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Bio 202 spring 2005 first web paper Forum


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Putting the Self in the Brain
Name: Joanna Sco
Date: 2005-02-19 15:11:32
Link to this Comment: 13016

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In a quest to separate ourselves from other species, we have attempted to distinguish humans as somehow special and superior. Before Nicholas Copernicus (1473-1543), it was assumed that we lived at the center of the universe. It is still widely accepted that humans have unique, more advanced capabilities that other species, even other higher primates, must lack. Philosophers and scientists have for years have attempted to tackle the problems of consciousnessperhaps one of the most important concepts in what it means to be human. Most animals (and to an extent, other organisms including plants) have some level of "awareness" in that they can sense and respond to environmental stimuli, although it is not commonplace to describe their behaviors in terms of awareness. Humans possess another type of awareness: awareness of themselves, both in terms of their body interacting with their environment and of their body as being whole and belonging to them. To explore this sense of self, cases where the body is an altered state from how the brain perceives it are particularly useful. Using the phantom limbs phenomenon as a model, can we put the self in the brain?

The occurrence of phantom limbs has been described throughout history. Silas Weir Mitchell first coined the name 'phantom limb' in 1871, after soldiers in the Civil War described vivid sensations in limbs that had been amputated after injury (5). Experiencing a phantom limb can, quite understandingly, cause a great deal of distress. The feeling is precise in its location and qualitatively very real. The most commonly reported sensations are pressure, warmth or cold, dampness, itchiness, and many different kinds of pain. As many as 70% of amputees experience pain in their missing limb (3). Phantom limbs often move in coordination with the rest of the body, behaving essentially as the normal limb would. For example, a phantom leg will bend when the amputee is in a sitting position. In some cases, though, the limb may feel stuck in an awkward position. In one case, a man turned sideways whenever moving through a doorway to avoid hitting the wall with his phantom limb, which he believed was stuck at a right angle from his body (3). These varying sensations persist throughout the course of the amputee's life. Children and adolescents also experience phantom limbs, especially in the case of traumatic amputations. One study found that 33% of individuals who were born without a limb or who had an amputation in the first 6 years of life still experienced phantoms (7). This finding is perhaps one of the most controversial, as it casts into doubt theories which explain phantom limb phenomenon in terms of nerve memory.

Ren Descartes (1596-1650) used phantoms as proof of his argument that all sensation is located in the brain. He reasoned that the "the whole mind seem[ed] to be united to the whole body", but noted that "if a foot or arm...is cut off, nothing has thereby been taken away from the mind" (1). Descartes believed the mind is unified, while the body is more fragmentary in nature. More recently, scientists in the field of cognitive informatics have described the mind's relationship to the brain as that of a program to a computer. Wang believed phantom limbs shows that the mind is "partially programmed and partially wired" and that phantom sensations occur at the lower (programmed) level of the brain which cannot be eliminated, even though higher layers may be overridden or modified (6). Descartes and Wang are essentially saying the same thing, although their terms (and potentially, their underlying beliefs about the mind/brain distinction) differ: there is something in the brain which causes sensation in the missing limbs and perhaps 'believes' this limb is still present.

One of the most fascinating characteristics of phantom limbs is that they are experienced as part of the self, not as foreign entities by any means. The missing arm or leg feels very much like part of the amputee's bodyit belongs to them. This is not unique to amputees; phantoms occur in numerous other conditions, including paraplegia, brachial plexus avulsion (where the nerves from the arm are disconnected from the spinal cord), and in patients whose spinal cords have been anesthetized. In these cases, the spinal cord is not operating normally by sending signals to the brain from the body. Yet they experience sensations in the affected extremities and identify those parts of the body as their own. This suggests that the sensations and the affected person's experience of their limbs in a certain position is generated in the brain.

A series of observations of brain lesions have highlighted the role of the right hemisphere in the sense of self. In a comparison left hemisphere (LH) and right hemisphere (RH) lesions, acute lesions on the RH caused more severe disruptions in self-image and self-awareness in relating the self, visually and emotionally, to the environment (2). In left-sided hemispatial motor neglect, lesions on the right side of the brain impair the movements of extremities on the left side of the body. The muscles are still functional and can be activated on commands from an observer. When the same lesion occurs on the LH, however, the RH is able to accommodate and activate the right-sided muscles. This suggests that the defect ultimately stems from impairment of the sense of self, which occurs with right-side damage. Unilateral neglect is more extreme; it can affect visual, tactile, and auditory stimuli in any combination. Again, the motor and sensory functions are still in tact, yet cannot be initiated or activated on the patient's own. In the case of Anosognosia, the affect patient can no longer identify their left arm as belonging to them and experience hemiparesis (weakness or slight paralysis) in the left-side. What is most remarkable in such cases is that the LH is oblivious to the damage and patients continue to hold false beliefs about their abilities even in the face of information (from doctors and from their own visual input). Patients with phantom limbs are able to 'correct' their feelings through visual and tactile input. Some have even found tactile input beneficial in coping with painful phantom sensations; massaging the stump and applying heat decrease the pain (2). Their sense of self is intact; they experience their sensations as part of them. Anosognosia, however, is essentially a delusional disorder and their sense of self is severely disturbed.

Another interesting case is that of the phantom supernumerary limb, sometimes called the 'alien hand syndrome'. As the name implies, people experiencing a phantom supernumerary limb experience an additional limb. Both the real and imagined limbare perceived simultaneously and, similarly to other phantoms, these sensations persist over time. The sense of self under normal conditions results in one, unified concept of the self and the body. With supernumerary phantoms, there are multiple conscious representations of a particular body part. McGoinigle, et. al studied one particular case, that of subject E.P., a stroke patient with a right frontomesial lesion. She experienced a 'ghost' left arm which she described as "having a will of its own," and less often, a ghost left leg. This began immediately after her operation. Similarly to phantom limb sufferers, E.P.'s perception of the ghost is "cancelled by vision of the normal left arm or leg" and prevented by "continual tactile stimulation" (4). Unlike phantom limbs, the supernumerary limb is the result of brain damage. E.P.'s phantom does not feel like an ordinary limb, but rather interferes with her body and feels out of her control. Her phantom conflicts with her sense of self and this distortion occurred after a RH lesion.

There are several theories which aim to explain phantom limbs and similar phenomenon in terms of the nervous system. Nerve memory is an older theory which essentially states that the stump of amputees continues to generate impulses. These impulses act as normal sensory signals, sending a message through the spinal cord and into the thalamus and cortex in the form of action potentials and resulting in sensations at the specific site. Yet how can there be a 'memory' in the case of people born without a limb? Another blow to this theory is the unsuccessful treatments for pain that cut the nerves above the neuroma, or at the roots where the sensory nerves divide into smaller branches before entering the spinal cord (3). Amazingly, the pain returns and the presence of the phantom itself never disappears. This follows from the phantoms that occur in paraplegics and other such patients, making it very unlikely that nerve endings alone can account for phantoms. Melzack has recently proposed that the brain contains a "neuromatrix" which responds to sensory inputs and "continuously generates a characteristic pattern of impulses indicating that the body is intact and unequivocally one's own" (3). He calls this pattern a "neurosignature" and suggests that that its connections are largely prewired and determined by genes. He does acknowledge a role for experience in modifying the synapses of the neuromatrix. In other words, connections may be added, deleted, strengthened, or weakened, through experience. His model implies that the neuromatrix can function on its ownthe brain is generating its own inputs in the absence of external stimuli. His proposal is a good fit with our current observations; it will be interesting to see how it holds up over time and with new information.

The right hemisphere has been implicated in various conditions affecting the sense of self and of the body in relation to space, yet it cannot be fully understood without considering the role of the left hemisphere. The LH has been identified as the site of language and communication processes. Although beyond the scope of this paper, language may play an important role in consciousness as a whole. The specialization of language in the LH may by responsible for the RH's dominance in self-awareness via a "crowing out" mechanism (2). At some point in our evolutionary history, both hemispheres may have been responsible for our perception of self and of spatial relations. The RH may have become increasingly responsible for these skills, as development of language took place in the LH. This could have several implications, including the possibility that animals lacking language and communication in the traditional sense may still have a self-awareness, although without the lateralization seen in humans. The concept of animals possessing awareness is a difficult pill for many to swallow. And what would this mean for our use of animals in experiments and the notion of humane treatment? Perhaps sense of self does not make humans special at all; but if the search for it will likely lead us to the brain.

References

1)Descartes, R. The Philosophical Writings of Descartes, Volume 2. Trans. J Cottingham, D Murdoch, and R Stoohoff. Cambridge: Cambridge P, 1984.

2)Devinsky, O. "Right cerebral hemisphere dominance for a sense of corporeal and emotional self." Epilepsy & Behavior 1. (2000): 60-73.

3)Melzack, R. "Phantom limbs". Scientific American: Mysteries of the Mind.(1997): 85-91.

4)McGoinigle, D.J., et al. "Whose arm is it anyway? An fMRI case study of supernumerary phantom limb." Brain 125. (2002): 1265-1274.

5)Wade, N.J. "The legacy of phantom limbs". Perception 32. (2003): 517-524

6)Wang, Y. "On cognitive informatics." Brain and Mind 4. (2003): 151-167.

7)Wilkins, K.L., et al. "Phantom limb sensations and phantom limb pain in child and adolescent amputees." Pain 78. (1998): 7-12.


Increased Incidence of Depression in Women
Name: Beverly Bu
Date: 2005-02-20 17:36:50
Link to this Comment: 13041

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip



Among psychiatric disorders, depression is one of the most prevalent. Studies conducted on worldwide populations suggest that women are two to three times as likely as men to become depressed in their lifetime (1). While there are similarities in the factors contributing to depression in both sexes, depression in women is subject to the influence of additional factors such as environmental and hormonal changes.


In general, depression is a psychiatric disorder caused by biochemical alterations in the brain. This description of the disease is useful in the broad view of the ailment, however, it is not completely understood what causes the changes that influence the disorder. The most common symptoms of depression include unexplained feelings of sadness, worthlessness, guilt, loss of interest in pleasurable activities, loss of appetite, anxiety, insomnia, inability to concentrate and thoughts of suicide (4). It is estimated that of those that suffer from depression, 15 percent commit suicide (2).


An understanding of how depression develops may be approached by examining some aspects of brain function, beginning with brain composition. The brain is made up of nerve cells called neurons that participate in an intricate form of communication via biochemicals called neurotransmitters. Many different neurotransmitters exist in the brain, but there is a class of three specific neurotransmitters called monoamines that play a role in of some of the drives and moods that we experience: serotonin, norepinephrine, and dopamine. These chemicals are generated within neuron cell bodies found in the brain stem and distributed to other parts of the brain via a branched system that spans many regions of the brain (3). Delivery of neurotransmitters takes place across a space between neurons called the synaptic cleft. One group of neurons, the presynaptic cells, sends neurotransmitters while another group of neurons, the postsynaptic cells, receives neurotransmitters. The signals from the presynaptic cells are responsible for activating or inhibiting a reaction in the postsynaptic cells. A malfunction of the presynaptic cells (the cells that generate monoamines) can prevent the proper functioning of brain regions such as the amygdala, the hypothalamus and the cortical areas all parts of the limbic system that control emotions, libido, appetite, sleep and cognition resulting in the symptoms defined as depression (2). For example, the excessive reuptake of serotonin and/or norepinephrine by the presynaptic cells can create chemical imbalances and has been implicated in most cases of depression. Further imbalances of monoamines may also be the result of monoamine oxidase, an enzyme that degrades neurotransmitters (2). Causes of monoamine insufficiency differ among individuals, but current treatment methods focus on inhibiting enzymes that degrade these neurotransmitters as well as blocking the presynaptic uptake of norepinephrine and/or serotonin. Ultimately, these treatments seek so maintain elevated levels of monoamines, specifically norepinephrine and/or serotonin as they are critical to the function of the limbic system (1).


Additional sources of depressed moods may also result from hormonal responses to stress. When an individual receives a stimulus that elicits the fight or flight mechanism within the body, a cascade of hormonal events follows which ultimately produces symptoms of depression such as appetite reduction, anxiety, and insomnia. The hypothalamic-pituitary-adrenal axis (HPA) is the control center for this physiological reaction to stress and hyperactivity in the HPA axis has been identified as the most likely source of stress related depression (2). While short term exposure to the HPA axis response may be beneficial in life threatening situations, the long term effects of HPA axis hyperactivity can be detrimental to the body's delicate sense of equilibrium.


Aside from the above mentioned factors that influence depression in both men and women, there are additional factors that influence the incidence of depression in women. The continuous yet fluctuating presence of estrogen in the system of a woman is believed to contribute to depression due to its varying effects on different biochemical substances and physiological processes. One substance that is generated in the HPA axis system is cortisol, a hormone that heightens the metabolic and immune system response to stress. Excessive levels of cortisol can result in a burn out of these systems. Estrogen has been found to indirectly increase cortisol levels by interfering with feedback mechanisms that naturally regulate its secretion thereby generating a more enduring and powerful stress response than that found in men (1). Estrogen levels are also believed to cause reductions in serotonin levels resulting in premenstrual syndrome (PMS). These findings suggest that the state of depression, agitation and irritability that characterize PMS is not simply a mentally fabricated ailment as was once believed by physicians (1).


Seasonal changes are also at fault for producing symptoms of depression, especially in women. Seasonal affective disorder (SAD) is a form of depression that results from the seasonal changes in the availability of natural light. The human body responds to a decrease in daylight by producing a hormone called melatonin, which creates a sense of sleepiness. As daylight approaches, melatonin levels fall off with a resulting increase in alertness (5). Studies have found that while melatonin levels in men are constant year round, melatonin levels in women decrease in the summer and increase in the winter. This winter time increase in the hormone is believed to be a factor in the higher incidence of SAD among women (1).


The additional contributors to depressive disorders in women such as estrogen and seasonal changes appear to be the differentiating factors between rates of depression among men and women. Although the situations referenced above are examples of the pathological extremes of these differences as they relate to depression, an interesting question that arises from this conclusion is how subtle variations of these differences influence women's behavior and the experience of being a woman in general.


References

1) Leibenluft, Ellen. "Why Are So Many Women Depressed?" Scientific American 1998: 31-35

2) Nemeroff, Charles B. "The Neurobiology of Depression" Scientific American June 1998: 42-49

3) A Brief Overview of Neurotransmitter Distribution and Function (abstracted from Physiology of Behavior 7th Ed, 2001, by Neil Carlson)

4) Depression , National Institutes of Mental Health, National Institutes of Health web site

5) Melatonin: The Basic Facts , The National Sleep Foundation web site


The Impact of Epilepsy on Memory
Name: Camilla Cu
Date: 2005-02-20 20:52:33
Link to this Comment: 13046

<mytitle> Biology 202, Spring 2005 First Web Papers On Serendip

Epilepsy is an enigma in many ways because scientists and clinicians are still searching for answers regarding causation, treatment, and how to differentiate it from other seizure disorders. Because of the unanswered questions concerning the disease, many people living with the disease are fearful of seizures, for the onset is abrupt and it can strike at any moment. My best friend from high school who was diagnosed with the disease at age 18 recently related to me an occurrence that had happened during one of her seizures. She was sitting in her room studying and all of a sudden she began to have a seizure with convulsions. Her roommate immediately called an ambulance. However, it appears that during the seizure my friend Liz got up from the floor and went to the door to greet the EMS workers. She then collapsed onto her bed. Interestingly, she had no memory of greeting the workers at the door and she only was aware that this event took place because her roommate told her later on. In fact she had no memory of the seizure at all, which is apparently the normal response for an epileptic post seizure. My friend Liz has primary generalized epilepsy, which means that when a seizure occurs the whole brain is impacted rather than a specific localized area (5). After hearing about this incident I was concerned about the affect that epilepsy has on memory. I was left wondering how the seizure itself can impact memory, which parts of the brain correspond to which types of memory, and why it is the case that Liz does not remember greeting the EMS workers?

An epileptic is defined as a person who has experienced multiple seizures and all other possible reasons for the onset of a seizure- besides origination in the brain- such as high fever or injury, have been ruled out. The seizure occurs when the chemical message being sent from the axon of a single neuron to the dendrite of a fellow neuron gets excited and the excitation overwhelms the inhibition. This chemical exchange happens on a grand scale in the epileptic brain. As we learned in class once an action potential is reached there is no turning back. Thus the neurological impulses are firing out of control with no inhibitory influences to counteract them (5). As a result of the firing the epileptic loses control, and they can experience severe convulsions, during which the person is not aware of their surroundings (1). When Liz got up to greet the workers she was in a cognitive state where her brain was unable to learn and acquire new knowledge of her surroundings. She was thus unaware, and in a temporary state of "post-ictal confusion" (1). Since the epileptic cannot describe the seizure incident clearly, because they have no memory of it, I can imagine that it is difficult for physicians to fully understand the patient's experience while the seizure is occurring. The only thing physicians can do is observe the behaviors of the patient and measure brain activity on an EEG. Thus the picture of epilepsy remains incomplete.

Besides being physically dangerous, (a person can hit their head or bang into something), seizures can also cause neurocognitive damage. An especially long series of convulsions or multiple seizures all at once are more dangerous to the brain than a single short episode, because brain damage is more likely (1). The term status epilepticus refers to repeated generalized seizures without return to consciousness between the events. Depending on which part of the brain the seizure affects, this will determine the type and extent of the damage if any that will take place. One region of the brain that has been found to be especially vulnerable to repeated seizures is the hippocampus. (6) The hippocampus is a region of the cerebral cortex located in the temporal lobe and is involved in learning and memory. The hippocampus plays a key role in allowing new information to be imputed in the brain's memory storage systems (3). The excitatory neurotransmitter, glutamate, and the excessive stimulation of glutamate receptors may be responsible for the neuronal damage in the hippocampus. This phenomenon has been referred to as excitotoxicity (6).

Liz reported problems recalling tasks that she needed to accomplish the next day that she had planned to do the day before her seizure. She had planned to go to the gym with two of her friends and when she didn't remember to show up they became alarmed. This forgetfulness of future events may have been due to slight damage sustained in the frontal lobe, which is responsible for recalling upcoming events and plans. It might also be due to the fact that she takes AEDs (anti-epileptic medications), which can affect your short-term memory. Other areas of the brain such as the temporal lobe affect learning, whereas long-term memory is distributed throughout the brain (4).

Besides her inability to remember to go to the gym, Liz described her feelings post seizure as being "foggy" and "confused". She took a lot of naps and felt like she couldn't concentrate on her homework. After a few days the feelings faded but they kept her out of commission for a while. Whether these feelings of fogginess were due to the seizure itself or the AEDs is questionable. Since AEDs can often cause you to feel tired and effect your capacity to learn (1), increasing the dosage after a seizure in order to limit the chances of another one occurring, will generally make the patient more susceptible to these side effects.

Interestingly, pre-seizure the feeling of fogginess was also present but in a more pleasant way. Described as a feeling of "Deja vu " or a "gratulant" feeling, a generalized euphoria or experience of altered consciousness can come over a person before they begin seizing (4). Experiencing an "aura" is another indicator of the onset of a seizure (2). The aura or fuzzy feeling is due to the onset of excessive firing of neurons in the brain (4). However, some people experience nothing unusual before a seizure and thus have no indication that they are going to have one.

After hearing my friend's account of her seizure and reading about the causes and effects the disease has on memory it seems that the main causes of memory disturbances are brain damage from the seizure itself, the side effects of the AEDs, the after effects of the seizure or "fogginess", and the"post-ictal" confusion experienced during the seizure. I am still left with the unanswered questions of why some patients experience the feeling of an "aura" while others don't, and how Elizabeth was physically able to get up and go to the door during a seizure. There are many aspects of epilepsy that are still not completely understood, which is the reason why more research is needed in this field. In order to pioneer a cure we must first have a more complete understanding of the disease itself.

References

1)National Society For Epilepsy, info on the disease, causation, and treatment
2)The Brain Matters, From the Serendip website list.
3) Bear, Mark F., Connors, Barry Q., and Paradiso, Michael A. Neuroscience Exploring The Brain (2nd ed.). Baltimore: Lippincott Williams & Wilkins, 2001.
4) Gellatly, Angus and Zarate, Oscar. Introducing Mind And Brain. New York: Totem Books, 1999.
5) Gumnit, Robert J. (2004). Neither Gods nor Demons But Misfiring Brains. Cerebrum, Vol 6, number 2, 27-40.
6) Jessell, Thomas M., Kandel, Eric R., and Schwartz, James H. (ed.). Principles of Neural Science (4th ed.). New York: McGraw-Hill, 2000.


Music Matters
Name: Kara Gilli
Date: 2005-02-21 15:14:05
Link to this Comment: 13070

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


gWithout music, life would be a mistakeh (1). Although the famous philosopher, Friedrich Nietzche, was referring to the importance of music in his personal everyday life, could he also unintentionally be commenting on the effects of music and the evolution of the human brain throughout time? Would life as we know it, and the human brain be what they are today, without the development of music? The newest wave of research is trying to solve the question of musicfs role in early development, as a tool for therapy, and as a contributing factor in the evolution of the human species.

The ever-expanding knowledge of how the brain works has been aided by the development of brain activity mapping techniques, such as magnetic resonance imaging
(2). The results of studies demonstrating the effects of music on the brain are astounding. Music has been found to affect many different parts of the brain, rather than one distinct region. This makes musicfs effects very hard to explain in terms of neurological pathways, but it does help explain why music had such a profound power over us. People have been using music for years to help with cognition, pattern recognition, and better mental health.

Music, or more generally sounds, enters the body through the outer ear and travel into the middle ear region. The middle ear region turns the sounds in vibrations that stimulate the inner ear region, or the cochlea. The spiral shaped cochlea functions to then turn these sound vibrations into nerve impulses, which can enter the brain through the auditory nerve. Sounds are actually turned into nerve impulses by the organ of Corti, located in the cochlea. The impulses travel from the inner ear until they reach auditory cortex, located near the temple region of the head
(3) . From there little is understood as to how, or why, music then affects so many other regions of the brain besides the main auditory sensory region. Part of the problem of explaining music is the fact that sounds are taken in through the ears, but recognition and responses are controlled by other sections of the brain. So in order to appreciate anything more than just random beats and rhythms, other parts of the brain need to be involved (2).
It is important to note that the ear contains mechanisms to turn external stimuli into nerve impulses, as well as the ability to respond to nerve impulses coming from the brain. So, as discussed extensively in class, signals can be created in the nervous system itself, without outside factors, as shown by neurons of inner ear hair cells
(3). This type of response explains why it is possible to get a song stuck in your head (2).
The impact of music starts when a child is still in the womb. Doctors have presented the idea that a babiesf first experience with music is a motherfs breath, heartbeat, and the steady flow of blood rushing into the placenta. This might not seem like music to grown adults, but the repetitive rhythm, and patterns, of these biological processes are imperative to the development of important neurological pathways in the developing fetus. It is believed that neurons start developing at the rapid pace of 50, 000 a second in the embryo stage, and the growth of dendrites, or neuron cell
body extensions, is aided by music stimulation
(4). Audiotapes of heartbeats and womb noise have been shown to reduce stress, and help with higher oxygenation in newborns (8). Clearly the effects of just constant a constant melodious noise can do a lot to help with development, however the study still raises questions as to why these effects are working. Children for thousands of generations have survived and thrived without excess music stimulation after birth. Little can be known about the conclusions of the study till these children grow up and can be studied in comparison to other children.

Another widely growing area of research has focused on the social implication of music and evolution. Currently there are many hypotheses as to what role music has played in our evolution. Some say that music has always existed in some form, and it aided in courtship by males to win over a female. If a male could dance/ sing/ make pleasurable music of some kind, he was considered physically fit, and therefore had ggoodh genes that would be beneficial to pass on to future generations
(5). A musician, Niccolo Paganini comments, gI am not handsome, but when women hear me play, they come crawling to my feeth (6). As Niccolo jokingly points out, even today, there exists something inherently attractive about a man who can play music, regardless of his physical appearance.

Others say that musicfs role was less involved in a Darwinian aspect, but it had a more social function. Music brought people together, in larger groups to interact and from there, higher forms of social organizations could be established. Both of these concepts still follow the idea that evolution selected for music, and therefore there must be some area of the brain responsible for its hold over us
(7).

In direct juxtaposition, Steven Pinker of Harvard, has coined the phase that music is gauditory cheesecakeh
(7)E He believes that music is not a mechanism for anything but a little pleasure, or a mere by product that occurs because of the design of the brain. In other words, music played no role in our expansion as a species. The debate continues on as more and more evidence is revealed about the brain.

Based on class discussions and my own research, I am inclined to believe that music played some role in our development. Music has had too much of an impact in our individual development as a baby, and all parts of our daily life for me to believe that musicfs power over us happened by accident. Maybe music has so much power over us because it is not controlled by one region, but it affects many regions of the brain, giving us, in a sense a mental neurological massage.

WWW sources

1. < a name=g1h>1)< a herf=http://www.laurasmidiheaven.com/Quotes/Without-music-life-would-be-a-mistakeFriedrich-Wilhelm-Nietzsche-Quote.shtml.> quotations page


2. < a name=g2h>2)< a herf=http://www.nature.com/cgitaf/DynaPage.taf?file=/nature/journal/v416/n6876/full416012a> Nature website

3. < a name=g3h>3)< a herf=http://cognet.mit.edu/library/books/view?isbn=0262032562 > Bryn Mawr online resourse


4. < a name=g4h>4)< a herf=ghttp://www.edu-cyberpg.com/Teachers/brain.htmlh > teaching resourse

5. < a name=g5h>5)< a herf=ghttp://www.nytimes.comh> New York Times article

6. < a name=g6h>6)< a herf=ghttp://www.menc.org/networks/genmus/openforum/messages/3490.htmlh> quotations page


7. < a name=g7h>7)
< a herf=ghttp://www.sciam.com/print_version.cfm?articleID=0007D716-71A1-1179-AF8683414B7h> Scientific American article


8. < a name=g8h>8)
< a herf=ghttp:// www.transitionsmusic.com/study.htmlh> web article


It's a Matter of Neurons
Name: Leslie Ben
Date: 2005-02-21 16:44:23
Link to this Comment: 13071

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


"I can't control my fingers I can't control my brain"
-- The Ramones ((1))

It was only after attempting unsuccessfully to forge a friendship with a young woman recently diagnosed with bipolar disorder that I was swept into her whirlwind rapid cycling. Sometimes without any prior provocation she would burst into tears making the most light-hearted situations tense. With her pressure cooker emotions leaving me exhausted and confused, I commenced on finding simple answers for complicated processes. The manic-on-top-of-the-world-highs and the-jump-off-a-building-lows were draining for us both. After probing her for information on what lead to her roller coaster emotions and finding she knew little about her own affliction; it lead me to ponder how bipolar disorder affects and alters her brain activity.


Medically defined as intense episodes of mania and depression that disrupt everyday life, each period of emotional instability can last as little as 24 hours, known as rapid cycling, or may stabilize for weeks or months at a time ((2)). Such symptoms are debilitating for sufferers; pushing them from delusional exuberance to suicidal lows. Classified as a mood disorder, bipolar disorder affects normal brain activity in the limbic system ((2)).


From known research, the limbic system appears as a major influence on mood regulation within the brain. This distinct structure is composed primarily of the hippocampus (memory center) and the amygdala (fear center). Gland secretions from the hypothalamus also appear to be an essential component in mood management and stability ((2)). More specifically, the amygdala functions as an epicenter in which the frequency of neuron firings increase when brought into contact with stimuli. If repeated and excessive stimuli exposure occurs in this area the response from the neurons associated with the input becomes increasingly less potent. Thus, as the amygdala acclimates itself with increased stimuli the response time for an output is lengthened and the habituate remains reactive longer ((7)). This process works in conjunction with the hippocampus. In patients not demonstrating bipolar characteristics a layer of the hippocampus is responsible for processing information in such a way as to recognize dangerous situations. When the hippocampus functions erratically or abnormally axon deterioration occurs which stops connections from being made between neurons. As these axon connections no longer situate themselves with the memory center or hippocampus, bipolar sufferers can experience a "constant state of anxiety because [they] can no longer identify safe situations" ((7)).


The abnormal brain activity attributed to bipolar patients has been shown to elevate electrical signals being processed across the cerebral cortex ((4)). This has been evidenced by brain scan reports taken by an imaging technique known as positron emission tomography (PET). One of many techniques for understanding and evaluating brain activity it non-invasively gauges brain metabolism, put more simply it measures brain activity ((8)). With the assistance of PET scans scientists have been able to view and monitor the areas of the brain most active during times of emotional highs and lows. The scans produced by these machines generally display hyperactivity in the brain during manic periods ((4)). Brainplace.com researchers also credit the limbic system with increased metabolism during manic periods as witnessed from scan results. These neuron firings which originate without an input to the central nervous system can be drawn into comparison with similar patterns of activity that occur in the brains of epilepsy patients.


Although controversial and only one way of thinking, some scientists have drawn comparisons between brain activity in bipolar individuals and sufferers of epilepsy. This approach and the similarities that can be established between the two disorders have yet to be scientifically based. This theory may help scientists to critically explore why random cycling of emotions may be so prevalent amongst bipolar individuals. These ideas originating from Dr. Jim Phelps come to focus on the functions of the cingulate which is located in the limbic system. Operating as a metaphorical mediator, allowing an individual to shift their "attention from thing to thing, to move from idea to idea, to see the options in life"; the cingulate appears instrumental in establishing a balanced lifestyle ((5)).


In terms of appearance the cingulate possesses the "same squiggly pattern, even though it is deep in the brain, as the outside part of the brain" ((3)). This "means that limbic cortex is cortex just like "motor cortex" (the outermost part of the brain)" ((3)). This is an important parallel to establish since it is the motor cortex that is affected by abnormally high brain metabolism in epilepsy patients. Thus, if the disturbance that takes place within the motor cortex during an epileptic seizure was moved to the cingulate it can be hypothesized that the same phenomenon of overactive excitatory neuron firing patterns would occur. It is believed this transpires because of a loss of inhibitory neurons. Interestingly, epilepsy.com describes a seizure as "a sudden surge of electrical activity [...] that usually affects how a person feels or acts for a short time" ((6)). This explanation appears almost interchangeable with the known effects of bipolar disorder. This "sudden surge" of electrical activity is the basis of both conditions. Phelps believes there is "no reason to think that [the] cingulate cortex is any less likely than [the] motor cortex to end up having an epileptic area" ((3)). Essentially meaning that instead of an uncontrollable physical seizure that comes from the motor cortex, the disturbance would occur in the limbic system and thus an emotional reaction would come from the increased brain activity. Thus, Phelps explains what would take place as "emotional epilepsy" and therefore an uncontrollable seizure of emotions ((3)).


The concept of "emotional epilepsy" makes further sense when considered in conjunction with the types of medications prescribed to bipolar patients. There is a plethora of possible options all clouted for their minute uniqueness but overall "5 out of the 6 known mood stabilizers are anti-seizure medications" ((3)). Ultimately, bipolar patients are being prescribed known epilepsy medications, ones in which lower the risk of seizures.


These ideas on brain and behavior all work themselves back to being one more instance in which Emily Dickinson's hypotheses hold true since the pattern of neurons is constantly changing within everyone's brain ((9)). The brain to some extent is equivalent to behavior because for bipolar patients it is the excitatory neurons of the brain that prompt their erratic functioning and this constant activity prompts changes in brain structure. Dickinson would say it is these small differences that influence the different behaviors of each person. Thus, each person afflicted with bipolar disorder or epilepsy would have slightly different mood variations/cycling patterns/seizure schedules because their brain composition is not precisely the same as other sufferers.


Ultimately, a vast array of interactions between genetics, environment, and the brain must take place before a person suffers the effects of bipolar disorder. Brain activity alone cannot account for why symptoms of the disorder occur. Everyone experiences manic episodes and depressed states of mind at one point in their lives. So what I am left pondering is what exactly forces the elongation of these episodes in some and not in others. Genetics plays a role in why some people are more predisposed to the disorder but at what point does the brain activity move from normal to abnormal? Understanding the connections that can be drawn between bipolar and epileptic patients shows the essentialness of anatomical specificity in producing specific reactions and behaviors in particular portions of the brain. Thus, if bipolar disorder is in fact connected to epilepsy, sufferers may someday call into their place of employment "Nope, can't come to work today...Having an emotional seizure... Be back soon."

References

1. 1) Ramones Lyrics

2. 2) Mood Disorder: Bipolar Disorder , Emedicine website

3. 3)Mood, Jim Phelps, M.D.

4. 4) Images of Bipolar Disorder and Schizophrenia , The Amen Clinics Inc.

5. 5) Brain Function and Physiology , The Amen Clinics Inc.

6. 6) What is a Seizure , The Epilepsy Project

7. 7) Young and Bipolar , Time magazine

8. 8) Open Mind , Mental Health Association of Greater St. Louis

9. 9) Emily Dickinson's The brain is wider than the sky


Ecstasy, Brain, and Behavior
Name: Sonnet Lof
Date: 2005-02-21 18:36:46
Link to this Comment: 13072

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Everybody wants to have a good time. The problem with this is that sometimes 'having too good of a time' can be dangerous. The popular hallucinogenic and amphetamine drug Ecstasy, also known as MDMA, and Adam, has become all the rage. Upon coming to college I had of course heard of ecstasy in reference to New York City clubbers and young Hollywood stars, but it was not until the first couple of months into school when I realized just how mainstream this club drug is.

It seems like Ecstasy is everywhere. People are either preparing for it's use by way of scheduling activities that will allow them to exert their newly gained energy, or they are desperately trying to get their hands on it for the upcoming weekend. At first sight it makes sense, who wouldn't want an energy booster for a night on the town? However, Ecstasy can be fatal. Giving into temptation just once could change things forever.

Recreational use of Ecstasy is dangerous because it is not regulated by the FDA or subject to quality control, and no one knows what amount is considered a safe dosage 1)University of Arkansas for Medical Sciences. So if the level of danger is relatively high, then is the state of euphoria caused by the party drug of choice worth it? This question is obviously debatable as everyone is different, but without having seen the effects of Ecstasy on the brain, we would not be able to see the relationship between the brain and behavior.

Ecstasy is absorbed quickly into the bloodstream. Upon ingestion, Ecstasy is extracted by the liver and transmitted through the blood vessel wall to the brain. Since Ecstasy is mostly in its nonpolar form in the bloodstream, it can reach the brain within 15 minutes 2)National Institute on Drug Abuse. This quick flow to the brain aids in the rapid effects felt by the brain. When an Ecstasy tablet reaches the brain, the neocortex as well as the structures that comprise the limbic system are all affected. The effect of Ecstasy on these structures of the brain lead to changes in memory, perceptions, thinking, mood, emotions, and the production of anxiety 2)National Institute on Drug Abuse.

Ecstasy has had widespread recreational use because of the influence of those who have already tried the drug. The state of euphoria which is experienced by Ecstasy users involves the neurotransmitter serotonin. The use of Ecstasy causes serotonin neurons to release a large amount of serotonin which are stored in the axon terminals. The attachment of a serotonin molecule to a receptor causes the chemical information to be sent down the dendrite to the cell body of a neuron 3)A page for the promotion of health and safety within the rave and nightclub community. Research concludes that mood is influenced in part by the amount of serotonin receptor binding 3)A page for the promotion of health and safety within the rave and nightclub community. This might lead one to believe that Ecstasy provides evidence to confirm that Brain=Behavior.

An increase in serotonin levels causes the high felt by Ecstasy, but once the serotonin molecule detaches from the receptor, Ecstasy begins to deplete the serotonin levels in the brain which once deficient, cause depression 4)A page promoting youth wellness. Brain imaging research in humans has shown that Ecstasy may affect neurons that rely on the chemical serotonin to communicate with other neurons 2)National Institute on Drug Abuse. The depletion of the normal serotonin supply causes physical damage to the neurons which are used to secrete serotonin. This damage can cause the serotonin nervous system to be 'fried' or 'burned down', leading to potential long lasting depression. A depleting or low supply of serotonin will directly affect the regulation of mood, sleep, sensitivity, and aggression.

The effect of Ecstasy on the brain illustrates that Brain=Behavior. If individuals are using Ecstasy tablets in order to increase empathy, happiness, sociableness, sensation of touch, etc.,it can therefore be seen that the brain is essentially equated to behavior. Ecstasy is used in order to create these feelings and behaviors which might otherwise be nonexistent. The argument that Brain=Behavior is controversial, but it seems clear that if individuals are ingesting a tablet in order to gear themselves towards feeling and acting in a certain way, the direct relationship between Brain and Behavior exists. Whether or not the use of this drug is the most adequate way to demonstrate this relationship is altogether another question, but it seems as though that the desire to experience euphoria can be all too tempting.

The chemical name of Ecstasy is 3, 4-methylenedioxymethamphetamine. Synthesized in clandestine laboratories by altering the structure of the amphetamine molecule, the probability that an Ecstasy tablet will contain other drugs is high 2)National Institute on Drug Abuse. Such drugs that are likely to find their way in an Ecstasy tablet are ephedrine and caffeine. Because the purity question is at play, users must be extra cautious of what it is that they are putting into their body. In addition, the danger of Ecstasy is heightened by other factors. For instance, Ecstasy causes an increase in blood pressure and heart rate which makes it increasingly dangerous for individuals with heart conditions or high blood pressure 4)A page promoting youth wellness. Whether taking Ecstasy is worth it is up to the person. There are a variety of things that should be considered before making the decision. After all, making oneself happy is not that easy.


WWW Sources

1.) http://www.uams.edu/today/2002/032102/club.htm; University of Arkansas for Medical Sciences
2.) http://www.drugabuse.gov/pubs/teaching/teaching4/Teaching2.html; National Institute on Drug Abuse
3.) http://www.dancesafe.org/slideshow/slide11.html; A page for the promotion of health and safety within the rave and nightclub community
4.) http://www.ayn.ca/health/en/addictions/addiction_ecstacy.asp; A page promoting youth wellness


Understanding Intelligence
Name: Xuan-Shi,
Date: 2005-02-21 19:05:57
Link to this Comment: 13073

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


What is intelligence? While it is common to relate intelligence to IQ, or intelligence quotient, one should understand that IQ is a social construct. It refers to the scores on psychometric intelligence tests, which are constructed to measure qualities that enable people to be successful within that culture (1). Although intelligent behavior has different manifestations across and within cultures, it is intuitive to think that there may be underlying similarities in the brains of intelligent people. Does higher intelligence equate to larger brains and/or more synaptic connections between neurons? Can intelligence be localized to specific brain regions? This paper examines the major theories of intelligence and attempts to understand the concept of intelligence in terms of neuroanatomy.

Presently, theories of intelligence are divided into two camps: the psychometric and multiple intelligences approaches. Intelligence tests, such as the Wechsler tests, are typical psychometric instruments used to measure general intelligence, or g, for assessment and research purposes. The g factor was first proposed by Charles Spearman who also developed factor analysis (2), a statistical tool that has uncovered correlations among people's performance on groups of test items; this suggests that g underlies groups of specific abilities, as outlined in Spearman's two-factor theory of intelligence (3). Test items or tasks that involve a high degree of complexity have also been found to tap more heavily on g (4); one example is the Raven's Advanced Progressive Matrices (5). Thus, there is reason to believe that g is related to cognitive abilities, although g is not a cognitive ability by itself (2). Other researchers have since expanded on the concept of g. Cattell and Horn proposed that there are many types of g, including fluid (Gf) and crystallized (Gc) intelligences; Gf is "essentially nonverbal, relatively culture-free mental efficiency," while Gc refers to the skills and information acquired through acculturation (6). Carroll later superimposed a g factor, akin to Spearman's g, above the different types of general mental abilities, which also include Gf and Gc; the general abilities are in turn composed of specific abilities, such as general reasoning and induction that comes under Gf (6).

Howard Gardner and Robert Sternberg, proponents of the multiple intelligences approach, believe that intelligence consists of several constructs. Briefly, Sternberg's successful intelligence theory states that intelligence is comprised of three components: practical, analytic, and creative abilities (1). Gardner's multiple intelligences theory consists of seven intelligences: linguistic, logical-mathematical, spatial, bodily kinesthetic, musical, interpersonal, and intrapersonal. He has since suggested other intelligences: naturalist, spiritual, and existential (7). Gardner believes that everyone possesses seven intelligences that are in constant interaction with one another; they are utilized in different combinations to complete a task (8). Gardner's theory is of special interest to this paper because he has attempted to map out the brain areas associated with each intelligence, presumably drawing most of his data from clinical studies of patients with brain injuries (8). The observations that selective damage to a brain area impairs only a specific ability or "intelligence" and leaves other abilities unaffected suggest to Gardner that there are different intelligences, each of which may be localized to different brain regions.

Sternberg and Kaufman observed that since 1997, there were no empirical studies to test whether the multiple intelligences theory is valid (1). Despite its unpopularity among researchers, Gardner's theory is well-received by many in the field of education, which also uses psychometric tests to assess students. The fact that intelligence tests measure Gc, in addition to Gf, may contribute to the association of g with performance in academics. According to Gardner, most intelligence tests focus mainly on "linguistic and logical faculties" (5); traditionally, schools have nurtured these abilities or "intelligences." Seen in this light, Gardner's theory expands the concept of intelligence beyond what is measured on IQ tests, acknowledging performance in other domains. Gardner's expansive concept of intelligence is complementary to the idea that learners are unique individuals, with different strengths and weaknesses. However, does this imply that psychometric g is a reductionistic model of intelligence?

Psychologist Arthur Jensen believes that the "g factor reflects individual differences in information processing (9)." According to Jensen, tests that yield an IQ score correlate to some extent (6). Because these cognitive tests differ in their content and requisite skills, Jensen reasons that the correlation among them is not contaminated by the tests or the statistical tool of factor analysis; instead, loadings on g reflect an attribute of the brain (9). It seems reasonable for Jensen to view g as closely related to information processing capacity. At the level of the organism, information processing encompasses a wide range of cognitive functions such as attention, memory, and problem-solving. At the cellular level, a neuron both receives and transmits signals. If g is related to information processing, and given that information processing is a fundamental aspect of our nervous system, it is possible that g has a biological basis.

How are the brains of individuals with high g and average g different? In terms of neuroanatomy, MRI studies has previously shown that there is about a +0.4 correlation between brain size and IQ (9). More recently, Richard Haier et al (2004) first discovered that more gray matter in specific brain regions is associated with higher IQ, as measured by the Wechsler Adult Intelligence Scale (WAIS) (10). These regions include several Brodmann areas within the frontal, temporal, and parietal lobes. Interestingly, Gardner has also associated these lobes with several intelligences, such as interpersonal and logical-mathematical (8), although he did not name specific areas. Haier's study appears to endorse the idea that differing strengths and weaknesses of people with the same IQ arise as a result of differences in cognitive abilities associated with information processing, rather than from interactions among various intelligences. Such cognitive differences may be explained by the variation of gray and white matter volumes in brain areas that are associated with IQ (10).

If it is assumed that an individual with a high IQ score has a high g, then it is questionable whether g may be associated with gray and white matter location and volume. Is g an abstract function or does it has a material existence? With respect to Gardner's theory, one wonders whether poets have more gray matter in the same frontal areas identified by Haier's study, when compared to scientists with the same IQ. Does more gray and white matter in specific IQ-associated brain areas also translate into enhanced performance in certain domains under Gardner's theory? Theoretically, psychometric g and multiple intelligences theories are starkly different in the way each has conceptualized intelligence. In reality, the two theories may be different interpretations of the same neural map, as the existence of g is contingent on the variety of abilities or "intelligences" which one possesses.

Haier's study has also reported that the location of increased gray matter associated with IQ varies across age groups, i.e. young and middle-aged adults (10). Specifically, more gray matter in the frontal and parietal lobes are associated with IQ in the middle-aged cohort, while in young adults, more gray matter in the temporal lobe and less in the frontal lobe are associated with IQ. Comparing gray matter within the frontal brain region, the researchers found that the location of gray matter associated with g varies across different age groups. Haier et al suggest that the shifting pattern may be a response to age-related neuronal loss that is more likely to affect the frontal region, particularly the anterior cingulated gyrus, an area reported by Wilke et al (2003) to be associated with IQ in children (10). Given that Gf decreases with age while Gc remains relatively stable, could these findings relate to decreases in Gf? Taken together, these findings provide a dynamic and developmentally-sensitive view of intelligence that is influenced by biological mechanisms. Although Gardner's theory has also taken development into account, it appears that experience is the primary factor that brings about changes in the brain; Gardner claims that the seven multiple intelligences evolve with age and follow developmental trajectories in terms of emerging expertise.

To conclude, both the psychometric and multiple intelligences approaches contribute to one's understanding of intelligence. Studies emerging from neuroscience and cognitive psychology are more promising because they help one to better understand intelligence, as the g factor, in terms of individual differences in neurological and information processing systems. The multiple intelligences approach as a whole seems to convey the important reminder that intelligence is also influenced by experience and that intelligence manifests itself in different aspects of behavior. Clearly, how a society defines intelligence is likely to affect the ways in which it allocates resources among individuals. Therefore, the presence of different theories of intelligence is necessary to emphasize the idea that intelligence is not a fixed and concrete entity (11), which may be measured by culturally biased intelligence tests.

References

1)Human Abilties, An article by Sternberg and Kaufman that explores the definition of intelligence and provides a good summary of theories from past to present

2)The G Factor: the Science of Mental Ability, An article by Arthur Jensen, provides comprehensive and critical overview of psychometric g

3)Key Players in the History and Development of Intelligence and Testing, A very brief but organized introduction to the major intelligence theories

4)The General Intelligence Factor, A reader-friendly article on g that also discusses how g is measured

5)The Importance of Spearman's g, Reviews major intelligence theories and contains an informative section on the importance of g as an "educational and social construct"

6) Sattler, J. M. Assessment of Children: Cognitive Applications. 4th Edition. San Diego: J. M. Sattler, 2001.

7)Howard Gardner and Multiple Intelligences, Evaluates Gardner's multiple intelligences theory

8) Armstrong, T. Multiple Intelligences in the Classroom. Virginia: Association for Supervision & Curriculum Development, 2000.

9) Jensen, A. R. "The g Factor and the Design of Education." Intelligence, Instruction, and Assessment. Ed. Robert J. Sternberg & Wendy M. Williams. New Jersey: Lawrence Erlbaum Associates, Inc, 1998.

10)Structural Brain Variation and General Intelligence, The first study to report that more gray matter in specific brain areas is associated with IQ

11)Current Views of Intelligence Testing, 1997 Lecture notes created by Elizabeth Johnson


Vmat2, or the God Gene: Reading Spirituality in th
Name: Student Contributor
Date: 2005-02-21 21:07:19
Link to this Comment: 13081

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip



As Ishmael, in the great American novel Moby Dick, stares into the water from atop the Pequod, he thinks to himself: "There are certain queer times and occasions in this strange mixed affair we call life when a man takes this whole universe for a vast practical joke" (2).It is only befitting to start a paper concerning the spirituality gene, a phenomenon that threatens to mutate the very nature of religion, with a novel that arguably claims truth is imperfect by default. With the discovery of vmat2, the assumed spirituality gene, it is hard not to think as Ishmael does; imagine if, as a cosmic joke, evolution led us to believe God was our creator, when in actuality He was nothing more than a creation of our neuronal imagination. This begs the question: Which came first, God or the need for God? Or, in other words, is religion a phenomenon that was induced from external signals, such as that from God above, or did evolution instill in us a sense of the divine? (3).While the above question is arguably unanswerable, Ishmael's conclusion in Moby Dick of a perfect universe interpreted by imperfect laws should serve as a warning against adhering to one school of thought, such as science, over another, such a religion, for they are both battling internal discrepancies. By examining the experiments concerning vmat2, this paper aims to consider the implications of a spirituality gene.

Imagine Mecca in the Islamic month of Al-Hijja, millions of pilgrims from all over the world gather around the holy site of the Kabaa, performing the appropriate rituals in their white garments in commemoration of Hagar's search for water in the desert. It's not too hard to see the divinity in the movement of the pilgrims, the symbolic stoning of the devil, the final visit to the prophet's grave in Medinah. It's there in the faces from the Middle East, Europe, North and South America, and Asia. If divinity is so easy to feel, then why is it so hard to explain? Ask any believer of any faith to describe divinity, and they'll most likely say it's a feeling a sense of a higher power (3).

Molecular biologist Dr. Dean Hamer, in his recently published book The God Gene: How Faith is Hardwired into our Genes explored this "sense," or feeling of a higher power, and has concluded that it could possibly be the result of a gene known as vmat2. This gene may be directly responsible for an inherited predisposition for spirituality. Dr. Hamer narrowed his search for the suspected spirituality gene to nine specific genes known to play major roles in the production of monoamines. These chemicals include serotonin, norepinephrine, and dopamine, which regulate functions such as mood and motor control. A variation in a gene known as vesicular monoamine transporter, or vmat2, seemed to be directly related to how volunteers for Dr. Hamer's experiment scored on his self-transcendence test. Those volunteers with the nucleic acid cytosine in one particular spot of the gene scored higher than those with the nucleic acid adenine in the same spot (1).A single change in a single base of the gene seems to be directly related not to the belief in God, but to the increased probability that that individual will identify as spiritual. The results of Dr. Hamer's experiments are not wholly impressive, mainly because his work has yet to be repeated, and much of his analysis is provisional, but it does demonstrate the belief by some in the scientific community that spirituality is not a result of transcendence; rather, it is a result of chemical signals.

Similar, and one could argue, more convincing, experiments were done in 1979 at the University of Minnesota where investigators began tracking down 53 pairs of identical twins and 31 pairs of fraternal twins that been separated at birth and raised in different environments. The investigators were looking for traits the members of each pair had in common, particularly their disposition towards spirituality, assuming that the characteristics shared more frequently by identical twins would be genetically based because of their identical DNA. Their findings demonstrated that identical twins have plenty of things in common, such as migraine headaches or similar fears, but most importantly, identical twins showed a similar overlap in their feelings towards spirituality and religion, much more so than fraternal twins. The disposition towards spirituality did not translate into a degree of observance of a particular faith, something that the investigators agreed was significantly impacted by environment, but it did translate into whether we're drawn to God from the beginning (3).

The theory that certain individuals are predisposed to spirituality, more so than others, throws the concept of religion in a questionable light. How fair is it to demand observance of a particular religion as the sole ticket to heaven, when an individual's ability to believe is a consequence of genes, something the individual has no control over? Did God selectively place the vmat2 gene in certain individuals over others, or is God merely an invention of the brain? These questions have dominated religious spheres since vmat2's introduction into the public sphere. The consequence of believing in vmat2's function is to reduce religion to a genetic predisposition, such as breast cancer, leaving believers to wonder how genuine their faith really is. On the other hand, Hamer disagrees with the notion that the discovery of vmat2 directly implies the death of God. In fact he states: "If God does exist, he would need a way for us to recognize his presence" (1).He seems to think that the discovery of vmat2 does not function to replace divination, but to confirm its existence.

As the research is still premature, it is difficult to formulate an opinion regarding the matter. The discovery of vmat2 seems to imply that spirituality is equivalent to a genetic phenomenon, such as eye color or the inherited predisposition for a particular disease. Incomplete penetrance could account for why some individuals are more spiritual than others, Mendel's 1st law of segregation could account for why spirituality may skip a few generations in a family, and genetic mutations could account for religious fanaticism. It all seems to fall into place and, yet, there still remains a sense of dubiety. To take these notions seriously would reduce the human experience to nothing more than a few interactions between brain chemicals. While some might find this notion comforting, others will find it unnerving, for "what is man that he should live out the lifetime of his God?" (2).This paper offers no solution to the above concerns for the sole reason that there is no solution, no answer that will result in the final 'aha' moment. It only offers this: a warning to those who try and claim truth either by scientific discoveries or religious revelations there will always be something lacking.

References

1) Hamer, Dean. The God Gene: How Faith is Hardwired into Our Genes. USA: Random House, Inc., 2004.

2) Herman, Melville. Moby Dick. New York: W. W. Norton & Company Inc., 2002.

3)Is God in Our Genes, Times 25 Oct 2004

4)God and Evolution, New York Times 12 Feb 2005


Compulsive Overeating Disorder: Genetics Vs. Behav
Name: Sofya Safr
Date: 2005-02-21 21:17:42
Link to this Comment: 13083

There was a case of two British children* who, from the age of four months, were overcome with an unappeasable hunger that came to control their lives. By the time Jenny was eight years old, she could no longer walk and had to be put into a wheelchair, while John, at the age of two, could eat 2,500 calories in just one sitting. As they grew older, their parents were forced to lock refrigerators and cabinets; however, the children would rummage through the trash and anywhere in the house trying to find some food they could eat. Professor Ellen Ruppel Shell published a book called "The Hunger Gene" and investigated the case of these two children (1). Her book touches upon some interesting discoveries.
There are more than 200 genes involved in appetite and weight regulation, and a missing gene, even one, can prevent a person from feel full. In 1994, a gene called Leptin was isolated and found to work as an appetite inhibitor. Those missing this gene may eat and eat because their bodies are telling their brains that they are starving. It turns out that Jenny and John were both missing this gene. Leptin injections fixed this problem and the children lost a significant amount of weight very quickly. We now know that in this case, the missing gene was the cause for their insatiable hunger and overeating. However, Shell touches upon the fact that only 12 people in the world have been found with this deficiency (1). A mutated gene may also be a problem: The melanocortin 4-receptor, as a healthy gene, makes a protein that controls appetite in the brain. A mutated version of this protein may cause it too be too small to affect appetite control, therefore making a person with this mutated gene feel less full (2).
How can we explain compulsive overeating for those who do have the Leptin gene? Is there another factor contributing to the feeling of being sated, or are compulsive overeaters to blame themselves for their overweight or obese conditions? Are our bodies in thrall to our genes, or can we also blame obesity on fast food chains and the huge portions of foods that are high in fat and sugars? Can an overeater overcome his or her problem with therapy? We can see that in Jenny and John's case, it was a genetic problem that was solved with the replacement of Leptin. What causes compulsive overeaters, without a genetic mutation, to develop this disorder? Are compulsive overeaters without genetic mutations afflicted with a chemical change in their brains following this disorder? Could this be compared to a drug addiction? Or is it environmental and social factors that begin early in childhood that cause behavior problems such as compulsive overeating? Let's explore this question.
Compulsive overeating is characterized as an addiction to food and relying on food for comfort or distraction from problems such as stress and emotions. People suffering from this disorder tend to feel guilt and embarrassment after eating too much, and this can lead to a destructive path, like drug use, which leads compulsive overeaters to turn to food once again to hide from this guilt and embarrassment (3). It is important to note that not all compulsive overeaters are overweight or obese; in fact, compulsive overeaters may be of "normal" weight by binging after overeating. This can be caused by many factors such as obsessing over body weight and dieting. Someone who attempts to lose weight by dieting may end up breaking down and overeating, and may perhaps end up throwing the food up (3). I know that when I have tried to cut back any carbs, sweets or sugars, I have ended up having caving in and overloading on carbohydrates and sugars. For people very concerned, even obsessed with their weight, this could become very dangerous and detrimental to their health.
This leads me to consider external environmental factors that could assist in a person's development of compulsive binging. Society today is very weight oriented: Everywhere one looks, one sees extremely thin models in magazines, television and movies, on the runways and in society. Most magazines such as "Glamour" or "Cosmopolitan" present cover girl models or actresses who are very fit, and therefore considered by our society as beautiful. The word thin clearly equals beauty and acceptance in our world today, while the word fat tends to be associated with lack of self-control, laziness, and many more unfair stereotypes. It is no surprise that people, especially women, feel the pressure to be thin.
For most people, it seems that medical treatment and continual monitoring can help compulsive overeaters overcome this disorder. Patients have tried psychotherapy and find it helpful, which hints that overeating may be a mind over matter problem. Perhaps a person can actually be full, and even feel full, yet for some reason they continue to eat. However, I believe that this is something that takes a great deal of will power and support to overcome. Psychotherapy focuses on the behaviors that are associated with compulsive overeating, and changing these behaviors in order to overcome compulsive overeating. It may also help to identify the causes of the disorder, such as personal issues, childhood problems, recent deaths or losses, relationship problems, etc. There has also been a discovery of several new medications that may adjust the brain chemistry that could be responsible for compulsive overeating. Compulsive overeating, which may be linked to depression, could also be treated with antidepressants (4).
In conclusion, compulsive overeating and compulsive binging may be caused either by genes, or by external environmental factors, which may change behavior and eating habits. I have learned that there is an "obesity" or "hungry" gene, which presupposes that victims of compulsive overeating are genetically inclined to have continual hunger, although their bodies may tell their brain that they are indeed full. On the other hand, it may be argued that this is not true for either all or any compulsive overeaters; it may be a problem of associating food and eating with getting away from one's problems. Either way, it is an issue that should be looked at both scientifically and sociologically to help determine a successful treatment.


Sources:
(1)http://www.telegraph.co.uk/health/main.jhtml?xml=/health/2003/01/14/hfat12.xml&sSheet=/health/2003/01/14/ixhmain.html
(2) http://cms.psychologytoday.com/articles/pto-20030325-000001.html
(3) http://cms.psychologytoday.com/conditions/overeating.html
(4) http://recovery.hiwaay.net/special/compulsive.html
* Names have been changed to protect identity
<mytitle>
Biology 202, Spring 2005
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The Nervous System: The Ultimate Athlete
Name: Amy Vendit
Date: 2005-02-21 21:31:39
Link to this Comment: 13084

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Biology 202, Spring 2005
First Web Papers
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What makes Terrell Owens of the Philadelphia Eagles such a fantastic football star? Or Tiger Woods a great golfer? How is 5 foot 11, 165 pound Allen Iverson, on the Philadelphia 76ers, able to maneuver his body in such a way allowing him to score 60 points over 7 foot players in a basketball game. Why was Michael Jordon, one of the best basketball players ever, not able to excel as a baseball player? How was hockey player Wayne Gretzky able to get a shot off so quickly? (1) Believe it or not, the answer to each of these questions is the same: the nervous system. It seems that it is not merely skill, training, practice, muscle mass, or drive that makes a super athlete. The nervous system is responsible for producing naturally amazing, record-breaking athletes.

Although the nervous system has the power to create highly successful athletes, it is also responsible for the failure of certain athletes. For example, the heavyweight champion, Muhammad Ali, developed Parkinson's disease due to the fact that he was born with a weak substantia nigra, an area of the brain that helps to control movement. Lou Gehrig, the only one of Babe Ruth's teammates who gave him a run for his money, suffered from the disease amyotrophic lateral sclerosis, now known as Lou Gehrig's disease. (2)It was this disease, stemming from Gehrig's nervous system, which ended his career as well as his life; however, it may have also been Gehrig's nervous system that allowed him to be such a tremendous baseball player. Mutations, or quirks, within the nervous system can cause diseases such as Lou Gehrig's disease, a stunted substantia nigra, and Tourette's syndrome, but it may also be these same quirks within the nervous system that cause extraordinary quickness, hand-eye coordination, and athleticism in general. (3)

If we assume that brain equals behavior, meaning that everything is encompassed within the brain, than it can also be assumed that athletic ability is in the brain. However, much like the nature verses nurture argument, it is argued as to where athletic skill originates; whether or not one is born athletic. Muscle control and movement occurs when the electrical signals are sent via neurons from the brain and spinal cord throughout the body to the muscles. The motor cortex area of the brain controls movement by keeping almost a diagram of muscles used throughout the body. This area of the brain remembers muscles that are used and enables them to be electrically stimulated when needed. (4)

In a newborn baby, the motor cortex area of the brain is not completely developed. This is why a newborn baby's movement is limited to sucking, swallowing, and breathing. As the motor cortex area, or motor strip, within the brain begins to develop, the baby is able to perform simple gross movements, such as lifting the head. Despite the simplicity of gross movement, muscle control is much more complicated than it seems. In short, an electric signal must be sent from the brain to the muscle; however, a multitude of nerves and neurons are involved in this process, which all must be working adequately. After the signal has been sent through nerves insulated with myelin, and the muscle cells receive the signal, the muscles must then respond. It is incredible that this whole process occurs all of the time within a fraction of a second. Therefore, it is no small feat for a young child to perfect a motor skill such as walking. (5)

Not only do all of the child's nerves, neurons, and muscle cells need to be working and in conversation with each other, but the child also has to perfect such skills as balance and posture. Recall that the motor cortex area of the brain has a diagram of muscles that need to be used throughout the body. In the brain of a newborn baby, this diagram consists of only the muscles needed to suck, swallow, and breath. As the child's brain begins to develop further, and new muscles are discovered, such as those needed for balance and posture, these muscles are added to the muscle diagram in the motor strip of the brain. Therefore, it can also be assumed that as athletes learn new skills involving the manipulation of different muscles in different ways, this is information is added onto the muscle diagram. Thus the brain is constantly growing wider and changing to accommodate new and different skills. (6)

Since muscle control obviously originates from the brain, and the brain expands when new skills are learned involving new muscles and new sequences of muscles, it can be stated that athleticism originates in the brain. Therefore, success on the court or the field depends as much on the neurology as it does on physiology. There are three separate motor systems of the brain and spinal cord that control movement: the pyramidal tract (corticospinal tract), the cerebellar system, and the extrapyramidal system. The pyramidal tract is the part of the brain that directs movement, in the sense that the pyramidal tract transports the message that movement is needed to the motor neurons. The message that is transported to the motor neurons directs the spinal cord as to what specific movement is desired. The pyramidal tract also tells the spinal cord the sequence in which the specific muscles should be moved. For example, think about shooting a basketball. The whole body is involved in this task, not just the arms and hands. Therefore, the pyramidal tract must tell the motor neurons and the spinal cord that they need to direct muscles to shoot a basketball. Then the pyramidal tract must tell the motor neurons and the spinal cord to first grip the basketball with the hand muscles, then bend both knees, bend elbows, push the ball up, etc. The pyramidal tract is the director of movement, thus the output of movement depends on this tract. (7)

The cerebellar system, which is in the cerebellum area of the brain, is working all of the time controlling synergy and coordination of muscles. The cerebellar system works whether one is moving or not. Going back to the example of shooting a basketball, the cerebellar system allows for the coordinated movement of each muscle to make a smooth basketball shot, as opposed to each muscle working on its own, which would result in jerky movement. So far, we have discovered that in order for one to shoot a basketball, the pyramidal system must first direct the movement and sequence of muscles to be moved. Then the cerebellar system coordinates and synergizes the movement, so that the basketball is released in on smooth continuous movement. (7)

Assuming that this is all that is needed to shoot a basketball, then why shouldn't one be able to score all of the time? The cortex has measured the distance from the basketball, the weight of the ball, and thus the amount and sequence of muscle needed. The cerebellar system is working automatically, coordinating muscles. The third tract within the motor strip of the nervous system is the extrapyramidal tract. This tract travels directly from the brain to the spinal cord. It is the extrapyramidal tract that controls posture and balance. As new skills are learned and new muscles used, the extrapyramidal tract must continue to grow and adjust so that balance and posture is maintained. Although all sports depend on the extrapyramidal tract as much as the pyramidal tract and the cerebellar system, golf is a sport in which the extrapyramidal tract is especially important. In order to hit the golf ball as well as he does, Tiger Woods must shift his weight and balance all of his muscles in a specific way at a precise time in a fraction of a second without even thinking about it. (7)

It is because the extrapyramidal tract always has the ability to grow and change that golfers usually mature into their sport as they age. Other sports, however, like baseball and basketball do not focus as much on balance and posture, but more on the tasks of the pyramidal and cerebellar systems. The pyramidal and cerebellar systems, unlike the extrapyramidal tract, do not continue to continue to change as new skills are being learned. Therefore, it is for this reason that Michael Jordon was not as spectacular a baseball player as he was a basketball player. The window of opportunity to learn such sports as baseball and basketball is smaller than that of golf. (8) Thus it makes sense that after retiring as a professional basketball player, Michael Jordon picked up golf. (7)

Therefore, despite common stereotypes that athletes lack brain power, it seems that athletics have as much to do with the brain and the nervous system as physique. So how was Wayne Gretzky able to get a hockey shot off so quickly? A Canadian neurologist determined that Gretzky has the quickest reflexes every measured by this specific neurologist. Gretzky's muscle movement controlled by long loops of brain cells within the motor cortex of the brain occurs exceptionally quickly. Thus, it is due to Gretzky's quick brain cells that he was able to excel as he did in hockey. (1)

The nervous system gives the body the ability to perform incredible athletic accomplishments. As an avid weight-lifter John Abdo stated, "no brain, no gain". (9) Muscle control is not the only aspect of athletics that is based on the nervous system. It is said that competition itself is between 80% and 90% mental. (9) Although muscle control and movement and their relation to the nervous system have been thoroughly discussed, there are still many questions that have been left unanswered. Whether athletes are made or born is still an unanswered question. However, we have determined that the motor cortex of the brain is imperative in muscle control, and thus in athletics. We have also determined that parts of the motor cortex can continue to grow and learn, creating new neural diagrams of muscles and muscle use with the creation of new skills. As new skills are learned in a specific sport, muscles grow, as does the brain and nervous system. It is continuously evolving and changing to specific needs.

Therefore, it must be true then, that Michael Jordan's brain is different that Lou Gehrig's brain, which is different then Tiger Wood's brain, which may be why Michael Jordan was not a great baseball player, but an extraordinary basketball player. It seems that maybe Allen Iverson has a particularly quick pyramidal tract, allowing him to dart past defenders and shoot the basketball quicker than the defenders can respond to him. Maybe Terrell Owens has an extrapyramidal tract that is more evolved than most, allowing him to have exceptional balance and posture, so when he is tackled by a 300 pound defender, he can continue to run, stay on his feet, and carry the football. So, when the Nike advertisements say "Just Do It", they should be talking to the nervous system instead of the body.


References


1)Psychology Today, What Makes Athletes Great

2)Neurology Channel, Amyotrophic Lateral Sclerosis

3)bmj.com, Why Michael Couldn't Hit

4)Science Museum, How Do We Move?

5)keepkidshealthy.com, Gross Motor Development

6) Dr. Harold L. Klawans, Why Michael Couldn't Hit, Chapter 5 The Bantam Ben Hogan, pp. 88-92

7)Online Sports, The Creative Athlete

8)Fitness Tech, No Brain No Gain

9)American Family Physician, Amyotrophic Lateral Sclerosis: Lou Gehrig's Disease

10)We Move, Normal Muscle Control

11)Building Baby's Brain, Prime Times for Learning

12)Competitive Edge, Sports PTSD

13)Baseball Think Factory, Swinging from the Heels


The Brain, Behavior and Obsessive Compulsive Disor
Name: Kristin Gi
Date: 2005-02-21 22:38:55
Link to this Comment: 13089

<mytitle>
Biology 202, Spring 2005
First Web Papers
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Approximately 3.3 million Americans suffer from Obsessive Compulsive Disorder (OCD) and this disease affects 2.3% of United States citizens between ages 18-54 (1) . This disorder is equally common in males and females and occurs at similar rates throughout the world (2) . In class and in the forum, we have discussed the notion that brain equals behavior as proposed by Emily Dickinson (3) . This paper investigates the differences in brain structure and behavior between individuals with OCD and those without the disorder in hopes of determining the validity of Emily's statement. Furthermore, two different types of treatment for this disease will be discussed. One form of therapy targets structures in the brain in order to modify behavior, while the other form aims to modify the behavior in hopes of altering the way in which the brain functions. Therefore, this paper aims to shed light on the question that was set forth in the first week of class, using OCD as a means to determine if brain equals behavior.

An obsession is defined to be an inappropriate and unwanted thought or image that stems from fear of danger or contamination, as well as the persistent need for order. Individuals with OCD also may be plagued with sexually explicit thoughts. A compulsion is defined as repetitive behavior, such as excessive checking, counting, and silent repetition of words, hand washing, cleaning, arranging or hoarding. Symptoms of OCD usually begin during childhood for males, while for females, the age of onset can occur during childhood or around the time of pregnancy or birth, perhaps due to the interactions between the hormones within the brain (2) . The actual cause of OCD has yet to be determined, but several theories as to why individuals are afflicted with this disorder have been proposed. One theory postulates that a stressful event in an individual's life can spark the onset of the disorder (4), while other scientists and doctors argue that the disorder is genetically inherited, because OCD seems run in families (2) .

During most of the 20th century, doctors and scientists speculated that OCD could be understood in terms of psychoanalytic and behavioral theory, meaning that individuals afflicted with OCD were stricken because they struggled with internal and external unresolved conflicts. At this time, it was also believed that an individual may contract OCD as a result of an internal struggle for control over their own lives (5) .

However, as science and technology advanced, it seemed there was more involved in this disorder than unresolved feelings and the need for control. Moreover, it was found that analyses of the structure of the brain might hold the answers. Lewis R. Baxter Jr. and his colleagues at the University of California at Los Angeles and the University of Alabama in Birmingham were the first group to use positron-emission tomography (PET) in order to study the brain's link to OCD. PET scans are able to produce color-coded images of the brain in order to provide information as to where metabolic activities are occurring. In this study, it was found that elevated activity occurred in the frontal lobes, in particular, the orbital cortex and the basal ganglia in individuals with OCD. The basal ganglia functions to integrate and process information that is being sent from all parts of the brain. Dr. Judith L. Rapport of the National Institute of Mental Health reported similar results. She found that the basal ganglia and connecting regions in the brain were turned on inappropriately in individuals with OCD. Furthermore, she believed the obsessions and compulsions were preprogrammed in the basal ganglia (5) .

Magnetic resonance imaging (MRI) has also been done on patients with OCD and it was found that there was less white matter in the brain of these subjects (6) . White matter refers to the portions of the brain and spinal cord that are able to facilitate and direct communication between regions of gray matter, as well as communication between the gray matter regions and other parts of the body (7) . Therefore, communication between the brain and the body is compromised in individuals with OCD.

Jeffrey Schwartz and his colleagues at the University of California at Los Angeles College of Medicine used similar techniques to investigate OCD and changes in the brain. This group used PET scans of the brain as well, on 18 patients between 25-51 years of age. Radioactively labeled glucose was injected into the patients in order to determine where in the brain the glucose was traveling, which would tell the researchers which areas of the brain were metabolically active in the subjects with OCD. Four main areas of the brain were under study: orbital cortex, caudate nucleus, cingulate gyrus, and the thalamus. It was found that the orbital cortex was hyperactive in the individuals with OCD. Studies performed on monkeys found that damage to the orbital cortex leads to repetitive behaviors. Therefore, the researchers believed that the orbital cortex sends out repetitive false alarms in those with OCD. Usually these false alarms can be turned off, however, with OCD, the alarms continue to be sent and eventually reach the caudate nucleus, which controls the movement of limbs. The signal then travels to the cingulate gyrus which causes the heart to pound and the stomach to churn, while the thalamus controls and integrates the information from the aforementioned three parts of the brain as well as other areas. Schwartz and his colleagues thus found that all four regions took up the glucose at high and similar rates, suggesting a linkage between these components of the brain. Confronted with these results, the researchers have speculated that this linkage and close relationship between these four parts of the brain is the cause of OCD (8) .

There is also a link between OCD and serotonin, a neurotransmitter that facilitates cell communication (9) . Most neuronal cells are separated by a fluid-filled space called a synapse. A neurotransmitter is released into this space, which then interacts with the receptor on this cell causing an electrical signal to be generated that is then directed to other areas in the brain in order to bring about a particular response or behavior. Released serotonin is usually taken back up by the cell from which it was released, enabling serotonin to be recycled for further use. This process also prevents excess levels of this neurotransmitter from clogging up synapses (10) .

Once these studies were performed, researchers then turned their attention to methods of treatment. Two major methods exist to treat OCD; one involves drug therapy while the other focuses on modifying a patient's behavior in hopes of alleviating the obsessive and compulsive behavior.

The drug therapy method attempts to alter the brain chemistry in hopes of modifying behavior. These drugs are mainly serotonin reuptake inhibitors (SRI's) or selective serotonin reuptake inhibitors (SSRI's). Both classes of drugs aim to increase serotonin levels. More specifically, they interfere with the recycling of serotonin, thereby allowing for the serotonin to linger in the synapse longer and affect the surrounding nerve cells for an extended period of time. Researchers have not yet determined how or why this helps to ameliorate the obsessions and compulsions (11) . Therefore, further research can be done in order to understand the chemistry of increasing serotonin levels in the brain and how this correlates to reducing the symptoms of OCD.

Anafranil (clomipramine) is the main SRI that is used in treatment of OCD. However, this drug not only alters serotonin levels, but it also can affect other neurotransmitter concentrations, therefore, this drug is not selective. The main SSRI's used for treatment are: prozac (fluoxatine), luvox (fluvoxamine), celexa (citalopram), zoloft (sertaline) and paxil (paroxatine) (11) . Studies have also been done in order to assess the effectiveness of these drugs on the patients. One study found that roughly 75 percent of patients were helped with these medications and more than half of the patients reported relief of symptoms because the drugs diminished the frequency and the intensity of their obsession and compulsions. During these studies, it took the patients about three weeks or longer for their symptoms to subside. If a particular SRI or SSRI is not working for an individual, researchers have determined that one of the SRI's can be used as the primary form of medication and then use another drug as an augmenter. However, if an individual opts to stop using the medication then a relapse will most likely follow and the symptoms of the disorder will start to manifest themselves again. Therefore, even if the symptoms subside, most people will need to continue to take the medications, albeit at a lower dosage, in order to control their obsessions and compulsions (12) .

The second method of treatment is called Cognitive-Behavioral Therapy (CBT), also referred to as exposure and response prevention, is supported by Dr. Jeffrey Schwartz author of Brain Lock. This form of treatment exposes the individual to his or her fear in hopes of having them confront their obsessions and compulsions (11) . After the exposure, their compulsive response is delayed. For example, if an individual has a fear of germs, the treatment would expose him or her to some form of contamination and then prevent the individual from compulsively washing their hands to rid themselves of the germs. The aim of this treatment is to ease the fear and stress in the individuals as well as make them less anxious by having them confront their anxieties. Schwartz believes this is the best form of therapy for individuals with OCD because they learn not to succumb to their obsession which is harmful behavior. Therefore, this form of therapy aims to dissuade individuals from engaging in their old destructive behavior. Schwartz also argues that the brain will respond to whatever form of behavior individuals engage in. Thus, if the individual continues to engage in healthy behavior, the brain will notice this and automatically begin to prevent the individual from reverting back to their potentially self-destructing behavior (11) .

In his book, Schwartz presents four steps that allow individuals with OCD to modify their behavior. The first step (relabel) involves naming the particular urges one feels as obsessions and compulsions. Individuals also must acknowledge that the urges they feel are false alarms and are not real problems. As this type of therapeutic behavior continues, the brain will recognize these as false alarms and these urges will, over time, subside. Step two (reattribute) involves acknowledging that the disorder causes these compulsions and obsessions in hopes of bolstering confidence and the willpower to ward off these feelings. The third step involves refocusing one's attention onto a more healthy activity when a false alarm occurs. Schwartz suggests finding a therapeutic hobby and putting one's energy towards this activity and learning to delay their response to the particular urges they may feel. The last step (revalue) involves placing less importance on the behaviors of OCD and he urges individuals to take charge and control of their behaviors rather than having them control you. Schwartz believes this is the best form of treatment for those with the disorder because it confronts the particular behaviors and urges that lead individuals to behave destructively (11) .

We began our class with the idea that brain and behavior are the same as proposed by Emily Dickinson. This paper looked at OCD in order to determine if this theory had any validity. Studies have been done on individuals with OCD and those without and it has been found that there are differences within their brains. These differences in the brain must then account for the differences in behavior, hinting at the fact that brain and behavior are the same. Two main types of treatment for this disorder were also discussed. Drug therapy involves altering the brain chemistry and neurotransmitters levels in hopes of modifying behavior by reducing the frequency and intensity of the obsessions and compulsions. The second form of therapy, CBT, involves altering one's behavior such that the brain chemistry will change as well. Therefore, these two therapies have diametrically opposed ways of healing. However, if the brain chemistry can be changed, causing behavior to change as well through the use of SRI's and SSRI's and one's behavior can be changed through CBT, which then causes the chemistry of the brain to change, then the brain must equal behavior. Based upon our discussions in class and in the forum, my thoughts as to whether brain equals behavior have been mixed, however, after investigating OCD, I have finally come to realize that the brain and behavior are synonymous. Using OCD as a lens with which to answer this elusive question has helped me come to a definite conclusion and a greater understanding of the points discussed in class and in the forum.

References

1)National Institute of Mental Health, National Institute of Mental Health site that offers information about OCD.


2)SA Mental Health, describes the genetics of OCD

3)Serendip Homepage, our class website and forum area

4)Help Guide for OCD , a site that provides an overview of OCD

5)Psych Central, a site that provides information about the probable causes of the disorder

6)Understanding Obsessive Compulsive Disorder, managed by the National Institute of Mental Health, this site also discusses possible causes of the disorder

7)Multiple Sclerosis Information, I used this site to find an informative definition of white matter

8)Chemistry of Obsession, a site that discusses the chemistry behind OCD

9)National Institute of Mental Health, I used this site maintained by the Nation's Voice on Mental Illness to search for information about OCD

10)Psych Central, this site discussed the various medications used to treat the disorder

11)Healthy Place OCD Community , this site also discussed treatments

12)OCD Support, this site discussed the various medications for the disorder


The Healthy Fat Craze; Fact or Fiction?
Name: Kate Matne
Date: 2005-02-21 22:43:22
Link to this Comment: 13091

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Biology 202, Spring 2005
First Web Papers
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A new health craze for the benefits of essential fatty acids (EFA) is gaining momentum in the United States and beyond. Supporters of EFA enriched diets believe that sufficient intake of these fats benefit health in seemingly endless ways. One suggested benefit of essential fatty acids is that it can treat arthritis. Recent studies propose that adequate intake of essential fatty acids not only reduces the inflammation of arthritic joints and relieves pain caused by joint-tissue degradation, but also inhibits cartilage-degrading enzymes that perpetuate the disease (5.) It is also believed that EFA supplementation improves cardiac health. In fact, the American Heart Association currently advises biweekly intake of fish because it supplies high quantities of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two essential fatty acids (4.)

These are just a couple of the areas where essential fatty acids may promote health. There are many other claims that other areas throughout the body benefit from a high dose of healthy fat. Perhaps the most striking of these claims is that essential fatty acids improve nervous system functioning. It is no surprise to us that drugs affect the chemical workings of our brain. Anti-depressants block re-uptake of serotonin and norepineephrine, dopamine receptor blockers are used to tame the spasms of epileptics, and even over-the-counter ibuprofen alleviates pain by intervening in biochemical pathways related to pain signal manufacturing. And yet, the concept that diet, like drugs, can alter brain functioning is a bit more difficult to trust. Is it possible that by consuming avocados (a source of essential fatty acids) we can improve our nervous system functioning and, by doing so make ourselves smarter? Is there anything to the Omega-3 health wave or is it just a fad of the holistic-medicinal world that with time will prove fictitious? In order to address these questions we must first understand what these health-facilitating fats are, where they work in the nervous system and how they are unique from any other fat.

There are three types of fatty acids (FA): Omega-3, Omega-6 and Omega-9 fatty acids. Omega-3 and Omega-6 are essential fatty acids (EFA) because the body cannot produce them independently. Essential fatty acids must come from the diet. Omega-9 fatty acid is not considered essential because the body can produce it without supplementation, although only in limited amounts. The dietary building blocks for fatty acids are three types of acids found in food. Omega-3 fatty acids are derived from Linolenic Acid, Omega-6 from Linoleic acid and Omega-9 fatty acids are derived from and Oleic Acid. Foods high in these acids include flaxseed oil, fish, and most nuts (2.)

On a molecular level the structural difference between bad and good fats is strikingly small. The difference lies in the presence of a single double bond in the carbon chain of the fatty acid. It is the absence of this double bond alone that makes bad fats saturated and its presence that makes good fats unsaturated. The number (three, six or nine) in the fatty acid name indicates the location of this critical double bond. It is fundamentally this double bond that yields great differences in the functioning of the fat and its derivatives in the body.

Although it does not directly involve the nervous system one crucial role of essential fatty acid in the endocrine system is worthy of note because of the parallel nature in which the endocrine system works with the nervous system to maintain body homeostasis. EFA is crucial in the production of a family of cell signalers involved with pain response, prostaglandin. Along with other endocrine signaling molecules (including prostacyclins, thromboxanes and leukotrienes,) essential fatty acid arachidonate is the precursor to this family of chemicals. Interestingly, the over-the-counter pain reliever aspirin works by actually inhibiting the cyclooxygenating step in the synthesis of prostaglandin from its fatty acid derivative (3.) It is the release of this fatty acid derived molecule that not only triggers pain development, but also fever and inflammation responses (7.) Hence, prostaglandin inhibition allows Advil to relieve pain and inflammation.

Beyond serving as a building block for cell signalers, essential fatty acids also play a direct structural role in the nervous system. Essential fatty acids make up 20% of neuronal membranes. Neuronal membranes play an integral role in the transmission and integration of information because it is between them that cell-to-cell communication and nervous system information processing occurs (8.) A recent study (April 2004) conducted by the Institute on Alcohol and Alcoholism in Rockville, Maryland confirmed the importance of essential fatty acids' presence in neuronal membranes (1.) Although the study looks at the consequence of reduced essential fatty acids in rat retinal cells, structural consistency throughout the nervous system makes the ramifications of the findings far reaching. Thus, their study uncovers much of the mechanisms behind the magic of healthy fats not just for vision, but also for information processing throughout the nervous system.

The experiment consisted of two groups of rats. One group was fed a diet deprived of the essential Omega-3 fatty acid, while the other group was given an Omega-3 adequate diet. The adequate diet differed only by its supplementation with flaxseed oil and fatty acid docosahexaenoic acid (DHA.) After ample time on the diets the rats' retinal rod outer segments (ROS), sensory neurons of the eye, were tested for the presence of DHA. They found that rats fed the deficient diet had about 80% less DHA in their retinal membranes. In the deprived rats the saturated poly-carbon chain, docosapentaenoic acid, largely replaced DHA. Bovine proteins were used to replace the rats' original ROS membrane proteins so as to eliminate the potential for differential protein functioning. This allowed the study to isolate the effects of membranous fats (essential and non-essential) on vision.

The speed and efficiency of the complex biochemical pathways of sight were then tested and compared in the two groups of rats. Because these pathways involve G protein-coupled receptors (GPCR), which are ubiquitous in biochemical pathways of cognitive function, the results support the potential for similar effects throughout the nervous system. The results showed that in deficiently dieted rats there was not only a reduced speed in the biochemical pathways of vision, but also weakened signaling strength in the GPCR pathway. Probable cause for the relative inefficiency of deprived rats is reduced flexibility of the cell membranes. Docosapentaenoic acid's saturated character results in less free volume than the unsaturated DHA's packing order. Since the GPCR pathway for ROS activation involves the formation of a membrane complex, less flexibility (caused by a lack of free volume) probably results in greater energy barriers for complex formation.

This study is not the first to correlate EFA deficiency with decreased neuronal functions. In fact, studies on humans confirm the indispensable role of essential fatty acids on learning. Infants deprived of Omega-3 fatty acid exhibit lower performance in neurodevelopment tests (1.) The study on ROS in rats suggests that essential fatty acids are critical not only in developmental learning but also in sensory input and stimulus response throughout the nervous system.

Since learning is the input and processing of sensory data, the assertion that ideal building blocks for biological machinery can improve learning follows logically. After all, it is only after we have received an input a photon, a sound wave, touch that we can respond. Although the effect of food on our nervous system is not as observable as that of drugs we should not overlook its importance. The studies are in and the essential fatty acid health trend is not unfounded. If we care about the health and ability of our minds then we have to provide our brains with building blocks that facilitate optimal functioning.

So, what do you say? I say pass the salmon.


References

1) Niu, S.L., Mitchell, D.C., Lim, S.Y., Wen, Z.M., Kim, H.Y., Salem, N.Jr., and Litman, B.J. "Reduced G Ptotein-coupled Signaling Efficiency in Retinal Rod Outer Segments in Response to n-3 Fatty Acid Deficiency-*." JBC Online (http://www.jbc.org/cgi/content/full/279/30/31098#FIG2) (2004): 1-14.

2) Omega3 Information Service home page

3) Stryer, Lubert. Biochemistry. New York: W.H. Freeman and Company, 1995.

4)American Heart Association , Fish and Omega3 Fatty Acids.

5) Omega-3 Fatty Acids and Arthritis Prevention and Remedy home page ,

6) HOPES Glossary home page , from Stanford University.

7)Biology Lecture Notes , from the University of Connecticut.

8)Psychology Today , Food n Mood homepage.


The Healthy Fat Craze; Fact or Fiction?
Name: Kate Matne
Date: 2005-02-21 22:50:28
Link to this Comment: 13093

<mytitle> Biology 202, Spring 2005 First Web Papers On Serendip

A new health craze for the benefits of essential fatty acids (EFA) is gaining momentum in the United States and beyond. Supporters of EFA enriched diets believe that sufficient intake of these fats benefit health in seemingly endless ways. One suggested benefit of essential fatty acids is that it can treat arthritis. Recent studies propose that adequate intake of essential fatty acids not only reduces the inflammation of arthritic joints and relieves pain caused by joint-tissue degradation, but also inhibits cartilage-degrading enzymes that perpetuate the disease (5.) It is also believed that EFA supplementation improves cardiac health. In fact, the American Heart Association currently advises biweekly intake of fish because it supplies high quantities of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), two essential fatty acids (4.)

These are just a couple of the areas where essential fatty acids may promote health. There are many other claims that other areas throughout the body benefit from a high dose of healthy fat. Perhaps the most striking of these claims is that essential fatty acids improve nervous system functioning. It is no surprise to us that drugs affect the chemical workings of our brain. Anti-depressants block re-uptake of serotonin and norepineephrine, dopamine receptor blockers are used to tame the spasms of epileptics, and even over-the-counter ibuprofen alleviates pain by intervening in biochemical pathways related to pain signal manufacturing. And yet, the concept that diet, like drugs, can alter brain functioning is a bit more difficult to trust. Is it possible that by consuming avocados (a source of essential fatty acids) we can improve our nervous system functioning and, by doing so make ourselves smarter? Is there anything to the Omega-3 health wave or is it just a fad of the holistic-medicinal world that with time will prove fictitious? In order to address these questions we must first understand what these health-facilitating fats are, where they work in the nervous system and how they are unique from any other fat.

There are three types of fatty acids (FA): Omega-3, Omega-6 and Omega-9 fatty acids. Omega-3 and Omega-6 are essential fatty acids (EFA) because the body cannot produce them independently. Essential fatty acids must come from the diet. Omega-9 fatty acid is not considered essential because the body can produce it without supplementation, although only in limited amounts. The dietary building blocks for fatty acids are three types of acids found in food. Omega-3 fatty acids are derived from Linolenic Acid, Omega-6 from Linoleic acid and Omega-9 fatty acids are derived from and Oleic Acid. Foods high in these acids include flaxseed oil, fish, and most nuts (2.)

On a molecular level the structural difference between bad and good fats is strikingly small. The difference lies in the presence of a single double bond in the carbon chain of the fatty acid. It is the absence of this double bond alone that makes bad fats saturated and its presence that makes good fats unsaturated. The number (three, six or nine) in the fatty acid name indicates the location of this critical double bond. It is fundamentally this double bond that yields great differences in the functioning of the fat and its derivatives in the body.

Although it does not directly involve the nervous system one crucial role of essential fatty acid in the endocrine system is worthy of note because of the parallel nature in which the endocrine system works with the nervous system to maintain body homeostasis. EFA is crucial in the production of a family of cell signalers involved with pain response, prostaglandin. Along with other endocrine signaling molecules (including prostacyclins, thromboxanes and leukotrienes,) essential fatty acid arachidonate is the precursor to this family of chemicals. Interestingly, the over-the-counter pain reliever aspirin works by actually inhibiting the cyclooxygenating step in the synthesis of prostaglandin from its fatty acid derivative (3.) It is the release of this fatty acid derived molecule that not only triggers pain development, but also fever and inflammation responses (7.) Hence, prostaglandin inhibition allows Advil to relieve pain and inflammation.

Beyond serving as a building block for cell signalers, essential fatty acids also play a direct structural role in the nervous system. Essential fatty acids make up 20% of neuronal membranes. Neuronal membranes play an integral role in the transmission and integration of information because it is between them that cell-to-cell communication and nervous system information processing occurs (8.) A recent study (April 2004) conducted by the Institute on Alcohol and Alcoholism in Rockville, Maryland confirmed the importance of essential fatty acids' presence in neuronal membranes (1.) Although the study looks at the consequence of reduced essential fatty acids in rat retinal cells, structural consistency throughout the nervous system makes the ramifications of the findings far reaching. Thus, their study uncovers much of the mechanisms behind the magic of healthy fats not just for vision, but also for information processing throughout the nervous system.

The experiment consisted of two groups of rats. One group was fed a diet deprived of the essential Omega-3 fatty acid, while the other group was given an Omega-3 adequate diet. The adequate diet differed only by its supplementation with flaxseed oil and fatty acid docosahexaenoic acid (DHA.) After ample time on the diets the rats' retinal rod outer segments (ROS), sensory neurons of the eye, were tested for the presence of DHA. They found that rats fed the deficient diet had about 80% less DHA in their retinal membranes. In the deprived rats the saturated poly-carbon chain, docosapentaenoic acid, largely replaced DHA. Bovine proteins were used to replace the rats' original ROS membrane proteins so as to eliminate the potential for differential protein functioning. This allowed the study to isolate the effects of membranous fats (essential and non-essential) on vision.

The speed and efficiency of the complex biochemical pathways of sight were then tested and compared in the two groups of rats. Because these pathways involve G protein-coupled receptors (GPCR), which are ubiquitous in biochemical pathways of cognitive function, the results support the potential for similar effects throughout the nervous system. The results showed that in deficiently dieted rats there was not only a reduced speed in the biochemical pathways of vision, but also weakened signaling strength in the GPCR pathway. Probable cause for the relative inefficiency of deprived rats is reduced flexibility of the cell membranes. Docosapentaenoic acid's saturated character results in less free volume than the unsaturated DHA's packing order. Since the GPCR pathway for ROS activation involves the formation of a membrane complex, less flexibility (caused by a lack of free volume) probably results in greater energy barriers for complex formation.

This study is not the first to correlate EFA deficiency with decreased neuronal functions. In fact, studies on humans confirm the indispensable role of essential fatty acids on learning. Infants deprived of Omega-3 fatty acid exhibit lower performance in neurodevelopment tests (1.) The study on ROS in rats suggests that essential fatty acids are critical not only in developmental learning but also in sensory input and stimulus response throughout the nervous system.

Since learning is the input and processing of sensory data, the assertion that ideal building blocks for biological machinery can improve learning follows logically. After all, it is only after we have received an input a photon, a sound wave, touch that we can respond. Although the effect of food on our nervous system is not as observable as that of drugs we should not overlook its importance. The studies are in and the essential fatty acid health trend is not unfounded. If we care about the health and ability of our minds then we have to provide our brains with building blocks that facilitate optimal functioning.

So, what do you say? I say pass the salmon.

References

1) Niu, S.L., Mitchell, D.C., Lim, S.Y., Wen, Z.M., Kim, H.Y., Salem, N.Jr., and Litman, B.J. "Reduced G Ptotein-coupled Signaling Efficiency in Retinal Rod Outer Segments in Response to n-3 Fatty Acid Deficiency-*." JBC Online (http://www.jbc.org/cgi/content/full/279/30/31098#FIG2) (2004): 1-14. 2) Omega3 Information Service home page 3) Stryer, Lubert. Biochemistry. New York: W.H. Freeman and Company, 1995. 4)American Heart Association , Fish and Omega3 Fatty Acids. 5) Omega-3 Fatty Acids and Arthritis Prevention and Remedy home page , 6) HOPES Glossary home page , from Stanford University. 7)Biology Lecture Notes , from the University of Connecticut. 8)Psychology Today , Food n Mood homepage.


What is the brain? What is the mind?What realation
Name: LF
Date: 2005-02-21 23:14:49
Link to this Comment: 13095

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


What is the brain? What is the mind? What relation does one have to the other?
LF
The central nervous system is a physiological system similar to the digestive system or respiratory system. The only difference is that it has a brain at the end, which in effect seems to be the rational and conscious mind of the rest of the body. An article I read stated that "the mental processes of Mind are attached to the molecular processes of Brain as a subjective addendum, so that we no longer have the brain and mind relationship of popular belief, but "brainmind" unity in one substance."
I would like to attempt to find out whether this is the only logical explanation to the much debated issue of brain vs. mind.
When the brain processes it translates to a mental processing and through that we experience emotion, pain, pleasure etc. However, using a dualistic approach, has no physical properties it cannot, be a direct part of a physical brain that necessitates real "micro joules of incoming synaptic energy" to modify its constant activity towards a mentally desired outcome.
Another suggestion is that the mind is entirely separate from the brain and that is it an entity with undefined substantial nature. However this would still raise many questions such as how is the mind connected at all with the brain? Does one influence the other. If this is the case, surely the non material mind cannot influence, control or take part in actions of the material brain.
In my opinion a mind can definitely not exist without a brain, because a brain perceives surroundings and registers emotions and feelings that thus formulate the mind. A brain can exist without a mind. But the question is then raised, what constitutes a mind? Is it what Philosophers refer to as a soul? Or is it simply the part of the brain that transfers signals from the nervous system into physical external actions? Is the term mind just another way to describe the brain. And, if a mind cannot exist without a brain, yet a brain can exist without a mind, then does the mind really exist, is it just a name without a meaning?


What and Where is Evil?
Name: Elizabeth
Date: 2005-02-22 00:24:17
Link to this Comment: 13099

The gradual process we call evolution in which one thing changes into a more complex and usually better form is a concept that I usually do not associate with personality. Yes, brain size, capacity, and the ability to comprehend are all derivatives of the millions of years humans have evolved. Personalities and traits that accompany them are a different concept. Throughout history there has always been documented cases of the good versus the bad or evil. Dating from first human societies to the our present, this concept has not changed. If evolution has done its job, why are there those among us that make up the evil side of this ancient battle? Or has evolution actually done its job by making the evil among us more complex and better at being evil through time? Where do the evil differ from the socially accepted good? What deviates? It is important to examine these differences and understand where our differences originate.

As a society, we try to offer explanations to why people behave as they do, however, once a heinous act is committed by an individual beyond a fathomable degree, instead of being called evil, the person is pronounced psychologically unfit, of an unsound mind, or horrible. Deeming someone as evil is not an option in any DSM manual or court, but the trait and concept are real and alive in society. The intentional wrongdoing that evil is (1) an act that the individual finds joy in and yearns to complete. Why do some of us yearn to do such things? To understand, both environmental and biological factors must be investigated further, but before we do this, examples to which we can refer to must be established. Perhaps the most obvious evil mastermind to our current western world thought process would be Osama Bin Laden (9), the man behind thousands of untimely deaths. Another might be Ted Bundy (2) who raped and killed innocent women. Finally we will take the case of John Wayne Gacy (3), who raped and killed over thirty boys. What made these individuals do what they did?

According to psychiatrist Robert I. Simon, "The capacity for evil is a human universal" (10). He concludes that there is a continuum of evil from lesser evils, stealing or cutting in line, to greater evils such as prejudices, and finally massive evils that encompass serial sexual killings. The motivation and drive to the extreme may be a biological or environmental factor or both. If we all possess certain evil traits, factors that could coax the evil in us to be proactive could be a variety of things. If one is abused emotionally or physically in any way, ones motivation and feelings change. As a child, one models their environment trying to find the best way to coexist with the immediate surroundings. If these surroundings are of a threatening nature, we learn early on how to defend ourselves and what we wish could be. To many of us these behaviors are far from consistent normal behavior, but for those individuals whom act in accordance with how they feel, their actions appear and feel completely normal.

As scientific methods concerning neural functioning and genetic traits progress, mysteries behind human behavior have become more evident and explainable. Frontal lobe dysfunction (8), among other neural abnormalities, has been blamed for violent and criminal behavior. In research done by Dr. B H Price (8), a correlation was found between frontal lobe dysfunction and increased aggressive behavior. Individuals with frontal lobe dysfunction have limited impulse inhibition, are trivially motivated, and are habitual aggression. Individuals also suffer from poor abstract conceptual thinking, the inability understand other's subjective experience, and extreme immature moral reasoning. Individuals examined, especially murderers, having frontal lobe dysfunction showed a significant decrease in cortical blood flow, these abnormalities to the brain are associated with repetitive and purposeless violent behavior.

Further research concerning the role of the amygdala has rendered interesting ideas behind certain behavioral tendencies. It is thought that through the interaction between the posterior cortex and subcortical (4) regions of the brain that conscious experiences and self identity are created and carried. Further research concludes that if the amygdala (5), which is responsible for impulse control, does not agree with prefrontal cortex it can override any decision. So are we constantly at the will of a tiny structure in our brain that if in a bad mood can make us pretty much anything it wants? This scares me.

The role of neurotransmitters (7) and their role in behavior is extremely important to examine where behaviors might originate. If for some reason reuptake is slow or does not exist at all, our mood can fluctuate and cause us to act in a way that inconsistent. Could there be a combination of neurotransmitters that could cause certain behaviors such as evil? This would thus allow pharmaceutical companies to invent a drug correcting neurotransmitter flow better known as the anti evil drug. If this drug were given to Bundy (3), Osama (9), or Gacy (2), would the past have been different?

I think both situational and biological factors can explain Osama Bin Laden's (9) behavior. Through his religious and spiritual beliefs, the acts he has committed are looked upon in favor and even praised. What strikes me as interesting is the ability to ignore the subjective experiences of others. Does this mean that frontal lobe dysfunction (8) is to blame for everything? Is it that easy? I do not think so. I would be willing to bet if all of al-qaeda were examined, the percentage of those with any kind of dysfunction would be extremely low. There is something to say about moral reasoning and their influence on ones actions.

In contrast, let us examine John Wayne Gacy (2), a former Chicago businessman convicted of raping and killing young boys. At his murder trial, his soul defense was that he was insane and no longer in control of his actions. The crimes and deaths he committed were extremely intricate and well planned something had to be in charge and thinking. Was it his amygdala that ordered him to do the things he did? Maybe, but to a jury this defense did not explain or excuse anything. Finally we examine the case of Ted Bundy(3), responsible for vicious sexual attacks and killings to young wome. As a child he was teased and became extremely shy. Were his later actions in retaliation to his childhood trauma? Was neurotransmitter activity upset? No matter the case, like Gacy (2), Bundy (3) was extremely careful and precise. Something was in charge.

Are these and other men like them evil? According to Dr. Michael Stone's 22-level hierarchy (11) of evil behavior they are. The hierarchy is based on the behavior of the 500 most violent criminals. Bundy and Gacy (2) are at the top of the hierarchy! To be diagnosed using this hierarchy individuals must take a 20 question personality test. From this test, Dr. Stone is able to deduce whether evil is the factor in control. Where does this hierarchy fit into Dr. Simon's continuum (10)? Where should one sit on the continuum to be able to claim the title of evil? Australian courts have concluded that invoking the concept of evil would risk adding moral and religious dimensions to judicial tradition and have opted to use the term of antisocial personality disorder in place of evil. I feel that separation of church and state is important, but I feel that hugely immoral acts should have a name that captivates the degree of its actions.

"The capacity for evil is a human universal" might be a little harsh, but I do believe that a little bit of evil exists in all of us. What provokes our actions, whether biological or environmental, is different in all of us. The battle for good and evil will never be won because we are constantly switching sides and playing for both teams, it is not evolution at work, but our own human nature. How evil are you (6)?


1)http://web1.infotrac.galegroup.com/itw/infomark/234/191/58517134w1/purl=rc1_ITOF_0_A87426033&dyn=3!xrn_5_0_A87426033?sw_aep=bryn52545

2)http://www.crimelibrary.com/serial_killers/notorious/gacy/trial_7.html

3)http://www.crimelibrary.com/serial_killers/notorious/bundy/index_1.html?sect=1

4)http://web1.infotrac.galegroup.com/itw/infomark/234/191/58517134w1/purl=rc1_ITOF_0_CA86530965&dyn=5!xrn_1_0_CA86530965?sw_aep=bryn52545

5)http://web1.infotrac.galegroup.com/itw/infomark/234/191/58517134w1/purl=rc1_ITOF_0_CA87490348&dyn=7!xrn_1_0_CA87490348?sw_aep=bryn52545

6)http://web.tickle.com/tests/standard/evil.jsp

7)http://web1.infotrac.galegroup.com/itw/infomark/234/191/58517134w1/purl=rc1_ITOF_0_CA86530965&dyn=9!xrn_1_0_CA86530965?sw_aep=bryn52545

8)http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11723190

9)http://www.fbi.gov/mostwant/topten/fugitives/laden.htm

10)http://web1.infotrac.galegroup.com/itw/infomark/805/247/58518119w1/purl=rc1_ITOF_0_A74633126&dyn=3!xrn_4_0_A74633126?sw_aep=bryn52545

11)http://www.timesonline.co.uk/article/0,,2087-1482339,00.html


Can You Judge a Brain Without the Mind?
Name: Lily Yoon
Date: 2005-02-22 00:50:46
Link to this Comment: 13100

Less than a week ago, my family experienced the unexpected death of my grandmother. Although she was supposed to celebrate her eightieth birthday this week, we all still felt like she had left too soon. During the funeral procession, I watched the members of my family fall apart one by one. My mother, the youngest of the sisters but oldest of the brothers, was the most emotionally expressive out of the six siblings. But despite who appeared to be the most sensitive, I believe that each child felt the same blow and suffered from the same emotional repercussions resulting from their mother's death. Therefore, I do not question the impact of the matter, because I know it was hard for everyone, however, I wonder about the long-term effects this might have on some and not so much on others.

When tested with the same traumatic experience, there exists certain amount of acceptable sadness and grieving on everyone's part, but what sets apart the one person who will suffer the longest and continue to be under the spell of depression, while others accept and move on? When a justifiably horrendous experience strikes, who comes out of it stronger and who buckles under the pressure? Is it circumstantial, biological, or both? If we can argue that depression is a disease of the mind and the brain can exist without the mind, the same does not go for the reverse, then we might be able to assume that the brain and its neurological functions does, in fact, play a role in clinical depression.

The actual trigger of depression is not yet known; however, there seems to be evidence of the influence of genetics, environment, and neurobiological factors. In a neurochemical perspective, norepinephrine, dopamine, and thyroid hormones are several examples of hormones that are linked to the development of depression, but "research studies have implicated disturbances in the serotonin (5-HT) system and the Limbic Hypothalamic-Pituitary-Adrenal (LHPA) axis as two of the neurobiological alterations most consistently associated with mood-altering illness" (1). All of these hormones are part of a monoamine class, which has been found to cause depression when it is low in level or inhibited in the brain (2).

Although, it cannot be definitely argued that the brain is the main cause of depression, its disturbance in circuits and neurotransmitters make a significant difference in depression (2). The adrenal glucocorticoid, produced by the adrenal gland, not only regulates metabolism, but also interacts with serotonin 5-HT during severe stressful periods. The adrenal gland is linked to the region where serotonin is produced by limbic HPA axis, the area in which arousal, sleep, appetite, pleasure, mood is regulated (1). Because the malfunctioning of these behaviors are some of the symptoms of clinical depression, it is hard to ignore the role it might play during stressful times and the ways in which people respond. Of course it can be asked whether the people who suffer from depression are born with slightly different brains and neurobiology or if the stressful event causes the brain to suddenly function differently.

Another example of the importance of the brain and its function in handling stress is the hippocampus and its ability to control hormones and higher thinking in response to stress. Two receptors in the hippocampus work to control cortisol levels, when found in overabundance can cause depression (1). The prefrontal cortex is also related to higher thinking and executive function, and there is a discrepancy in these areas of the brains of depressed or suicidal patients (1). Now if this is true, then one might be able to assume that those who normally cannot display appropriate "higher thinking and executive function" throughout their lives might be more prone to depression.

Although we cannot say that stress actually causes depression, according to Lopez, stress very likely interacts with genetic disposition in the more vulnerable individuals, which can then lead to a mood disorder (1). But even with this hypothesis, the concept of stress seems so arbitrary. What might be considered a severe stressful situation in one life might be an everyday situation in another. Then, we can question the validity of the "genetic disposition of the more vulnerable individuals". Do the people who face dangerous situations everyday possess the exemplary genetic strength to live each day without resulting in some sort of emotional breakdown? Are these people just wired to deal better than those who live in a more comfortable environment? If not, then are those who lack the likely environmental influence to lead to depression not justified in their sufferings?

In addition, studies of identical and fraternal twins have shown that there is a higher and more consistent diagnosis of manic-depression for both individuals of identical twin siblings than those of fraternal twins (2). And since identical twins are genetically identical, while the fraternal twins are as genetically similar as any other sibling pairs, there is evidence that there also exists a genetic basis to depression.

These studies, like much of science, do not possess a definitive conclusion. There is an idea of what parts of the brain is linked to depression, but there is no definite cause. The continued studying in this area might ultimately bring about a cure or a means to avoid depression, yet there are certain biological factors that can never fully fathom much of the emotional and spiritual turmoil that the depressed patients must face. Edgar Cayce wrote,

"Yet, while the brain and the cords through which the nerves function are the channels, these are not the mental consciousness; though it is through the nerve plasm that the nervous systems carry impulses to the various forces of the system. There are the spiritual attributes, - desire, hope, will, - that function through the organs of reproduction, as well as becoming the import or motivative force in expression even in a material manner through the senses of the body ... In this instance we find that the glands of the body form the greater portion of such associations or activities" (3).

(1) http://www.thedoctorwillseeyounow.com/articles/behavior/depressn_5/; on thedoctorwillseeyounow website.

(2) http://www.lib.calpoly.edu/infocomp/modules/05_evaluate/WIC2b.html; on the Scientific American website.

(3) http://www.meridianinstitute.com/ceu/ceu14dep.html; on the meridian institute website.


Habits
Name: MK McGover
Date: 2005-02-22 00:54:04
Link to this Comment: 13101

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Have you ever arrived at home or work with no memory of how you got there? When you started on your journey, you thought about the first few steps on that familiar path, but somewhere along the way, your brain moved onto more interesting topics, and the next thing you knew, you'd arrived. This is the essence of habits - once you start on a familiar series of actions, you stop thinking about them, and you are able to complete them without conscious thought or attention (3,4). This can be both a boon and a bane to humans as it frees up our minds from dull or repetitive tasks, but also makes it difficult to stop a habit once it's started. What differentiates the learning that forms habits from other types of learning? How do habits form? Why are habits so hard to break? How does the brain know which learned behaviors to translate into habits? What does this imply about our day-to-day behavior?

Habits are a series of steps learned gradually and sometimes without conscious awareness (2,3,4). Habit formation is a type of procedural learning in which the basal ganglia, a cluster of nuclei located in the forebrain between the cortex and the brainstem (1,11), play a key role (1,2,3). The location of the basal ganglia provides access to both the cognitive areas of the brain involved in decision making (forebrain) and also the midbrain which controls motor movement (1,11). It is the only place in the brain that deals with both physical and cognitive actions simultaneously, linking thought to movement (10). This linking occurs via projections from the basal ganglia into the thalamic nuclei (associated with the frontal cortex and cognitive functions) and the brainstem nuclei (associated with motor control) (1).

The area of the basal ganglia that has been particularly associated with habit formation is called the striatum. This area receives the most input from the cortex and may be involved in cortico-basal ganglia loops using the thalamic connections mentioned above. These loops may be involved in the decision to select certain actions, e.g. the automatized response of habits. In addition, the striatum receives input from dopamine-containing neurons in the midbrain or brainstem. Together, these inputs may create a loop with the striatum that leads to habit formation by associating rewards (dopamine) with a particular context (1,3).

In experiments involving rats with striatal neuron sensors, a restructuring of neural response patterns was indicated during habit formation. As a sequence of steps was learned, basal ganglia activity was present during all steps, but as training continued, this activity became centered around the beginning and end of the task. The dopamine-containing midbrain neurons shifted their firing pattern to respond to the earliest indicator of reward, e.g. the start of the habit task (3). Essentially, the dopamine-containing neurons fired predictively, which suggests the development of an action template in the striatum so the steps of a task are treated as one behavioral unit (1,3).

There are several possible mechanisms for the development of this action template: the gradual tuning of certain modules of striatal neurons, spatiotemporal binding by striatal neurons, and convergence of information on striatal targets (2). Although the exact mechanism remains unknown at this point, the coding of tasks into units or chunks is supported by behaviors like obsessive-compulsive disorder (OCD). The striatum of OCD patients shows consistent abnormal patterns of activity that abate with treatment. The symptoms of OCD involve sequential repetitive behaviors driven by extraordinary compulsions. These behaviors are performed as chunks and are directly linked to the striatum by the patterns of activity mentioned above (2). Additionally, after monkeys were trained in a three step task, the monkeys continued onto the third step even when the reward was given at the second step, indicating a chunking of the task. This chunking was linked to the striatum when pretraining damage to the monkey's striatum led it to stop at the second step instead. This indicated that damage to the striatum prevented the binding of the task into a unit as had been previously observed (2).

Chunking of tasks allows for the automated nature of habit behavior. In fact, attention to the tasks involved in a habit could lead to its disruption (2). This emphasizes the importance of slow learning in habits. This gradual development provides a selection mechanism for which task sequences will be encoded as habits. Only those tasks which are repeated over a period of time have the potential to become habits. This is particularly important since the predictive firing of dopamine-containing neurons and the chunking of habit steps makes it especially difficult to break a habit once it is formed (2).

Since a habit is a series of behaviors bound together and initiated by a particular context, avoiding this initiating step could be key to breaking a habit (8). Habits are formed by the repetition of a particular neural pathway leading to a reward. When a habit is being formed, learning creates a bombardment of action potentials that strongly depolarize a target cell so that fewer action potentials are need to trigger depolarization in the future. This can create a neural pathway - a series of connected neurons whose polarization is permanently raised closer to the threshold potential making it easier to propagate action potentials down this path. In order to break a habit, it might be necessary to prevent particular neural pathways from being selected (11). This could be done by creating new neural pathways that are preferred, i.e. making a new habit to take the place of the undesirable one (8).

The importance of the initiating step in performance of habits is underscored by certain behaviors associated with Parkinson's. Since the release of dopamine is associated with the beginning step of a habit, a lack of predictive capacity, i.e. the ability to anticipate a reward and release dopamine at the start of a habit chunk, could impair sensorimotor functionality (2). This would lead to behaviors similar to those displayed by Parkinson's patients, in which they have particular difficulty starting and stopping movement sequences, or switching from one sequence to another (3). The role of the basal ganglia in task switching is illustrated by a decrease in this ability by patients with basal ganglia damage. For example, patients with Huntington's disease made significantly more errors in selecting a sample item from a group of items which were identical to the sample along one dimension (6). This indicates a difficulty in switching attention between dimensions, thus linking the basal ganglia with the ability to readily switch between learned procedures or habits (6).

Once a habit chunk has been initiated, problems can occur if there are defects in the inhibitory influence of output neurons in the basal ganglia (4). Neuroimaging of patients with Tourette's Syndrome shows abnormal levels of activity in the striatum (1) indicating a connection between overactivity in the basal ganglia and tics (4,7). In fact, tics have been suggested as the building blocks of habits (4), so overactivity along habit pathways could lead to the uncontrolled tic behaviors characteristic of Tourette's.

The acquisition and performance of habits can also be manipulated by certain drugs. It is in fact this manipulation of the habit formation process that could be the underlying mechanism of addiction (9). For example, there is heightened activity in the striatum which is associated with a proportionate increase in stereotyped behavior when rats are treated with drugs such as cocaine or amphetamine (1). This heightened activity may act like a switch in the basal ganglia which changes a habit into an addiction (9). In addition, if a small surgical change is made in the addicted rat's basal ganglia, it loses its addiction immediately (7). Since even one dose of these drugs can be addictive, the gradual, repetitive nature of habit formation is circumvented, possibly due to a chemical change from the sudden, massive reward of a high (9).

The idea of the basal ganglia as a key player in habit formation is further strengthened by studies which dissociate other areas of the brain associated with learning and memory, e.g. the hippocampus and the amygdala, from habit formation. The hippocampus is involved in explicit, factual learning and memories (11). The amygdala maintains emotional memory (11). Experiments in which rats are given a choice between a cue response (striatal use) and a spatial response (hippocampus use) for a trained habit task follow along structural damage lines. That is, rats with hippocampus damage show a cue response and those with striatal damage show a spatial response. Similarly, rats were able to acquire habits with amygdala damage, but did not show acquisition of stimulus-reward information, and vice-versa with striatal damage. This pattern indicates parallel and simultaneous acquisition of the task during habit learning for the hippocampus, amygdala, and striatum along with a shift in strategy based on location of damage (5). Further, it indicates a dissociation of learning and memory functions among these structures (5).

Habits are differentiated from other types of learning both structurally (basal ganglia changes) and behaviorally (incrementally, unconsciously acquired). They are essentially discrete, quantized patterns of behavior that comprise major portions of individual everyday existence. The complexity of conscious behaviors requires the surrender of routine tasks to the unconscious in order to allow a basic level of multi-tasking. For example, habits allow us to walk around the block and talk to companion at the same time, to eat while we watch TV, to find our way home while dissecting the exam we just took in our mind. While this is certainly convenient in many ways, this surrender of control also leads to questions regarding free will. Can habits alter one's brain structure in such a way that free will is lost? Isn't this the essence of addictions? How is the conflict between one's conscious will and the unconscious force of habits reconciled?

References

Note that starred (*) sources are accessible only to Bryn Mawr, Haverford, and Swarthmore students through Tripod

1) Graybiel, Ann. (2000). "The Basal Ganglia." Current Biology, 10(14), R509-511.

2) Graybiel, Ann. (1998). "The Basal Ganglia and Chunking of Action Repertoires." Neurobiology of Learning and Memory, 70, 119-136.*

3) Jog, Mandar, Yasuo Kubota, Christopher Connolly, Viveka Hillegaart, and Ann Graybiel. (1999). "Building Neural Representations of Habits." Science, 286, 1745-1749.*

4) Leckman, James and Mark Riddle. (2000). "Tourette's Syndrome: When Habit-Forming Systems Form Habits of Their Own?" Neuron, 28, 349-354.*

5) McDonald, R.J. and N.S. Hong. (2004). "A Dissociation of Dorso-Lateral Striatum and Amygdala Function on the Same Stimulus-Response Habit Task." Neuroscience, 124, 507-513.*

6) Packard, Mark and Barbara Knowlton. (2002). "Learning and Memory Functions of the Basal Ganglia." Annual Review of Neuroscience, 25, 563-593.*

7) Anthony, Richard. (2001). "Changing Habits: Brain Studies May Help Us Overcome Destructive Behaviors." Spectrum, MIT, online.

8) Eveld, Edward. (2000). "It's Time to Break Those Bad Habits; Here's How." The Kansas City Star, online.

9) "The Infinite Mind: Habit." (2003). The Infinite Mind, online.

10) Halber, Deborah. (1999). "Work Probes Why Habits Are Hard to Make, Break." News Office, MIT, online.

11) Campbell, Neil and Jane Reece. (2002). Biology (Sixth Edition). San Francisco: Pearson Education, Inc.


A Neurobiology of Dreaming: Dreams and Biologic Re
Name: Elizabeth
Date: 2005-02-22 01:02:13
Link to this Comment: 13102

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Dreaming is one of the brain’s more perplexing and fascinating phenomena. Sometimes
vivid, colorful and bizarre, other times simply odd or mundane, dreams create an entirely
different world for the sleeper out of often-random images, sounds or other sensations.
But how can it be explained? Is there a “dream center” in the brain that is activated
during sleep, or is there a change in brain chemistry during REM sleep that brings about
these nightly visions? Several neurobiological factors contribute to dreaming, and this
paper asserts that dreams can be explained through said biological processes alone, and
that to dream is no different from performing any other waking function, a hypothesis
that is rather pejoratively referred to as “biologic reductionism.” The term in this paper, however, is not used so negatively, but rather is used to support the working model of brain=behavior in our class lectures.

To start off, people have always wondered whether or not there is a function or
evolutionary advantage to dreaming. If so, what would this function be? Some
researchers are fond of comparing the brain’s sleeping processes to that of defragmenting
a computer: “For Nobel laureate Francis Crick of the Salk Institute in San Diego, dreams
are nothing but random attempts, without any deeper meaning, to clear from the brain
unneeded or even harmful memory. Crick claims this is a necessary step to reset the brain
for the next day, much as one erases old data from a floppy disc” (1). Others, such as
psychologist J. Allan Hobson, proposed that dreams are the result of random impulses in
sleeping neurons of the brain, and that dreams arise from the brain’s attempt to make
sense of these spontaneous neural impulses. (1)

However, current research suggests that dreaming serves neither a discernible biological
purpose, nor do dreams result from random firing patterns. Rather, dreams are simply a
form of “sleep thinking,” a good example of nerves firing on their own in the brain and
creating their own signals"the autonomous function of what we refer to in class as the
individual “boxes” within the brain. These firing patterns of the neurons are far from
random; psychologist Bill Domhoff’s work in studies of sleep and dreaming would
indicate a very organized network of brain structures that continue to function during
sleep in very much the same way they function in our waking hours.

What is interesting to consider is not why, but how we dream. The ability to dream in an
organized, almost story-like progression arises from what psychologist Bill Domhoff
calls a human “cognitive achievement.” As far as we know, animals do not dream, at
least in the same story-line format that humans are able to create. Neither do very young human children; in lab settings, children under the age of 9 reported mostly static images or feelings whenever awakened during an REM dreaming episode. Older children
seemed to develop the ability for story dreams, that is, a dynamic situation within the
dream that reflected certain activities or emotions (4). These studies performed by
Domhoff and David Foulkes bring up the idea of the “cognitive achievement principle,”
that is, certain neural networks in the forebrain (particularly parietal) areas must be well established before vivid, story-like dreaming can occur (4). In children under the age of 9, these areas of the brain are not yet as complexly developed as in the older children who more frequently report the story dreams.

A second question that has also fascinated researchers: do dreams have meaning or a
universal symbolism as described by such analysts as Carl Jung? According to Dumhoff,
they do not; dreams are simply a reflection of everyday occurrences or going through
familiar tasks. This is what Domhoff refers to as the “cognitive continuity principle,” (4) or the fact that experiences and emotions that occur during waking hours are very much active during sleep as well. Often, though certain objects in a dream may seem out of place or from another situation altogether, the brain will put these elements together and work them into the typical story-dream format that, surprising and bizarre as the dream may seem, actually makes sense in terms of a story progression. The supposed
phenomenon of dreaming as a problem-solving device works similarly, but it must be
stressed that the dream itself does not offer a some solution outside of our knowledge to
problems mulled over during the day. Whether or not a possible solution arises from
later consideration of the dream is one thing, but dreaming is not problem-solving: a
dream may serve as an inspirational tool to artists, for example, but in fact a dream more often than not reflects the waking worries of the person (2). This is a prime example of Domhoff’s third principle, the “repetition principle” (4) which states that we cannot dream of what we do not know, and that what we do dream is largely made up of familiar activities, situations, and fears we experience in everyday life. But again, without the complex network of brain structures in the parietal lobes, the brain would most likely lose this ability to create a cogent dreaming situation from our experiences, further stressing the importance of biological mechanics in dreaming.

Another piece of evidence in favor of biologic reductionism is the study of REM sleep:
Studying the physiology of the sleeping brain reveals a different brain chemistry during
sleep, according to the “random firings” hypothesis proposed by neurophysiologist J.
Allan Hobson: “Random firings, Hobson says, are due to a very different composition of
signal-transmitting chemicals, called neurotransmitters, in the brain during REM sleep as
compared to the waking brain. According to Hobson, a different brain chemistry also
explains"through chaotic nerve impulses"our wild and bizarre dreamscapes during
REM sleep” (1).

But the idea of chaotic randomness goes against Domhoff’s view of higher-order
processes, such as the continuity and cognitive achievements that allow for organized
story-dreaming. If the signals were simply random and uncoordinated, the things we
dream about would not be integrated into any recognizable form at all, and sleepers
would report the static dream images or feelings as witnessed in patients with damage to
critical structures of the brain. Therefore, these higher processes cannot, and should not, be thought of as a process that occurs outside of neurology. Important structures in the limbic system, parietal and occipital lobes have been shown to play important roles in the story-format of dreams. Dreaming should not be interpreted as anything more
meaningful or mystical than waking thoughts, which admittedly can often be as strange
as any dream fragment. The important thing to remember, though, is that changes in the
brain lead to changes in dreaming; brain damage, drugs, or disruptions of neural networks
have all been shown to have an effect on the nature of a person’s dreams (4), a strong
argument for the neurobiological basis of dreaming. Although sometimes it may seem
that a certain “prop” or object in a dream is put there to represent something more
significant or is the product of the subconscious, this cannot be the case according to so called “biologic reductionism,” or the idea that dreams can be explained solely through the firing patterns of neurons. Yet Domhoff and Foulkes are themselves wary of biologic reductionism’s attempts to explain the nature of dreaming through simple measurements of brain activities: “‘I am always very wary about neurobiological findings. Dreams are not just eye movements,” Domhoff says. ‘There might be a neurobiology of dreaming, but never a neurobiology of dreams’” (1).

Domhoff is right when he says dreams are not simply “eye movements;” REM sleep is
merely characterized by such eye movement and does not even always indicate a dream:
dreaming can also occur in other deep stages of sleep (3). Yet why should dreaming be anything governed by principles outside of the brain? Even with all the accumulated evidence for a relatively simple explanation of how we dream, researchers are still wary of tackling the question of why we do it. If there is no greater significance in dreaming other than “thinking while we sleep,” why do we want to believe in a greater meaning for our dreams? Why should our brains create a sleeping reality impossible to explain through the normal firing patterns of “waking” neurons? After all, no one believes that waking thoughts are so unusual, no matter how off-the-wall any one fleeting thought may be. Why then, should dreams hold such a mystic quality if they are nothing more than a sleeping biological process?

References


1)Science Notes, 1998, A site summarizing the work of noted psychologists and neurophysiologists in the field of dream research

2)Domhoff, G. W. (2003). The Case Against the Problem-Solving Theory of Dreaming., A paper refuting the so-called "problem solving" method of dreams.

3)The Purpose of Dreams, a short paper on dreaming's function and meanings in society.

4) Domhoff, G. W. (2001). A new neurocognitive theory of dreams. Dreaming, 11, 13-
33.

5)The Quantitative Study of Dreams, A comprehensive database of dream studies, researchers and published papers.


ADD and ADHD, What is Really Inhibiting Bright Min
Name: Nadine Hun
Date: 2005-02-22 01:02:29
Link to this Comment: 13103

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Nadine Exie Huntington
Bryn Mawr College
Spring Semester 2005
Neurobiology 202
ADD and ADHD
What is Really Inhibiting Bright Minds of the Future?

Attention Deficit Disorder and Attention Deficit Hyperactivity Disorder are learning disabilities which are being detected and treated with startling frequency in America today. There are a plethora of medications and treatments currently being prescribed, also with astounding regularity, and often with little regard for their repercussion. While each drug and treatment has physical and medical side-effects, one must also consider the broader and longer term consequences, not only on the afflicted individual, but on society as a whole.
Medications such as Adderall, Concerta, Dexedrine and Ritalin are now being prescribed 49% more often than they were in 2003 and at ages as young as three years old. Due to the nature of its symptoms (lack of concentration, inability to focus, and impulsivity ) children are frequently misdiagnosed with the disorder, when they are simply displaying normal adolescent or infantile behavior. While 12% of American children have been labeled with one of these two learning disabilities many families are refusing to put their children on medication because of its mind-altering effects .
Although with each patient the symptoms of ADD and ADHD vary, one common thread they tend to share is an abundance of creativity. ADD and ADHD are speculated to be linked to such brilliant minds as Thomas Edison, Albert Einstein, Salvador Dali, Winston Churchill, Leonardo DaVinci, Mozart, Benjamin Franklin, Maria Montessori, and David Neeleman (CEO of JetBlue Airways). Their out-of-the-box creativity and spontaneity caused them to succeed in their field of genius, where more closed-minded individuals lack the ingenuity and imagination to stray from conventional ideas. In general those with ADD or ADHD are non-conformists whose insatiable curiosity and exuberance causes them to succeed tremendously in their interests. These individuals, however, are unable to focus on material which does not excite them, and tend to score significantly lower marks in school subjects which do not grab them. Parents in search of an honor roll student are quick to put their children on Ritalin or a similar drug, while parents who embrace their childs creative, if at times exasperating, personality maintain that these drugs have debilitating repercussions.
One must wonder whether Einstein would have made as many contributions to the world as he did if his inventive mind had been chemically modified. As the rate of children diagnosed with learning disabilities grows, and the number of children on Ritalin increases, will the input of original and daring ideas decrease? The association between ADD and brilliance is strong, but so too is the correlation between medicated students and the extinguishing of creative sparks. Are we as a developing society prepared to loose some of the brilliant minds of today, merely to facilitate order and concentration in our classrooms?
Teachers criticize children with ADD or ADHD as being unstable, uncooperative and inattentive. Dr. Othmer argues, however, that the brain is just like any other mechanism, and as such can be rendered unstable because of the amount of strain or activity to which it is exposed. He urges parents and teachers to look at the brain as a control system. Any feedback control system obeys the general rule that as higher overall gains are approached, the system runs the risk of becoming unstable. If high mental performance is connected with high gain then the correlation with brain instability would be explained. Children with ADD and ADHD are indeed sporadic in their interests and diligence in everyday activities (chores and homework), but are performing magnificently in other venues. Their brains are not lazy or recalcitrant, but directed at a specific focus or goal of interest, causing other tasks to be cast aside, or performed with irregularity and indifference.
Just as many suffering from ADD and ADHD are being robbed of the opportunity to lead normally functioning and orderly lives, our culture is running the risk of being robbed of its most clever minds. Numerous artists, business executives, scientists and other geniuses of today describe their past troubles in school, and their parents refusal to use medication for their problems with gratitude, as they feel that they would not have attained their success with the hampering of their creative intellect through Ritalin, Adderall or other such drugs . These medications are too new to be able to study their long term social and cultural impacts, but we must carefully consider the consequences of their profuse use among children.

(YOUR REFERENCE NUMBER).

References

SUCCESSIVE REFERENCES, LIKE PARAGRAPHS, SHOULD BE SEPARATED BY BLANK LINES (OR WTIH

, BUT NOT BOTH)

FOR WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY

REFERENCE NUMBER)NAME OF YOUR FIRST WEB REFERENCE SITE, COMMENTS ABOUT IT

FOR NON-WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY

REFERENCE NUMBER) STANDARD PRINT REFERENCE FORMAT


The Role of Optimism in Neurobiology and Behavior
Name: Liz Bitler
Date: 2005-02-22 01:09:21
Link to this Comment: 13104

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


"Life is Good." It's a motto that appears everywhere: from tee-shirts to water bottles, and even bumper stickers. It's what I say to my friend whenever he mocks me for being an optimistic. It is my belief that having an optimistic outlook on life can lead to a more enjoyable experience of life. And the phrase "Life is Good" is what got me interested in the implications that optimism may have on our neurobiology as humans.

Different individuals have very different outlooks on life, and I'm curious about the impacts that particular outlooks may have on one's brain or their behavior. There is the proverbial water glass to consider. If an 8oz glass contains 4oz of water, there are those that consider the glass to be half full, and those that consider it to be half empty. Recent studies have found that optimists, that is to say, those who see the glass as half full, generally live about twelve years longer than pessimists.(1) This has interesting biological implications, and I think that the way that neurobiology affects one's ability to be optimistic, and the way that optimism in turn affects human biology is worth investigating. I think that people have the ability to change their experiences of the world by changing their outlook and the way in which they perceive their surroundings, but I believe that there may be something on a neurobiological level that is capable of affecting one's ability to be optimistic.

On a biological level, there have been studies concerning the implications of perception of one's life experiences. For example, studies have shown that it is not the actual amount of stress, but rather one's perception of the amount of stress that correlates to biological responses. (1) I feel that this provides evidence that the interpretation of experiences plays a strong role in the biological responses to such inputs. If a person is able to change the way that life experiences are input in the brain, or the way that the inputs are interpreted by the brain, they may be able to achieve a more optimistic disposition.

Let me begin with possible ways to change the method of inputting experiences into the brain and the results that may ensue. I think that the most obvious way of changing the input to make more one optimistic is just by changing one's outlook on life. Simply telling one's self positive things may allow them to appreciate the world more. For example, upon looking outside and seeing snow, there are many different outlooks that would result in the input of such information differently. A person could say "This is awful, now I'm going to have to shovel my car out again and trudge through the snow to get to class." On the other hand, one could say "The snow is beautiful, and it really makes the campus appear more peaceful." Such outlooks would then lead to different inputs, resulting in different moods and amounts of enjoyment of the snow. I realize however that a possible objection to this is that there may be a predetermined outlook created by the brain that results in the manner in which the situation is assessed.

Another way to change the way that the information is input into the brain relies on the concept of perceptual accentuation.(2) That is, while one may acknowledge both the positive aspects and the negative aspects that are associated with freshly fallen snow, they can accentuate those that are positive by focusing on them more. This can be done by spending more time reveling in the pleasantries of the snow than thinking about the difficulties that may also be acquired. I think that this would be possible because selective attention enables people to attend most to what meets their wants and needs. (2)

An impact of altering the way that information is input could be similar to the results of the Pollyanna Effect, in which you see what you want to see. The Pollyanna Effect results in different cognitive appraisals of information of different types. Input that is pleasing and enjoyable is more greatly cognized, that is to say that it is more detailed in the mind, it is better remembered, and it is given a higher status in the mind than less pleasing inputs.(3) For example, if a person is given a stack of 100 one dollar bills and a stack of 100 ten dollar bills, they will characterize the stack of ten dollar bills as weighing more than the stack of one dollar bills because it is a more pleasing stimulus and it is given more status, although the two stacks will have the same weights.

Methods of changing the interpretation of inputs are of interest as well. William James believed that an external event results in physical changes in the body, and that the physical bodily responses are then experienced in an individual as emotion. Because, like many of my classmates, James believed in the concept of free will, he accounted for this in his theory as well. He believed that one could change their physical responses by will, thus changing their emotional responses.(4) This implies that if a person wants to be happier, they simply have to change their body to what it would be if they were happy (for example by smiling), and happiness will follow. There have in fact been experiments to test this hypothesis (called the "facial-feedback hypothesis" (5)) and the results have supported his theory. In one study, participants read cartoons with a pen in their mouth (without knowing why the pens were in their mouths.) Some held the pen between their teeth, utilizing the facial muscles involved in smiling, and others held the pen directly between their lips, utilizing the muscles involved in expressions of displeasure or disgust. Those that had the "happier" expressions found the comics to be more pleasing than did those with the less happy faces. (5)

Stanley Schachter and Jerome Singer had a different concept of the way that information is interpreted by the brain. They believed that there was both a physical response and a cognitive response to input. The cognitive response results from the assessment of the situation and what it means to an individual. In one of their studies, people were given injections of adrenaline and exposed to situations that would induce happiness. There was an informed group, which knew that they had been given the adrenaline, and an ignorant group that did not. Because the informed group attributed their physiological responses (such as an increased heart rate) to the adrenaline on a subconscious level and the ignorant group only attributed it to the pleasing situation, the ignorant group had a stronger experience of happiness. (6) In this way, it seems to follow that people can be more optimistic if they let themselves feel good about a situation, rather than trying to attribute a situation to something greater than their own experiences of it.

Cognitive coping strategies have resulted from concepts of the role of cognition on people's enjoyment of life. It has had very real impacts, particularly in patients suffering from chronic diseases. Under the direction of psychotherapists, such patients were able to lessen the amounts of perceived stress and pain, as well as having physiological impacts. The level of arousal of the sympathetic nervous system decreased, as was the amount of cortisol released internally. Feeling better emotionally enabled these patients to feel better physically and some of them were able to increase their amounts of physical activity and resume some of their daily activities. (7)

Another example in which altering the assessment of a situation results in physiological changes is that of the Placebo effect. Placebos are substances that are given to patients under the assumption that it is a type of medication that has expected results. However, it is nothing more than a sugar pill, saline solution, or other inert substance that will not cause any physiological side effects. It has been proven time and again that many patients that receive a placebo and expect their physical or emotional ailments to improve have actual improvements.(8) The mere suggestion that they should get better enables them to do so.

Neurotransmitters also play a strong role in a person's mental processing and thus ability to enjoy life. Dopamine in particular is released in a person's brain when they experience pleasurable occurrences. Dopamine also has great impacts in the pharmaceutical treatment of depression. It acts as a selective serotonin reuptake inhibitor, which results in an increased amount of serotonin in the synapse of neurons in the brain, and has been shown to alter the mental state of those who take it.(9) In this way, people are able to alter their optimism levels on a chemical and cellular level of the brain.

Optimism is clearly a combination of both biological and cognitive aspects of the brain. But I am still left wondering what role free will plays on the mind and it's interpretation of the world around (or possibly in) it. We know that a person is capable of changing their attitude and the way that they perceive things so as to make their life experiences more enjoyable, but what is it specifically that enables them to do so? Can we will our brains on a chemical level to produce more serotonin or dopamine? Can we change our cognitive process so that information is translated into the brain in a different manner? Or do we simply have to tell ourselves that "today is a good day," and "life is good?"

References

1)Annie Appleseed Project, an article about Optimism and Longevity

2)The Interpersonal Communication Book 10th Edition, online lecture notes

3)Pollyanna Discussion Homepage, a discussion of the Pollyanna Effect as Experiment Results

4)Classics in the History of Psychology, Writings by William James

5)Grounding Language in Bodily States: The Case for Emotion, contains a description of Strack's experiment, as well as other information concerning emotions and their expression through body language

6)Cognitive, Social and Physiological Determinants of Emotional State, a detailed description of Schachter and Singer's experiment

7)Stress and Health: Psychological, Behavioral, and Biological Determinants, an in-depth discussion of the effects of stress

8)The Placebo Effect, an article in the Skeptic's Dictionary describing briefly the Placebo Effect

9)Novel Antipsychotics for Treatment-Resistant Depression, information about several antidepressants and the ways in which depression may not respond to pharmecutical treatment


Congenital Insensitivity to Pain with Anhidrosis
Name: Sarah Mala
Date: 2005-02-22 01:50:15
Link to this Comment: 13108

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Congenital Insensitivity to Pain with Anhidrosis (CIPA) is a rare disease which causes one to lose their feeling of pain. I read this article a couple of weeks ago about a girl who has this rare disease and is incapable of feeling pain and will never know what pain is. It intrigued me and sparked my web paper topic. I wanted to know everything there is to know about this disease and my research to give me answers, but, of course, this was not the case. The more and more I researched I began to wonder if this supports our notion of the "Brain =Behavior". There is so much more to learn about this fairly young disease and with that please take into account that these are sources off the internet and one could not know if they are fully accurate or not. As for the deep detail of the topic, such as names of different genes and etc, I do not fully understand their full meaning so I will write about what I took from all the different information about CIPA.

CIPA is a disease that is very new and that very few people have. There are only thirty-five US Citizens that have CIPA, and most people with this disease usually do not live past 25, which makes it very difficult to study and to come closer to "getting it less wrong". ((1)) This one particular girl, Ashlyn Blocker, has CIPA which causes her life to be very difficult. Since the young girl was born with CPI, she would have no idea what pain feels like and cannot relate to most people. Most of us, from the day we are born, have this intuitive notion about pain. We feel it and know to be aware of it from learning from our experiences. Imagine being unable to learn what pain is because you are unable to have similar experiences. Well, that is how this young girl was born.
Most people would think it would be great to live without pain, but pain is an indication to our brain that our body needs something. Ashlyn is incapable of living a normal life and has to be examined regularly because there is no way to know if she is endanger of killing herself through high fevers because of the inability to sweat, unknown injuries, and etc. ((4))
Ashlyn's case is rare within the world, but there are other studies of people from different ethnic background which also get CIPA. Through these few studies there has been extensive research done and there are many correlations found. So far, CIPA is defined as an autosomal-recessive disorder ((2)) which is a developmental defect (not necessarily hereditary) ((3)) that usually is caused by a history of some kind of trauma. The person affected by this is unable to feel pain, even though they seem to show a normal central and peripheral nervous system. ((3))

With is young disease there are many questions and hypotheses brought up. There are many correlations and observations. On one study of CIPA, many different people having CIPA were observed and Clinical features, Pathological findings, and Molecular Genetics were all taken into account. Under the Clinical features one finding showed that in CIPA patients there is an overproduction of brain endorphins which could be some how interrelated to this disorder. ((3))

Another study was done by taking a biopsy of the cutaneous branch of the radial nerve of two patients with CIPA, differing in gender and age. Within the older of the two patient's biopsy of the radial nerve, there showed to be no small myelinated and unmyelinated fibers but within the younger of the patient the biopsy showed that they were lacking unmyelinated fibers and that the amount of small myelinated fibers was decreased. This suggests "that the disorder was not a hereditary sensory neuropathy, but rather a developmental defect" ((3)). Another pathological finding was that patients with a very small amount of nerve fibers were more likely to have rare nerve fibers in the dermis and no nerve branches or endings on the epidermis. These patients are classified as HSAN4 patients. The studied concluded that these patients "have a hereditary developmental defect of nerve outgrowth"((3)).
Lastly, the study of Molecular Genetics within CIPA patients gives the most substantial information. The study of a gene tyrosine kinase (NTRK1) which is related to the nerve growth factor (NGF) within the patients having CIPA seemed to be the mutation causing CIPA. This study also suggests that there are other TRK and neurotrophin genes might be the cause of developmental defects of the nervous system. ((3))

As for these studies, they just bring me closer to understanding what I want to understand between the brain and its behaviors. So far within this semester I have been trying to find something to show me that the brain and behavior are not equal, but I still cannot find anything. This rare disease, CIPA, shows that the brain and behavior are equal. People affected by this disease feel no pain and will never understand what pain is. Their behavior is equivalent with their brain state.

I find it interesting though that these people affected by CIPA act the function normally other than them not being able to feel pain and sweat. I wonder is there also something different within their brain. One study did show that there was an increase of endorphins within patients' brains that have CIPA, what does that show? Does it change anything? Why is their behavior still the same as most people other than the feeling of no pain? Is the only difference within their brain their insensitivity to pain?

I went into this research wondering about this disease and if it actually went against "brain=behavior" and it has not so far. It only makes the argument less wrong. This disease affects ones nerves because of a mutation of some sort, most likely a gene mutation within the NTRK1. The behavior still reflects ones brain state.

References


1)American girl feels no pain and smiles to her own Blood

2)Congenital Insensitivity to Pain with Anhidrosis


3)Insensitivity to Pain, Congenital, with Anhidrosis; CIPA

4)Girl with rare disease doesn't know pain


Dopamine and Addiction
Name: Imran Sidd
Date: 2005-02-22 02:09:36
Link to this Comment: 13109

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Dopamine is neurotransmitter in the brain that plays vital roles in a variety of different behaviors. The major behaviors dopamine affects are movement, cognition, pleasure, and motivation (1). Dopamine is an essential component of the basal ganglia motor loop, as well as the neurotransmitter responsible for controlling the exchange of information from one brain area to another (1). However, it is the role that dopamine plays in pleasure and motivation that attracts the most neurobiologists attention as well as mine.

In certain areas of the brain when dopamine is released it gives one the feeling of pleasure or satisfaction (1). These feelings of satisfaction become desired, and the person will grow a desire for the satisfaction. To satisfy that desire the person will repeat behaviors that cause the release of dopamine (2). For example food and sex release dopamine (2). That is why people want food even though their body does not need it and why people sometimes need sex. These two behaviors scientifically make sense since the body needs food to survive, and humans need to have sex to allow the race to survive. However, other, less natural behaviors have the same effect on one's dopamine levels, and at times can even be more powerful. Often these behaviors can result in addiction due their effect on dopamine, and that addiction can have negative effects on a person's well-being. Two of such behaviors are

Cocaine is by far the more severe of the two in terms of addiction. Cocaine chemically inhibits the natural dopamine cycle. Normally, after dopamine is released, it is recycled back into a dopamine transmitting neuron. However, cocaine binds to the dopamine, and does not allow it to be recycled. Thus there is a buildup of dopamine, and it floods certain neural areas (3). The flood ends after about 30 minutes, and the person is left yearning to feel as he or she once did (3). That is how the addiction begins. Progressively a tolerance builds up due to the fact that the person is constantly trying to repeat the feeling that he or she had the first time (2). However, the person cannot, because dopamine is also released when something pleasurable yet unexpected occurs (4). After the first time, the person expects the effect, thus less dopamine is released, and the experience is less satisfying. This principal is the foundation of why gambling releases dopamine.

Several studies have been conducted which targeted neural response to rewards. The results were unanimous in the fact that when one performed an action over and over again, and was given a reward randomly, dopamine levels rose. If the reward was given consistently, i.e. every four time the action was performed, the dopamine levels remained constant. Finally, if no reward was given dopamine levels dropped (4). These same random rewards can be seen in gambling. Because the outcome is based on chance, one does not know prior if he or she will win. Therefore, if the person one wins, dopamine levels increase (4). However, unlike cocaine, gambling causes addiction in only 4% of participants. This is due to the fact that Cocaine's chemical input is much more influential on dopamine levels than gambling's behavioral input. Therefore, only people whose dopamine levels are low, become addicted to gambling (5).

This brings up a very interesting topic of discussion. How do some people have lower dopamine levels than others? Is it genetic, environment related, something else, or a combination of factors? One study concluded that pathological gamblers most often experienced traumatizing experiences when they were younger (5). Because most people who become addicted to gambling have low dopamine levels, and also that same group usually has endured a traumatic experience, we have support for the observation that overall dopamine levels can change due to environmental factors. This then supports the observation that both the mind and brain can change to environmental factors. However, another study has observed that a gene related to dopamine is found twice as often in pathological gamblers than non-gamblers (5). This supports the observation that dopamine levels are genetic. Therefore, there are two plausible observations that can be made. Either both genetics and environmental factors effect ones brain anatomy and mind simultaneously, or that environmental factors can affect genes which in turn affect ones brain and mind. Because the observations in the studies show such a strong correlation between pathological gambling, traumatic experiences, and genetic influence, it the later which seems to be the least wrong observation.

Another important question, however more philosophical, is why is risk and reward a trigger for the release of dopamine? As stated earlier, it is scientifically logical that sex and food release dopamine, because they are essential for the sustained life of man. Risk and reward are not, are they? It is my belief that in nature everything happens for a reason; therefore, there must be a scientific explanation for the increase of dopamine levels in result of risk and reward. It seems to me that the human race separates itself from other species on this planet by not only its ability to reason, but its ability to create and innovate. I feel that nature wants humans to create and innovate, and in order to do this a person has to feel satisfaction when one accomplishes an innovation. To accomplish an innovation one has to take risks. It is risky to try to do something that no other being on earth has ever accomplished. Therefore, there must be a reward other than material that one gets when he or she accomplishes the innovation, or that person would not take the risk. The reward is the release of dopamine and the feeling of satisfaction. The problem with this process is that not only can one be satisfied after a major risk and accomplishment, but one can also be satisfied through constant minute risks and accomplishments. Gambling is an example of this.

These feelings of satisfaction that dopamine exhibits are so strong that one can often loses one's ability to reason in order to achieve satisfaction (4). It is then the unconscious that takes over and begins to make certain decisions. The brain develops neural circuits that unconsciously assess reward (4). Because the dopamine plays an active role in these circuits, a person will act in what they think is in their best interest, when in fact the only interest it satisfies is the release of dopamine. This can be exemplified in gambling where one insists on gambling even though he or she knows that the odds are against them (4). This is the case in all casino games, where the games are structured for the house to win. Probability and reason no longer are the most important factors in decision making. The unconscious need for the release of dopamine becomes most important. This supports the observation that the unconscious plays a vital role in decision making.

From this discussion of dopamine and addiction I was able to make some fairly general observations abut the brain. I observed that both a chemical (cocaine) and a behavior (gambling) can have the same effect on the brain. Furthermore, I observed that the brain is affected by both genes and environmental factors, and that most likely the environmental factors affect genes which affect the brain. Also, I was able to observe that dopamine makes humans take risks so that they may achieve greater innovations. And finally it was observable through gambling that the unconscious is constantly making important decisions. It is amazing how one specific topic can generate so many general observations about how the brain, mind, and nature function.

References

1) Dopamine

2) The Dopamine Connection

3) Cocaine Abuse and Addiction

4) Hijacking the Brain Circuits with a Nickel Slot Machine

5) Mental and Physical Status of Gamblers: Physiological Findings


Are Drugs Prevalent during the Menstrual Cycle?
Name: Sophia Lou
Date: 2005-02-22 02:57:46
Link to this Comment: 13110

Sophia Louis 2/21/05
Web Assignment #1: Are Drugs Prevalent in the Menstrual Cycle?
Start with something you're interested in, "surf", don't be afraid to get away from your initial question. Learn something. Being left with these instructions, I began to do exactly that. What I ended up with is a list of topics, which I will bring up in our regular postings, and an interest in something that had never crossed my mind. This past weekend I decided to write my paper on the science behind tickling, and why we cannot tickle ourselves. Today, while shadowing an Obstetrician, Gynecologist, I found an article on PMS and its connection to drug withdrawal. What is usually considered a reproductive process, a monthly emotional and physical setback, is now being connected to withdrawal. According to Dr. Joseph F. Smith, drug withdrawal is a syndrome, which occurs in drug and alcohol addicted individuals who discontinue or reduce the use of their drug of choice. This process of eliminating drugs and alcohol from the body is known as detoxification. Anxiety, insomnia, perspiration, body aches, and tremors are just a few of the physical and psychological symptoms of drug and alcohol withdrawal that may occur during detoxification (1). Like me, Im sure you are all asking what drug is involved in PMS? When and how do we become addicted? Why are we lacking it every month? How does this drug and lack thereof, affect our bodies?

Many women know without even looking at the calendar that their menstrual cycle is about to begin. Common signals are breast tenderness, a feeling of bloatedness or weight gain, feeling tired or "down" or more irritable (2). These changes are entirely normal. But for a small proportion of women there are emotional and behavioral symptoms that are more severe. They affect the way they do their jobs, their relationships with others, or the way they see themselves. It is not normal when premenstrual symptoms interfere with women's lives. These symptoms are a result of Premenstrual Syndrome (PMS).

PMS is a cluster of emotional, behavioral and physical symptoms that have a cyclic pattern related to the menstrual cycle. They usually occur in the week or two weeks before a woman's period. In severe cases, the predominant symptoms are likely to include at least five of the following symptoms: irritability or persistent anger; tension, headaches, anxiety; feeling depressed, upset stomach, bloatedness, joint or muscle pain, mood swings; difficulty concentrating; food cravings or changes in appetite; fatigue, lack of energy; sleep problems; physical symptoms such as breast tenderness, swelling, and aches. The causes of PMS are not yet clear but researchers believe that some women may be more sensitive than others to changing hormone levels during the menstrual cycle.

Recent research studies suggest that PMS may be caused by something similar to drug withdrawal-in this case, the woman's own hormones (3). Hormones are the chemicals "messengers" that, in concert with the nervous system, coordinate the activities of billions of cells in the human body- in this case, menstruation. Throughout this discourse, the drug, so to speak, is a woman's own hormones. Research is being done at Allegheny University that tests the effects of progesterone in the body during menstruation (4). Progesterone is a hormone prevalent in the menstrual cycle and during pregnancy. Progesterone levels are elevated in the second half of the menstrual cycle, and drops to very low levels right before the premenstrual period. The problem with hormones during menstruation occurs when progesterone is converted into another hormone called allopregnanolone, which acts like a sedative, or valium, or even alcohol. This hormone can make you feel relaxed, reduce anxiety, and even reduces seizures. Its effects are to increase the effectiveness of a transmitter in the brain called GABA (Gamma amino buteric acid). GABA is a key transmitter in the nervous system, acting almost like a "plug and socket" between the nerves that communicate in drug use, its receptors are found all over the brain (5). These are the drugs that our body is "begging" for during PMS. Allopregnanolone is like the other drugs (valium, alcohol) in terms of acting as the GABA receptor. So basically, high doses of progesterone and allopregnanolene cause less anxiety and other symptoms of PMS.

As I mentioned before, withdrawal occurs after the drug is discontinued (low levels of allopregnanolone). Although PMS is more subtle, the symptoms are similar to actual "drug" addicts, even women who are epileptic report more seizures during the premenstrual period. Drugs affect mood by altering brain chemistry, specifically the production of neurotransmitters. Neurotransmitters enable nerve impulses to travel through the CNS and regulate thought process, behavior, and emotion. Allopregnanolone acts like a depressant, decreasing neurotransmitter levels. When drug consumption becomes regular, the body adjusts to its constant presence by changing its normal production of neurotransmitters. If the usage suddenly stops or decreases the body and the CNS react to the normal dosage's absence with the symptoms that I have already mentioned.

One study was done on rats that were given progesterone for three weeks and then suddenly discontinued (4). The rats became more anxious; seizures were more easily induced in these rats than the rats that were not given progesterone. The rats were going through withdrawal. When the scientist looked at the actual brain cells, they found that GABA was less effective in calming brain cells after withdrawal from the hormone. GABA normally acts to calm brain cells, so maybe the nerve cells were more excitable, thus leading to the behavioral changes like anxiety, aggression or irritability.

The research being done on PMS has major implications for the future of women. The symptoms of PMS can make a woman's week absolutely miserable, and will not only affect her, but everyone around her. The results of the aforementioned study led to the discovery of a substance that can prevent receptor abnormality thus decreasing the behavioral effects of progesterone and allopregnanolone withdrawal. Even though this drug was rat specific, I am sure that they will be able to find the humans equivalent, and prevent some of the undesirable symptoms associated with PMS. In the meantime, I do not understand why increased levels of progesterone and allopregnanolone are not administered to PMS sufferers. Throughout my research, I did not find any articles suggesting that solution. My suggestion would be to administer some kind of pill containing higher levels of progesterone for women to take during their menstrual cycle. Other studies have been done questioning the causes of PMS. One study conducted by David Rubinow and Peter Schmidt was done at the NIMH in 1998 (6). They found that hormones alone were not the cause of premenstrual symptoms. Another study was done concluding that calcium deficiencies were the cause of the premenstrual symptoms (6). Clearly, the exact causes of PMS remains a mystery. At the beginning of my research I thought PMS was routine, that everyone suffered from mild cramps and had cravings. I assumed it was a regular part of the menstrual cycle. Now, coming to the end of my paper I realized that there are so many more factors involved. Physiological, biological, neural, emotional, behavioral, and societal factors are the most prevalent. This leads me to raise more questions. Can theories of "mind over matter" be included in this discussion? The power of the mind and its effect on behavior does play a role. How can the symptoms be measured, and when does mild become severe? Young women are usually taught about the menstrual cycle before onset. They also talk amongst their peers. Many women are taught to believe that the onset of their menstrual cycles leads to pain and discomfort, many women, like myself, accept PMS as a normal reproductive/biological/physiological process. As was said in class, our minds have strong influences over our behavior.

WWW Sources

1) Withdrawal syndromes Dr. Joseph F. Smith: Medical http://www.chclibrary.org/micromed/00070960.htmlLibrary


2)Premenstrual Syndrome National Women's Health Information Center
www.4woman.gov

3)Understanding PMS-UPENN health system
http://www.obgyn.upenn.edu/mudd/PMSarticle.html

4)The Health Report 1998
http://www.abc.net.au/rn/talks/8.30/helthrpt/stories/s11123.htm

5)Biochemistry of Neurotransmitters
web,indstate.edu

6)PMS and PMDD Cause Serious Suffering

7) Slade, P. (1984) Premenstrual emotional changes in normal women: Fact or fiction?
Journal of Psychosomatic Research, 28. 1-7.


Are Drugs Prevalent during the Menstrual Cycle?
Name: Sophia Lou
Date: 2005-02-22 02:57:56
Link to this Comment: 13111

Start with something you're interested in, "surf", don't be afraid to get away from your initial question. Learn something. Being left with these instructions, I began to do exactly that. What I ended up with is a list of topics, which I will bring up in our regular postings, and an interest in something that had never crossed my mind. This past weekend I decided to write my paper on the science behind tickling, and why we cannot tickle ourselves. Today, while shadowing an Obstetrician, Gynecologist, I found an article on PMS and its connection to drug withdrawal. What is usually considered a reproductive process, a monthly emotional and physical setback, is now being connected to withdrawal. According to Dr. Joseph F. Smith, drug withdrawal is a syndrome, which occurs in drug and alcohol addicted individuals who discontinue or reduce the use of their drug of choice. This process of eliminating drugs and alcohol from the body is known as detoxification. Anxiety, insomnia, perspiration, body aches, and tremors are just a few of the physical and psychological symptoms of drug and alcohol withdrawal that may occur during detoxification (1). Like me, Im sure you are all asking what drug is involved in PMS? When and how do we become addicted? Why are we lacking it every month? How does this drug and lack thereof, affect our bodies?

Many women know without even looking at the calendar that their menstrual cycle is about to begin. Common signals are breast tenderness, a feeling of bloatedness or weight gain, feeling tired or "down" or more irritable (2). These changes are entirely normal. But for a small proportion of women there are emotional and behavioral symptoms that are more severe. They affect the way they do their jobs, their relationships with others, or the way they see themselves. It is not normal when premenstrual symptoms interfere with women's lives. These symptoms are a result of Premenstrual Syndrome (PMS).

PMS is a cluster of emotional, behavioral and physical symptoms that have a cyclic pattern related to the menstrual cycle. They usually occur in the week or two weeks before a woman's period. In severe cases, the predominant symptoms are likely to include at least five of the following symptoms: irritability or persistent anger; tension, headaches, anxiety; feeling depressed, upset stomach, bloatedness, joint or muscle pain, mood swings; difficulty concentrating; food cravings or changes in appetite; fatigue, lack of energy; sleep problems; physical symptoms such as breast tenderness, swelling, and aches. The causes of PMS are not yet clear but researchers believe that some women may be more sensitive than others to changing hormone levels during the menstrual cycle.

Recent research studies suggest that PMS may be caused by something similar to drug withdrawal-in this case, the woman's own hormones (3). Hormones are the chemicals "messengers" that, in concert with the nervous system, coordinate the activities of billions of cells in the human body- in this case, menstruation. Throughout this discourse, the drug, so to speak, is a woman's own hormones. Research is being done at Allegheny University that tests the effects of progesterone in the body during menstruation (4). Progesterone is a hormone prevalent in the menstrual cycle and during pregnancy. Progesterone levels are elevated in the second half of the menstrual cycle, and drops to very low levels right before the premenstrual period. The problem with hormones during menstruation occurs when progesterone is converted into another hormone called allopregnanolone, which acts like a sedative, or valium, or even alcohol. This hormone can make you feel relaxed, reduce anxiety, and even reduces seizures. Its effects are to increase the effectiveness of a transmitter in the brain called GABA (Gamma amino buteric acid). GABA is a key transmitter in the nervous system, acting almost like a "plug and socket" between the nerves that communicate in drug use, its receptors are found all over the brain (5). These are the drugs that our body is "begging" for during PMS. Allopregnanolone is like the other drugs (valium, alcohol) in terms of acting as the GABA receptor. So basically, high doses of progesterone and allopregnanolene cause less anxiety and other symptoms of PMS.

As I mentioned before, withdrawal occurs after the drug is discontinued (low levels of allopregnanolone). Although PMS is more subtle, the symptoms are similar to actual "drug" addicts, even women who are epileptic report more seizures during the premenstrual period. Drugs affect mood by altering brain chemistry, specifically the production of neurotransmitters. Neurotransmitters enable nerve impulses to travel through the CNS and regulate thought process, behavior, and emotion. Allopregnanolone acts like a depressant, decreasing neurotransmitter levels. When drug consumption becomes regular, the body adjusts to its constant presence by changing its normal production of neurotransmitters. If the usage suddenly stops or decreases the body and the CNS react to the normal dosage's absence with the symptoms that I have already mentioned.

One study was done on rats that were given progesterone for three weeks and then suddenly discontinued (4). The rats became more anxious; seizures were more easily induced in these rats than the rats that were not given progesterone. The rats were going through withdrawal. When the scientist looked at the actual brain cells, they found that GABA was less effective in calming brain cells after withdrawal from the hormone. GABA normally acts to calm brain cells, so maybe the nerve cells were more excitable, thus leading to the behavioral changes like anxiety, aggression or irritability.

The research being done on PMS has major implications for the future of women. The symptoms of PMS can make a woman's week absolutely miserable, and will not only affect her, but everyone around her. The results of the aforementioned study led to the discovery of a substance that can prevent receptor abnormality thus decreasing the behavioral effects of progesterone and allopregnanolone withdrawal. Even though this drug was rat specific, I am sure that they will be able to find the humans equivalent, and prevent some of the undesirable symptoms associated with PMS. In the meantime, I do not understand why increased levels of progesterone and allopregnanolone are not administered to PMS sufferers. Throughout my research, I did not find any articles suggesting that solution. My suggestion would be to administer some kind of pill containing higher levels of progesterone for women to take during their menstrual cycle. Other studies have been done questioning the causes of PMS. One study conducted by David Rubinow and Peter Schmidt was done at the NIMH in 1998 (6). They found that hormones alone were not the cause of premenstrual symptoms. Another study was done concluding that calcium deficiencies were the cause of the premenstrual symptoms (6). Clearly, the exact causes of PMS remains a mystery. At the beginning of my research I thought PMS was routine, that everyone suffered from mild cramps and had cravings. I assumed it was a regular part of the menstrual cycle. Now, coming to the end of my paper I realized that there are so many more factors involved. Physiological, biological, neural, emotional, behavioral, and societal factors are the most prevalent. This leads me to raise more questions. Can theories of "mind over matter" be included in this discussion? The power of the mind and its effect on behavior does play a role. How can the symptoms be measured, and when does mild become severe? Young women are usually taught about the menstrual cycle before onset. They also talk amongst their peers. Many women are taught to believe that the onset of their menstrual cycles leads to pain and discomfort, many women, like myself, accept PMS as a normal reproductive/biological/physiological process. As was said in class, our minds have strong influences over our behavior.

WWW Sources

1) Withdrawal syndromes Dr. Joseph F. Smith: Medical http://www.chclibrary.org/micromed/00070960.htmlLibrary


2)Premenstrual Syndrome National Women's Health Information Center
www.4woman.gov

3)Understanding PMS-UPENN health system
http://www.obgyn.upenn.edu/mudd/PMSarticle.html

4)The Health Report 1998
http://www.abc.net.au/rn/talks/8.30/helthrpt/stories/s11123.htm

5)Biochemistry of Neurotransmitters
web,indstate.edu

6)PMS and PMDD Cause Serious Suffering

7) Slade, P. (1984) Premenstrual emotional changes in normal women: Fact or fiction?
Journal of Psychosomatic Research, 28. 1-7.


The Human Behavior of Communication
Name: Alfredo Sk
Date: 2005-02-22 03:00:53
Link to this Comment: 13112

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


A person's need to communicate and form close and complex relationships with other people is one of the most well studied of all the human behaviors. Its applications can be seen in almost all the major fields of social science, sometimes being the sole focus of a specific subfield (i.e. social psychology). Although these fields often deal with the effects and benefits that communication with others can have on an individual, when it comes to the natural sciences, biologists are only interested in its most observable manifestation, language. One of the most recent trends of thought in neurobiology is the idea that all of human behavior, thought, and emotion originate from the lump of matter that sits atop our body, the brain. When applied to the study of language, this assertion requires that two conditions are met: 1) that there must be an anatomical area of the brain that is responsible for language in humans and 2) that this area of the brain must be different for people who speak different languages.

For determining the validity of the first condition, it was often more valuable to use a backwards technique of discovery. For example, researchers would examine cases in which there was a loss or inability to communicate through language and find out what cause the problem rather than performing experiments on patients without language impairments. It is assumed that the area of the brain that was damaged was responsible for the ability that the patient lacked. Now let us pick apart the processes involved with communication through language, starting with the comprehension of spoken language.

The first step in this process is the physical recognition of the sound waves produced by produced by another's speech. This is a very detailed and complex process whose specifics are not entirely relevant to the comprehension of language. However, it is important to keep in some of the details, such as the fact that the sensory information received by the organs of our inner ear through sound waves is processed on the sensory cortex in the temporal lobe (1). Knowing this, it makes sense that the portion of the brain responsible for the comprehension of spoken language be located in the temporal lobe of the brain. This area, named Wernicke's area after the neurologist that discovered it, was first identified in a patient who suffered from what is now referred to as Wernicke's Aphasia (2). This is a condition often associated with a brain lesion in Wernicke's area in which the patient, although he is able to speak, is unable to understand the speech of others. In fact when the patient does speak, it is with meaningless, unrelated sentences whose words often do not relate to one another. Surprisingly, however, they tend to have little trouble with the grammar of their sentences (2).

Once speech is comprehended and interpreted, one then gathers their thoughts in an attempt to produce a response in the form of spoken language. Just as with Wernicke's area, the location Broca's area, the region of the brain responsible for the act of speaking, is determined by its function. It is located near the area of the motor cortex responsible for the muscles in our face because the production of speech would not be possible without the physical movement of our tong and mouth (1). Paul Broca, for whom the region is named after, made his discovery after performing an autopsy on one of his patients who had suffered severe brain damage to it. "Tan", the name given to the patient because that was the only word he could say, had no trouble understanding someone speak but could not do it himself. In some cases of Broca's Aphasia, the patient may be able to produce slurred speech; however, it is usually expressed in very poor grammar (i.e. it will be missing the ed ending to words in the past tense) (2).

Now that we have covered the basics of spoken language, we can turn our attention to understanding and construction of written language. Once again, the idea of anatomic specificity is maintained with the angular gyrus, the brain region responsible for written language, being located in the brain's occipital lobe near the visual cortex (2). This is expected because one's ability to read and write is directly related with their visual perception. Recently, problems with the angular gyrus have been linked to conditions that result in poor reading or writing activities. More specifically, it is thought that low activity levels in this region in the brains of people with dyslexia (difficulty with reading) and agraphia (inability to write) has caused them to use other, less efficient areas of the brain to perform these tasks (3).

We now turn our attention to the second condition. There has been some support for the idea that people with different behavior related to language also have differences in brain structure and the way that they process and produce language. For example, recent findings have found that bilingual children who are bilingual have a larger amount of grey matter in the brain areas responsible for language when compared to people who only speak one language (4). There also seems to be a specific pattern of lateralization of these language centers between right and left handed people (they are located on the left hemisphere for right handed people and vise-versa for left handed people) (2). This pattern of specialization between the two hemispheres as far as language is concerned seems to deteriorate as people get older and they begin using both sides more equally.

This evidence, however, does not account for differences in brain anatomy and function in the language areas of two people who speak different languages. In fact, it has been shown that there is little or no difference between the two. Although this fact would seem to contradict our initial contention that all behavior results from processes in the nervous system, one must consider an important fact about all languages that was discovered by Noam Chomsky. Chomsky's nativist theory of language states that all languages have a universal grammar, syntax, and follow a general organizational patter. Furthermore, Chomsky believes that these laws of language are "hard-wired" into our brains from birth as language acquisition devices (LAD) (5). The fact that all languages are understood, spoken, and written using the same basic rules explains why the brains of two people who speak different languages would not appear different. There is no need for a specialized brain region for each language if they are all, at their root, the same. An important correlation to the nativist theory proposed by Eric Lenneberg is the idea that there is a critical period for the learning of language. If a language (it does not matter which one) is not learned before this period and the proper neural connections are not formed, it then becomes impossible for the individual to ever learn a language (5).

After having resolved this issue, we can confidant that our original assertion, that the behaviors associated with language are a product of our brain and its neural connections, is a step in the right direction in understanding the role of the nervous system in relation to human behavior. We were able to identify the specific areas of the brain that were responsible for language and were able to show that differences in behavior in relation to languages caused (or were caused by) differences in brain anatomy and processing. And in the cases that these behavioral differences did not correspond to anatomical differences, we were able to explain why.

References

1)sparknotes neurobiology webpage,

2)website created by Dr. C. George Boeree,

3)the Society for Neuroscience webpage about dyslexia,

4)article posted on the UCSF website,

5)the Wikipedia site about language acquisition and Noam Chomsky,


Autism as evidence for the brain being responsible
Name: Lauren Doc
Date: 2005-02-22 03:40:20
Link to this Comment: 13114

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


In fairly recent years medical and social awareness of autism has grown to the level that more and more individuals are being diagnosed with the disorder and the diagnosis is coming at earlier stages in a child's development. Especially with the awareness brought by the movie "Rainman", autism has jumped to the forefront of medical issues as a disorder that affects approximately 425,000 Americans under the age of 18 (1) . This developmental disorder can provide an example to support the theory that the brain is responsible for all human behavior, rather than a soul or other element that could define personality and/or behavior.

Autism affects many important functions of human behavior, usually manifesting in early childhood, sometimes seemingly overnight. Most of the effects of this disorder impair an individual's social behaviors and can cause other behaviors such as repetitive actions and perseverations (2). Until recently the only diagnostic tests and defining characteristics that existed for autism involved behavioral studies. Researchers are now looking at the physical manifestations of autism in the brain structure of individuals with the disorder. More evidence is being uncovered to suggest that structural differences or abnormalities in the brain are what lead to the changes in behaviors observed in individuals upon the onset of autism (2). The cause for these structural and developmental changes in the brain cannot yet be determined, however a possibility exists that environmental factors contribute to the onset; even inflammation and vaccinations are being examined as possible causes.

Researchers have been able to map out areas of brain activity in autistic individuals and compare them to the active regions and amounts of activity in a control group of non-autistic individuals. It is estimated by some that autistic individual's brains are wired differently from birth which causes the different behaviors and effects of autism (1) . Whether the changes are present at birth or whether they occur gradually cannot be determined as of yet, but either way provides evidence to the fact that the changes in the brain bring about changes in behavior. Data to support the brain being responsible for behavior can be exemplified by Dr Fred Volkmar's statement. '"If you put 100 people with autism in a room, the first thing that would strike you is how different they are, the next thing that would strike you is the similarity'" (1) . In this respect different people's brains function in different ways accounting for the diverse variations of behaviors among a sample population which could be said to happen within a population of autistic individuals. However, the autistic individuals all possess similar changes in brain structure and development which cause them to behave in manners that are more similar to each other than to non-autistic individuals.

Two specific malfunctions are currently under research by scientists as the cause of the changes in behavior when a child first displays signs of autism: an abnormal pruning process (2), and abnormal changes in the limbic system; more specifically in the amygdala of the brain (4). In the first instance, pruning is a process that occurs several times during development to rid the brain of abnormally functioning neural connections. Pruning can help to maximize coordination of neural circuits (2). When pruning fails to function as may be the case in autism, brain size will increase and neural functioning and synapse will be decreased (2). This fits with studies conducted that found the brains of autistic children to be markedly larger in their early years as compared to a child without autism. This increased brain size is attributed to an increase in both grey and white matter that some feel causes a deluge of stimuli in the autistic brain; more than can be handled naturally. By adolescence the brain size of autistic children tends to have evened out in respect to those of non-autistic individuals, and in some cases they are even smaller than non-autistic children (1). However, by this point the damage has already occurred and the lack of pruning has left the brain with too many inefficient and damaged circuits.

A second difference or abnormality in the brain that could explain the change in behavior lies in the amygdala, which is part of the limbic system. The current definition of the limbic system includes parts of the hypothalamus, the septal area, the nucleus accumbens, the neocortical areas, and most importantly the amygdala. The amygdala is the part of this particular system that is most specifically involved in feelings and emotions. The amygdala is involved with the memory of specific cues that recognize fear and apprehension in human faces (3), which could explain the abnormal social behaviors of autistic individuals. This area also mediates emotional responses that humans possess from birth as well as learned emotional responses (3) and in the case of autism this could explain the lack of social responses and the flat manner of dealing with emotions and other people.

Although autism is not a newly discovered developmental disorder, many things are still unknown regarding the neurobiology of the disease and the exact definition of its effects on humans. The brain is such a complex organ and no two people possess the same brain which makes it difficult to measure and contrast brain differences among autistic individuals as compared to non-autistic individuals. However, with what little is known about brain structure and abnormalities in autism it is apparent that these changes can be considered responsible for the behavioral changes that often characterize autism.


References

1) New York Times, good overview of characteristics of autism

2) Hill, Elisabeth L. and Uta Frith. Understanding autism: insights from mind and brain. London: The Royal Society, 2003.

3) Kandel, Eric R. et al. Principles of Neural Science 4th edition. New York: McGraw Hill, 2000.

4) Salmond, C.H. et al. Investigating individual differences in brain abnormalities in autism. London: The Royal Society, 2003.


Social Implications of Lead Poisoning in Children
Name: Jenna Rosa
Date: 2005-02-22 03:52:29
Link to this Comment: 13115

<mytitle> Biology 202, Spring 2005 First Web Papers On Serendip

For decades, lead has been known to be a hazardous toxicant, especially for children. The children who are usually exposed to lead, particularly in this age of better understanding about the effects lead can have on neurological development, tend to live in older homes and come from poorer families who cannot afford to replace the two most common sources of lead to children, lead paint and lead plumbing (leadpoisoning.net). Although lead can affect several areas of the body, the neurological damage is often quite severe for individuals exposed to even slight amounts of lead during brain development. This damage often results in behavioral problems, reasoning and attention deficits, and low IQ and mental retardation, conditions that occasionally lead to deviant behavior. In these areas where lead exposure is so common and unavoidable due to the impoverished state of the inhabitants, the lead exposure of the children that develop neurological deficits and subsequently exhibit deviant behavior must be considered when determining their degree of culpability for a crime. If the physical state and composition of the brain determine the behavior of an individual, a brain damaged by lead poisoning can be the source of socially abnormal behavior.

Lead is referred to as xenobiotic, meaning it is a foreign substance with no useful role in human physiology, toxic even in minute quantities. Rather than breaking down to be eliminated as a waste product, lead accumulates in the body's bones and tissues because the body recognizes it as if it were calcium. It may be absorbed from the gastrointestinal tract or through the respiratory system. Lead exposure can result in low sperm counts in men and can increase the risk of miscarriage or still birth among women. It damages the kidneys and gastrointestinal tract, and it can lead to a host of neurological problems including decreased cognitive abilities and increased behavior problems in children (Konopka, 2003). The trigger level for lead in children, or the level at which it is deemed harmful, has been lowered over the decades and currently stands at 10g/dL, although recent studies suggest that adverse health effects exist in children at blood lead levels less than 10 g/dL (Canfield et al., 2003).

The most common source of exposure to lead in the household is dust from lead paint, commonly used before 1978 when the federal government banned lead as an additive to paint used for housing (CDC). Lead may also leach into water that travels through antiquated lead pipes, particularly if the water flowing through the pipes is heated, acidic, or treated with chloramines, an alternative anti-bacterial additive to chlorine. Other common sources of exposure outside the home are remnants of used leaded fuel or other lead products in soil, older painted toys, furniture, or jewelry, food and liquids stored in lead crystal or lead-glazed pottery or porcelain, lead particles released into the air from lead smelters and cosmetics or folk remedies that contain lead, such as "greta" and "azarcon" used to treat upset stomachs (EPA).

Although lead can cause harm to children and adults alike, the most seriously deleterious effects of lead poisoning are experienced by children still developing mentally and physically. Children are more likely to be exposed to lead because are more likely to be exposed to certain toxins because they play outdoors. They are shorter than adults, which means they can breathe dust, soil, and vapors close to the ground. Children are smaller than adults, therefore childhood exposure results in higher doses of chemicals per body weight (CDC). They are more likely to be irrevocably damaged by lead poisoning because lead causes damage to the nerve cells of the brain while the brain is still developing. The dendrites of nerve cells in developing brains are cut short by lead, thereby reducing the connections between axons among adjacent neurons. Dendrites are most plentiful during the early years of childhood, especially between the ages of 1 and 5, and thin naturally with age. Thus it is crucial for healthy development to establish as many connections between neurons in the brain as possible through education and stimulation between the ages of 1 and 5. When children are exposed to lead which limits the connections being made during this important developmental period, the brain is irrevocably disadvantaged, resulting in decreased amounts of gray matter (braininjury.com). Chelation therapy, which involves reducing the lead concentrations in the bloodstream by orally administering succimer, or injecting ethylenediaminetetraacetic acid (EDTA), has been shown to be ineffective at increasing already damaged neurons and increasing diminished IQ (Rogan et al., 2001). Therefore, even when individuals undergo treatment during childhood, the damaged areas cannot be recovered.

The neurological damage resulting from exposure to lead can result in abnormal behavior, exhibited through increased irritability and violence, learning disabilities, mental retardation, and other functional difficulties. The social effects of these abnormal behaviors through teasing, peer isolation, falling behind in school, drug abuse, domestic abuse, and a lack of understanding about the basis of an individual's impairments may also compound the neurological damage, resulting in psychological trauma, which studies show can cause other types of brain damage. (Rosen, 2001) All these conditions have been known to result in an individual's inability to function in society or possess adaptive skills. Inability to function in society often results in deviancy of various kinds, and at times the deviancy that is a symptom of an individual's neurological damage is so seriously a breach of the mores of social structure that it is viewed by our legal system as criminal.

In a landmark capital trial, Atkins v. Virginia, ruled in 2002, the defendant was given life without parole rather than the death sentence because it was proved he was mentally retarded. His lawyer argued that to put to death someone who had obvious mental deficits and an inability to cope in society was against the eighth amendment guaranteeing no use of cruel and unusual punishment as well as society's standards of decency:

Clinical definitions of mental retardation require not only subaverage intellectual functioning, but also significant limitations in adaptive skills. Mentally retarded persons frequently know the difference between right and wrong and are competent to stand trial, but, by definition, they have diminished capacities to understand and process information, to communicate, to abstract from mistakes and learn from experience, to engage in logical reasoning, to control impulses, and to understand others' reactions. Their deficiencies do not warrant an exemption from criminal sanctions, but diminish their personal culpability. (536 U.S. 304, 122 S.Ct. 2242)

In light of the distinction between sanctioning criminality and administering justice fairly by acknowledging an individual's culpability, it is necessary to see that if the state of the brain determines the behavior of the individual, and if the brain is damaged by a toxin which condemned it from the earliest years of childhood, the resulting behavior can be seen as a symptom of the brain. If that behavior is criminal, and if what made the individual's actions a crime can be attributed to known symptoms of a type of brain damage, then the amount of fault of that individual cannot be as great as if the crime were committed by someone without brain damage.

References

USEPA: http://www.epa.gov/reg3wcmd/lp-childrenrisk.htm accessed 2/21/05

http://www.epa.gov/lead/ accessed 2/21/05

Center for Disease Control: http://www.cdc.gov/nceh/lead/spotLights/changeBLL.htm accessed 2/21/05

New England Journal of Medicine, http://content.nejm.org: Rosen J. F., Mushak P., Primary Prevention of Childhood Lead Poisoning The Only Solution, New England Journal of Medicine, Volume 344, 2001

Rogan W. J., Dietrich K. N., et al., The Effect of Chelation Therapy with Succimer on Neuropsychological Development in Children Exposed to Lead, New England Journal of Medicine, Volume 344, 2001

Science Direct, www.sciencedirect.com: Canfield R. L., Henderson C. R. Jr., et al., Intellectual Impairment in Children with Blood Lead Concentrations below 10 g per Deciliter, New England Journal of Medicine, Volume 348, 2003

Konopka, Allan, The Secret Life of Lead, Living on Earth and World Media Foundation, 2003.

http://www.braininjury.com/children.html accessed 2/21/05

www.westlaw.com: Atkins V. Virginia, 536 U.S. 304, 122 S.Ct. 2242

http://www.emedicine.com/neuro/topic185.htm accessed 2/21/05

http://www.leadpoison.net/press-release3.htm accessed 2/21/05


Social Implications of Lead Poisoning in Children
Name: Jenna Rosa
Date: 2005-02-22 03:52:40
Link to this Comment: 13116

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip




For decades, lead has been known to be a hazardous toxicant, especially for children. The children who are usually exposed to lead, particularly in this age of better understanding about the effects lead can have on neurological development, tend to live in older homes and come from poorer families who cannot afford to replace the two most common sources of lead to children, lead paint and lead plumbing (leadpoisoning.net). Although lead can affect several areas of the body, the neurological damage is often quite severe for individuals exposed to even slight amounts of lead during brain development. This damage often results in behavioral problems, reasoning and attention deficits, and low IQ and mental retardation, conditions that occasionally lead to deviant behavior. In these areas where lead exposure is so common and unavoidable due to the impoverished state of the inhabitants, the lead exposure of the children that develop neurological deficits and subsequently exhibit deviant behavior must be considered when determining their degree of culpability for a crime. If the physical state and composition of the brain determine the behavior of an individual, a brain damaged by lead poisoning can be the source of socially abnormal behavior.


Lead is referred to as xenobiotic, meaning it is a foreign substance with no useful role in human physiology, toxic even in minute quantities. Rather than breaking down to be eliminated as a waste product, lead accumulates in the body's bones and tissues because the body recognizes it as if it were calcium. It may be absorbed from the gastrointestinal tract or through the respiratory system. Lead exposure can result in low sperm counts in men and can increase the risk of miscarriage or still birth among women. It damages the kidneys and gastrointestinal tract, and it can lead to a host of neurological problems including decreased cognitive abilities and increased behavior problems in children (Konopka, 2003). The trigger level for lead in children, or the level at which it is deemed harmful, has been lowered over the decades and currently stands at 10g/dL, although recent studies suggest that adverse health effects exist in children at blood lead levels less than 10 g/dL (Canfield et al., 2003).


The most common source of exposure to lead in the household is dust from lead paint, commonly used before 1978 when the federal government banned lead as an additive to paint used for housing (CDC). Lead may also leach into water that travels through antiquated lead pipes, particularly if the water flowing through the pipes is heated, acidic, or treated with chloramines, an alternative anti-bacterial additive to chlorine. Other common sources of exposure outside the home are remnants of used leaded fuel or other lead products in soil, older painted toys, furniture, or jewelry, food and liquids stored in lead crystal or lead-glazed pottery or porcelain, lead particles released into the air from lead smelters and cosmetics or folk remedies that contain lead, such as "greta" and "azarcon" used to treat upset stomachs (EPA).


Although lead can cause harm to children and adults alike, the most seriously deleterious effects of lead poisoning are experienced by children still developing mentally and physically. Children are more likely to be exposed to lead because are more likely to be exposed to certain toxins because they play outdoors. They are shorter than adults, which means they can breathe dust, soil, and vapors close to the ground. Children are smaller than adults, therefore childhood exposure results in higher doses of chemicals per body weight (CDC). They are more likely to be irrevocably damaged by lead poisoning because lead causes damage to the nerve cells of the brain while the brain is still developing. The dendrites of nerve cells in developing brains are cut short by lead, thereby reducing the connections between axons among adjacent neurons. Dendrites are most plentiful during the early years of childhood, especially between the ages of 1 and 5, and thin naturally with age. Thus it is crucial for healthy development to establish as many connections between neurons in the brain as possible through education and stimulation between the ages of 1 and 5. When children are exposed to lead which limits the connections being made during this important developmental period, the brain is irrevocably disadvantaged, resulting in decreased amounts of gray matter (braininjury.com). Chelation therapy, which involves reducing the lead concentrations in the bloodstream by orally administering succimer, or injecting ethylenediaminetetraacetic acid (EDTA), has been shown to be ineffective at increasing already damaged neurons and increasing diminished IQ (Rogan et al., 2001). Therefore, even when individuals undergo treatment during childhood, the damaged areas cannot be recovered.


The neurological damage resulting from exposure to lead can result in abnormal behavior, exhibited through increased irritability and violence, learning disabilities, mental retardation, and other functional difficulties. The social effects of these abnormal behaviors through teasing, peer isolation, falling behind in school, drug abuse, domestic abuse, and a lack of understanding about the basis of an individual's impairments may also compound the neurological damage, resulting in psychological trauma, which studies show can cause other types of brain damage. (Rosen, 2001) All these conditions have been known to result in an individual's inability to function in society or possess adaptive skills. Inability to function in society often results in deviancy of various kinds, and at times the deviancy that is a symptom of an individual's neurological damage is so seriously a breach of the mores of social structure that it is viewed by our legal system as criminal.


In a landmark capital trial, Atkins v. Virginia, ruled in 2002, the defendant was given life without parole rather than the death sentence because it was proved he was mentally retarded. His lawyer argued that to put to death someone who had obvious mental deficits and an inability to cope in society was against the eighth amendment guaranteeing no use of cruel and unusual punishment as well as society's standards of decency:

Clinical definitions of mental retardation require not only subaverage intellectual functioning, but also significant limitations in adaptive skills. Mentally retarded persons frequently know the difference between right and wrong and are competent to stand trial, but, by definition, they have diminished capacities to understand and process information, to communicate, to abstract from mistakes and learn from experience, to engage in logical reasoning, to control impulses, and to understand others' reactions. Their deficiencies do not warrant an exemption from criminal sanctions, but diminish their personal culpability. (536 U.S. 304, 122 S.Ct. 2242)

In light of the distinction between sanctioning criminality and administering justice fairly by acknowledging an individual's culpability, it is necessary to see that if the state of the brain determines the behavior of the individual, and if the brain is damaged by a toxin which condemned it from the earliest years of childhood, the resulting behavior can be seen as a symptom of the brain. If that behavior is criminal, and if what made the individual's actions a crime can be attributed to known symptoms of a type of brain damage, then the amount of fault of that individual cannot be as great as if the crime were committed by someone without brain damage.


References

USEPA:
http://www.epa.gov/reg3wcmd/lp-childrenrisk.htm accessed 2/21/05


http://www.epa.gov/lead/ accessed 2/21/05

Center for Disease Control:
http://www.cdc.gov/nceh/lead/spotLights/changeBLL.htm accessed 2/21/05

New England Journal of Medicine, http://content.nejm.org:
Rosen J. F., Mushak P., Primary Prevention of Childhood Lead Poisoning The Only Solution, New England Journal of Medicine, Volume 344, 2001

Rogan W. J., Dietrich K. N., et al., The Effect of Chelation Therapy with Succimer on Neuropsychological Development in Children Exposed to Lead, New England Journal of Medicine, Volume 344, 2001

Science Direct, www.sciencedirect.com:
Canfield R. L., Henderson C. R. Jr., et al., Intellectual Impairment in Children with Blood Lead Concentrations below 10 g per Deciliter, New England Journal of Medicine, Volume 348, 2003

Konopka, Allan, The Secret Life of Lead, Living on Earth and World Media Foundation, 2003.

http://www.braininjury.com/children.html accessed 2/21/05

www.westlaw.com:
Atkins V. Virginia, 536 U.S. 304, 122 S.Ct. 2242

http://www.emedicine.com/neuro/topic185.htm accessed 2/21/05

http://www.leadpoison.net/press-release3.htm accessed 2/21/05


Sensory Perception Limitations? Unreal!
Name: Rhianon Pr
Date: 2005-02-22 05:20:22
Link to this Comment: 13117

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Human beings have five external senses sight, touch, smell, hearing, and taste. Our interpretation and understanding of the world in which we live is based on these five sensory inputs. What they are able to tell us about the world we inhabit, however, is far from the only data available. While our senses allow us as organisms to interpret our environments, they do not provide us with all the possibilities for sensory input. We are, in fact, limited in comprehension of reality based on the limitations of our flesh.

For example, our senses may be much less sensitive than the same sense of another animal or completely unable to distinguish something in the same way even utilizing the same sense. Bees, for instance, can see infrared, invisible to the human eye ((1)); owls can see mice 150 feet away from them in very dim light ((7)). Dolphins, bats, and some whales, among other animals, use sound to navigate their surroundings through echolocation of objects ((2)). Dogs can tell the difference between two people based on scent alone; dogs and horses can smell emotions such as fear ((3)). A spider can distinguish between strong wind and a bug trapped in its web based on sense of touch ((5)). While we share these senses with these animals, they are able to glean information that, given the same data, we would be unable to duplicate without technological aid or without using another sense.

Even within the scope of human sensory input capabilities there is variation humans do not have uniform senses. Those entirely lacking certain normal human sensory perceptions aside (like the deaf or blind), some individuals possess certain genetic abnormalities or variations that allow them heightened or lowered senses in comparison to the average person. For example, the average human has approximately 184 taste buds per square centimeter; however, there are those who can boast 425 taste buds per cm2 and those who can only claim around 96 taste buds per cm2 supertasters and non-tasters, respectively ((4)); the former group has a greater than normal sensitivity to taste, while the latter has a less than normal sensitivity. Furthermore, some women are tetrachromatic rather than the normal trichromatic (which occurs when X chromosomes do not have identical photopigment genes for green or red so they see both pigments of the color), allowing them a broader color palette than most ((6)). Also, individuals may be born without certain smell receptors, leaving them unable to detect certain scents (such as the odor of a skunk, which is most common); this is known as anosia ((8)).

Because of these variations in sensory receptors, human brains are not always able to process certain data that is detectable to others. Our experiences, then, can be seen as not only completely relative, but also limited. With these sensory inabilities seen within our species and compared to others', why, then, do we think we have such a good grasp of the world around us? If there is so much data that we are unable to process, how can we be certain of any truth? How can we find definiteness when there is so much of which to be unsure?

We usually would understand "reality" to be something that all "normal" people can clearly identify and that they share. However, as reality to humans is based on our interpretations of what our senses show us to be extant, but we do not have uniform sensory analysis, can it be argued that individual humans do not share the same reality? While one may accept that what another tells her is in existence based on faith, she can never verify or experience it for herself; while it may be real to others, it is nothing more than a mental construct for her. Furthermore, as we know that there is sensory data available that human beings cannot interpret, as we lack the proper hardware, could it be said that humans lack the ability to experience reality at all? Human reality is not the same as an earthworm's; my reality is not the same as yours. Can reality really be so relative?

It is, however, overly dramatic to claim that we have no perception of reality just because we cannot experience all of it. Our sensory receptors do an entirely adequate job of allowing our species to propagate and thrive. It is a mistake, though, to think that humans have the world figured out we have discovered so much, but there is still much more that will likely remain forever beyond our comprehension and thus our reach.


References

1) Seeing, hearing, and smelling the world , from the Howard Hughes Medical Institute.

2) Echolocation, from the Academy for the Advancement of Science and Technology and the Smithsonian Institution.

3) Olfaction , from Cardiff University.

4) Minutes from Me: Tasting , from the Franklin Institute.

5)A Spider's Sense of Touch, from Compton's Encyclopedia On-Line.


6)Yes, men and women do see the world differently, from connected.telegraph.

7)Sense of Sight , from The Yuckiest Site on the Internet.


8)I Can't Smell a Skunk!, from About Children's Health.


Location, Location, Location: Identifying States a
Name: Laura Cyck
Date: 2005-02-22 07:49:15
Link to this Comment: 13118

<mytitle> Biology 202, Spring 2005 First Web Papers On Serendip

With each day the reaches of science stretch further and further. Within the field of neural sciences, with every new neurotransmitter discovered, every new molecule stumbled upon, every new hormone identified, new pieces of a bigger puzzle are pieced together. This puzzle aims to explain one of the biggest topics in neural and cognitive sciences, psychology, and even philosophy, and that topic is how human behavior works. Over the years, our view of the human brain has become ever more detailed. Specific loci down to the microscopic level have been identified with highly specific functions, such as visual or olfactory tracts. Even specific reflexes, vomiting for example, have been traced to a particular structure in a certain location. Student textbooks offer diagrams of the brain marked to show specific areas specialized for functions like memory, motor activity, or face recognition. There's once piece in the puzzle, though, that's been missing and shows no signs of being found anytime soon. That is the piece which holds the key to understanding consciousness. Where does consciousness fit in the big picture? Is it a small piece of the puzzle- that can be related to a particular brain structure- or is it the result of a number of structures coming together and thus the "big picture"?

In trying to answer these questions, the first problem to arise is defining consciousness. Most definitions include the idea of awareness of one's internal and external environment; definitions also usually include the idea that consciousness is something subjective and qualitative. The inevitable concern about whether animals are in a conscious state similar to humans has led to two different types of consciousness: phenomenal consciousness and self-consciousness. The first refers to a strictly empirical state of perception. When we see, hear, taste, smell, and feel things we become conscious of them. Under this definition, humans and animals alike are considered to be conscious. The most famous description of this type of consciousness comes from Nagel, who proposes there is a feeling of "what it is to be like" a particular species. To be in a self-conscious state, however, is to be capable of "second-order representation of [one's] own mental states... to be capable of attributing mental states to others" (1) and to "consider oneself as an agent." (2) Perceiving things like sounds, sights, and so on is included under a phenomenal consciousness only, and would not be included in self-consciousness. For example, hearing a sound would not be a self-conscious state but anticipating or thinking about hearing a sound would be.

Scientists come to a fork in the road when dualism and reductionism enter the picture. To a dualist, the brain and all of its neurons are one type of matter which is subordinate to thought, consciousness, and the mind or soul, which is not material entities. A reductionist view collapses the two into one category. The brain and all of it's activities give rise to "things" which we conceive as non-material, namely thought, consciousness, and mind/soul. At one extreme, consciousness might be considered something material since it would have to arise from a cellular level: neuronal firings. Consciousness is then simply an emergent phenomena, a higher function of the brain. Phenomenal consciousness might then be explained by a "building-block approach." (2) A feeling of "overall" consciousness is achieved by an aggregate of various perceptual or sensory experiences. That is to say that visual consciousness could be independent from olfactory consciousness and so on. The question then of which brain structures consciousness could be pinned too is redundant, as a collective consciousness it would be a sum of "sub-consciousnesses" which are manifested throughout the brain.

An interesting case supporting the building-block approach is the phenomenon of blind sight. In cases of blind sight, a patient will be blind in parts of the visual field but still be able to accurately guess locations of objects he or she cannot perceive. Neurologists have suggested damage or interruption in the pathway which splits and leads to a structure where consciousness might be involved. (3) A case highlighting interference with consciousness (or lack thereof) of output processing is jargon (Wernicke's) aphasia, in which there is damage to structures associated with language. Afflicted patients are not conscious of their speech-output and often substitute phonetically similar words and thus produce nonsense words and sentences. In both blind sight and jargon aphasia, consciousness of all other senses remain intact, which still supports a building-block theory.

A consideration incorporating ideas of both phenomenal and self-consciousness is whether or not input originates externally (in the environment) or internally ("within the brain" itself). Many theories of phenomenal consciousness assume sensory input from the environment-- sights we see, sounds we hear, etc. However, sleeping and subsequently dreaming, which are usually considered conscious states (albeit "altered"), need attention. Is dreaming to be considered phenomenal or a higher-order-self-consciousness? What about the events occurring around us while we sleep? If we're awoken by something in the environment it indicates we were still in a state of phenomenal consciousness. But what about our dreams? Are the visual cues during dreams to be considered higher-order because they do not originate from the environment? Some sleep researches suggest that during deep sleep or dreamless sleep we are "alive and [our] brain is functioning, but there are no mental events occurring in which there is any element of consciousness." (4)

In cases of patients being "brain dead" or in a "vegetative state", patients are often described in terms of consciousness on a gradable scale. That is, most usually they are diagnosed "minimally conscious." In a brain imaging study, researchers using MRIs concluded that patients thought to be totally unaware and responsive to any input showed mental activity. In several cases, patients showed brain activity in response to a family member's or friend's voice. (5) These patients may not seem to be in state of self-consciousness but could been seen to be in a state of phenomenal consciousness, in that their "sub-consciousness for hearing" was still present. The building block theory does not, however, hold true. If evidence can be shown for perception awareness in brain dead patients, there should be an "overall" or "emergent" consciousness even if it is not complete, as in blind sight patients. A unified field theory attempts to validate phenomenal and self-conscious states. According to this theory, phenomenal consciousness subsumes self-consciousness, rather than vice versa. In order to experience phenomenal consciousness, a person must already be in a state of consciousness. (5) The so-called "second-order" self-consciousness state is not emergent in relation to phenomenal consciousness but vice versa. This might apply to brain dead patients, who may process input but are not phenomenally conscious because whatever is responsible for the self-conscious state has been impaired.

Patients with split-brains might shed light on which parts of the brain, if any, may be responsible for such states. In such patients, many with epilepsy, the corpus callosum is severed so communication between the right and left hemisphere is suspended, though information may still be sent from the right hemisphere to the left through the brain stem. In one experiment, a researcher showed pictures to the left and right hemisphere of a female split-brain patient. Among the pictures was one of a nude person, which when shown to the patient's left hemisphere. She laughed and was able to explain why and what she saw. When a similar "funny" picture was shown to her right hemisphere, however, she laughed but was unable to explain why. (6) Among the implications with these results is again the question of where consciousness might be rooted-- if it is localized or collective-- and conscious control of outputs, such as laughing. If the picture was shown to the patient's right hemisphere and she laughed, but didn't know why, this might raiser other implications concerning unconscious behavior. It follows that free will is dependent on consciousness. Researchers on split-brains have also found that "basic responses (heart rate, visual conditioned stimulus)" cross hemispheres by way of lower-pathways within the brain and spinal cord. Researches imply this is related to evolution of human consciousness and conclude animals are conscious but at "lower" states. It might be said, then, that animals are incapable of experiencing free will.

Given all of the data, research, and special cases relating to behavior and consciousness, it's easy to piece together conclusions in a number of ways that all yield explanations to satisfy the observations. Whether or not our picture of behavior and consciousness will ever be complete, if a particular brain state is equal to a particular conscious state (or vice versa) then the equation brain equals behavior is irresistible-- which may make Cartesians feel a little "self-conscious."

References

1. Primate Consciousness.

2. John R. Searle, Consciousness.

3. Roger Penrose, Real Brains and Model Brains.

4. Consciousness.

5. Benedict Carey, New Signs of Awareness Seen In Some Brain-Injured Patients.

6. Split Brain Consciousness.


Intelligence
Name: Amanda Dav
Date: 2005-02-22 08:10:29
Link to this Comment: 13119

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


As a Mawrtyr, I would like to think that I am relatively intelligent to the rest of the population. If I was not I would not be at Bryn Mawr. What does it mean to be intelligent? I thought of it in terms of number of neuropathways, how fast one processes information, and brain to body ratio. I think of human evolution and the proposed progression of our ancestors. I think of the invention of tools, fire, and most importantly symbolism as exhibits of our intelligence. I had thought of other animals, such as great apes and dolphins as being intelligent in similar ways that humans are. I had not, however, thought of different types of intelligence. The notion that intelligence evolves in different ways for each species in order to provide for that species (1). had not occurred to me. The neocortex, not necessarily the size of the brain is what is important in relation to intelligence (1). All mammals have a neocortex, but some mammalian species have more folding in their cortex than others (1). A human's neocortex is more important to functioning than that of a mouse (1).

How does one determine what aspect of the brain is responsible for intelligence? Brain mass does not seem to be responsible (2). For example, men have a higher average brain mass than women, but it has not been shown that men are overall more intelligent than women (2). Also, the person with the largest brain mass ever recorded (2850g) was also recorded to be an epileptic "idiot" (2). Larger animals tend to have larger brains than smaller animals, so brain mass in and of itself is not an "accurate comparative measure" (9). Body weight (S) to brain weight (E) ratios also do not appear to be responsible for intelligence (3). Mice and human E/S ratios are approximately equal, as are those of horses and elephants (3). It is clear that mice and humans are not equally intelligent, nor are horses and elephants. Additionally, an animal's body mass may fluctuate throughout its lifetime while brain mass in an adult animal remains much more constant (9). In order to correct the inconsistency of brain and body mass increasing proportionately, but not in relation to intelligence, an equation to find the encephalization quotient (EQ) is used (3). This is the ratio of a cephalization factor (C) which is a constant to the average mammalian value (3). Thus, an EQ of 3.0 would mean that the C constant is three times as high as would be expected in a mammal of that size and brain mass (3). Humans' EQ is higher than that of chimpanzees whose EQ is higher than a whale's (3). Common knowledge would verify that humans are more intelligent than chimpanzees that are more intelligent than whales. This however, does not imply causation, just a correlation.

The folding of the cortex may influence intelligence (4). The grooves are called sulci and bumps called gyri (4). Animals that are considered to be more evolved have more cerebral cortex and the "higher" animals within this group have more sulci and gyri in their cerebral cortex (4). The functions of the cerebral cortex include thought, memory, voluntary movement, language, reasoning, perception and information processing (5). The thickness of the cerebral cortex is fairly uniform in all mammals, so that aspect has no correlation to intelligence (5). Humans' brains with more folding correlates to our ability to reason and use language (5). Humans and primates do not, however have more neocortex than other mammals (6). Are different neurons then responsible for intelligence? There are twenty-seven times more other neural substances (i.e. glial cells, intracellular space) than neural cell bodies (7). All neurons are the same however. Neurons are the same in a starfish as in a frog as in a human. Neurons themselves may not be responsible for intelligence (7). What about brain structures? Are they different in animals of different intelligence? Higher primates and humans have a higher amount of neocortex than lower primates (8).

Measuring "brainpower" in relation to physical structures in the brain is crucial for understanding how intelligence is related to them (9). This proves to be much more difficult done than said (9). It is not known how to measure cognitive ability across species (9). There have been social implications in the evolution of primate intelligence (9). Since primates are social creatures, perhaps evolution has favored brain structures that support social behaviors (9). The temporal and prefrontal cortices have been implicated as these structures (9). There are many studies yet to be done to give us more insight into primate intelligence (9). "While ecology may have provided the initial conditions, cognitive evolution undoubtedly soon spiraled into a complex, interconnected web of adaptation, coevolution, and cooption of cerebral traits to cope with changing ecological and social conditions" (9).

It seems that there is still a significant amount of information about intelligence that is unknown. Before one can understand what makes one person more intelligent than another, it is crucial to understand what makes some species more intelligent than others. If the answer is in their brain structures, then possibly it is minor differences in these structures between human individuals that are responsible for differences in intelligence. As much diversity of intelligence exists among our own species, it is dwarfed by the diversity of intelligence in the animal kingdom.

References

1)What is Intelligence, Anyway??, Click on "Go here for a discussion" link.

2)The question of intelligence continues, on the Serendip website.

3)Thinking about brain size, on the Serendip website.

4)Cortical folding and intelligence, on the Serendip website.

5)More cortical folding and intelligence, on the Serendip website.

6) Neocortex, on the Serendip website.

7) Neurons and intelligence, on the Serendip website.

8) Brain structures and intelligence, on the Serendip website.

9) Evolution of Primate Evolution, by Scott Rifkin at Harvard.


Hammering a Myth into the Ground
Name: Samantha T
Date: 2005-02-22 08:44:18
Link to this Comment: 13120

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Last month a Colorado man was admitted to the hospital after x-rays revealed a 4-inch nail wedged into the front portion of his skull, millimeters away from his optic nerve. After hours of surgery to remove the foreign object from this delicate portion of the brain, doctors assured friends and family that he would be pain-free and back to normal in no time (1). People nationwide agreed he was lucky to have missed all important areas of the brain. They wondered what would have happened to this unassuming construction worker if the nail had hit part of the functioning 10% of his brain. Or did he actually hit part of the 10%, and if so, is it a miracle that he survived? The world may never know...well, not necessarily.

For generations and generations and even among well-educated people today, a myth has circulated about the "useable" percentage of the brain; many argued, and still believe today that one only uses 10% of his or her brain. Recent studies have since provided overwhelming evidence to suggest that this theory is much more than 10% wrong.

The myth is thought to have originated from a few main sources. One such source is behaviourist psychologist Karl Lashley, who in the 1920s spent time executing experiments on lab rats to determine where in the cortex the neural bulge for memory was located (2). He first taught the rats how to complete a particular maze; he then proceeded to cut portions of their cortex away to determine the area that housed the function of memory. Instead of finding a distinct location, Lashley determined that memory seemed to be spread evenly throughout the layers of the cortex. This once misinterpreted concept is now understood as "'redundancy' and is found throughout the nervous system. Multiple pathways for the same function may be a type of "safety mechanism" should one of the pathways fail."(3)

With modern-day technology, former ambiguities such as these are now understood more thoroughly. Metabolic rates of particular sections of the brain can be mapped over time from different stimuli with such instruments as Functional Magnetic Resonance Imaging machines (fMRIs). "Today the entire brain is mapped in extensive detail, and a specific function has been found for each part of the brain."(4) This source goes on to explain that most functions of the brain reside on either the left or right portion of the brain (most functions are lateralized). One obvious exception, however, are the frontal lobes, where there is an extensive network of redundant structures. Over time, mapping and autopsy exploration have exposed a type of hierarchy of functioning portions of the brain. This is to say that over the course of the day one uses all of his or her brain, but at any given moment in time only part is being used depending on what task is being performed; some parts are also noticeably more metabolically active than others (5). For example, calculating a complicated algorithm will produce a completely different neural pattern than that generated while knitting a scarf. One then naturally wonders, what happens when particular portions of the brain are deformed, or altered in some way? Do these neural pathways find a new route to complete a particular function, or does the function simply not transpire due to an incomplete processing signal? What about other organisms and their lack or presence of particular portions of the human brain?

In January of 2005, Pediatric News published the results of a study on the brains of children diagnosed with Attention Deficit Hyperactivity Disorder (ADHD). This study provided evidence that portions of the frontal cortex, basal ganglia, brainstem, and cerebellum of children diagnosed with ADHD are significantly smaller than normal. The study also provided evidence that such physical and behavioral abnormalities are less pronounced in children who have received pharmaceutical intervention (6) (7). The change in function of the brain is thought to be caused by the extensive remyelination of axons in treated individuals; in other words, the brain grows and changes into a more socially accepted functioning brain.

One could conclude from this study that increased volume, or mass, of the brain means increased complexity and integration of function. Tracing the size and complexity of the brain through time, one distinguishes a general trend of increased complexity and mass of neuroanatomy (8). Even though the cerebrum of many mammals has enlarged over time, a progressively smaller proportion of it correlates with motor/sensory duties. While elephants and some whales have larger brains than humans, evidence does not support the theory that they exhibit a more sophisticated level of reasoning. Given the high demand for motor and sensory requirements to integrate movement in the bodies of these immense organisms, bigger brains are naturally essential. Also, bigger brains are not necessarily an evolutionary advantage; since they require such extensive nourishment, they have the possibility of overheating and organisms must find solutions to this problem with mechanisms to diffuse heat without sacrificing a significant amount of energy.

This, however, is not the whole story. Not only is it important to note the differences in body size of animals and their varied neural metabolic rates, it is also imperative to trace the percentage of neocortex present in the brains of differing species. "Neocortex enhances both the capacity to make use of variability in behavior and the capacity to deal with resulting ambiguities and uncertainties."(9) Examples of such ambiguities reside in differing interpretations of sensory input. Whereas monkeys and humans are thought to have over 50 differentiated neocortical areas, small-brained mammals characteristically have about 15 (10). Not only do different species establish differing responses to external stimuli, but individuals within species exhibit such ambiguities as well; a child with ADHD may respond differently to a loud classroom than a physiologically "normal" child. Even over time, humans are said to lose the function of 100,000 neurons each day after the age of 30; the "useable" size of their brains is therefore forever decreasing.

So is the Colorado man lucky? Well, yes of course, for he most likely hit a "useable" portion of his brain and is lucky to still be alive. It will be interesting to follow the story to determine if because of the altered shape of his brain, noticeable behavioral differences will later ensue.

References

1)MSNBC, Man Survives 4-inch Nail in Skull.
2)Science and Consciousness Review, Exploiting the 10 Percent Myth.
3)Washington.edu faculty page, Neuroscience for Kids - 10% of the Brain Myth.
4)The New England Skeptical Society, Don't You Believe It: 90% of the Brain is a Terrible Thing to Waste.
5)Urban Legends Reference Page, The Ten-Percent Myth.
6)Thomson Learning, InfoTrac College Edition
7) Pediatric News, Jan 2005 v39 i1 p7(1)
8)University of Claifornia San Diego - user: jmoore, Allometry.
9)Serendip Website, Brain size and evolution.
10)nature.com, Evolutionary neurobiology: The neocortex comes together.


Sleep Deprivation and Effects on Everyday Life
Name: Amy Johnso
Date: 2005-02-22 08:45:17
Link to this Comment: 13121

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Amy Johnson
Professor Grobstein
Neurobiology and Behavior
February 22, 2005

Sleep Deprivation and Effects on Everyday Life

Walking around Bryn Mawr's campus and sitting in its classrooms it seems like every student is yawning and struggling to stay awake. Everyday people struggle to stay awake because they did not get enough sleep the night before or have deprived themselves of sleep for a while. Yet, if there is a test the next day students (at least I always try) will go to sleep early so as to be able to perform optimally. So if wanting to be successful in a special task is so important what about the tasks we perform daily that need complete alertness? Do they not deserve the same treatment?

Sleep deprivation can cause forgetfulness, exhaustion, and fatigue, to name a few. When a person is exhausted and fatigued it causes pessimism, sadness, stress, and anger, none of which are appreciated by other people. When I come across one of my friends in a bad mood I try to avoid them; when someone is perpetually in a bad mood they will not maintain many friends (5).

In addition, lack of sleep affects the brains ability to solve problems. Everyday people are faced with simple problems that need to be solved, but sleep deprivation makes it much more difficult for people to complete the tasks (sleep-deprivation.com). This is given support by a study done by UCSD. Researchers studied the brain activity of subjects who were sleep deprived and noted that the parts of the brain usually associated with the particular task was not active, but another part of the brain was. When asked to perform a verbal task the parietal lobes were more active than the temporal lobe, which is usually involved in language processing. At the same time, subjects were given arithmetic problems to solve, and the same was found. In the sleep-deprived subject the parts of the brain stimulated were not the same as in the rested subjects, and in addition the deprived subjects skipped and got more questions wrong (1).

These findings suggest that while doing even simple tasks different parts of the brain are being stimulated, parts of the brain that would not under normal circumstances be used. This means that the neurons are maybe not firing as fast as normal or maybe not even at all, making it seem as if brain is not working as well as usual, and that this can have unfortunate consequences.

Most people drive a car on a regular basis, but driving a car while sleep deprived is just as bad as driving a car while under the influence of alcohol. People who have been awake for upwards of fifteen to twenty hours performed worse than a person with a blood alcohol level of .05, which is just under the legal limit for most states and is the legal limit in most of Europe. What is even more interesting about this is that of all fatalities related to drowsiness behind the wheel fifty-five percent occur to drivers under the age of twenty-five (4).

The same way people tend to get more sleep the night before a test people also tend to get more sleep the night before a big game or other sort of athletics meet. This is also in direct relation to the fact that the brain is not working correctly without sufficient sleep. Lack of sleep can cause recovery time to decrease and can cause hypoglycemia, both of which hinder athletic performance greatly. In addition these could lead to injury, an athlete's worst nightmare (3). Not everyone is an athlete, but everyone does use his or her body all day every day. So even a non-athlete's body will be affected by sleep deprivation.

Sleep deprivation even affects weight. Sleep has been found to be an important aspect in body weight and metabolism. When a person is sleep-deprived, chemicals that make one hungry are in excess and chemicals that show how healthy appetite are at low levels, thus making a person eat more (6).

Why then, when I do a survey of people I see, do they all seem sleep deprived? Sleep deprivation is bad for their health and well being. It makes people cranky and unhappy. Not only that, but it also has seriously detrimental effects on the health of people, and their ability to recover from illness and injury.


References

1)
Brain Activity is visible Altered Following Sleep Deprivation
, an article on a study done at UCSD

2)
Sleep Deprived at Stanford: What all Undergraduates Should Know about how Their Sleeping Lives Affect Their Waking Lives
, an article by William Dement

3)Sleep Deprivation can Hinder Sports Performance, an article by Elizabeth Quinn


4)Sleep Deprivation as bad as alcohol impairment, study suggests

5)Sleep Deprivation Symptoms: Lack of Energy, Fatigue and Exhaustion.

6)Sleep Deprivation Tied to Shifts in Hunger Hormones


Relooking at the Two Opposing Dream Theories in a
Name: Elizabeth
Date: 2005-02-22 09:07:59
Link to this Comment: 13122

<mytitle> Biology 202, Spring 2005 First Web Papers On Serendip

The first time I learned about the major theories for why dreaming occurs, I remember feeling intrigued but perplexed. Theories that account for why dreaming occurs can be placed into two basic categories: psychology or physiological (1). My high school psychology teacher obviously had no intentions of flushing out why physiological theories were the most acceptable, but at the time I was forced to accept this, albeit with many doubts.

Revisiting the topic of dreaming after having almost half of a semester of Neurobiology and Behavior has helped to shed new light on these two competing theories. I have learned that one way of thinking about the nervous system is as equal to behavior, which is broadly defined to include human experience. Thus, a change in one causes a change in the other. Also, it is important to note that the organization or pattern of activity is critical for causing changes in behavior. This means that when neurons fire in certain patterns, one may walk, but if it changes the firing pattern, one may dance. It is the same neurons that are firing, but the patterning is different. However, what happens when the person is sleeping and they cannot display any changes in behavior? Is that why dreams occur? And if the firing patterns are different, could this explain different dreams? Furthermore, how does this tie into environmental influences during wakefulness? Aristotle explains dreaming as a perceptionless state where our senses of our outside stimulus are shut off. If this is the case, our human experience is momentarily "shut off". (2). Thus, there should be no change in the brain. However, how do dreams occur if this is the case? To answer some of these questions, it is important to look at two major opposing theories that have been created in an effort to explain why dreaming occurs.

Freud was the first to theorize about why people have dreams. Like most of his ideas, he believed that dreams were a result of underlying desires tied to the Id. During Freud's time period, the nervous system was thought to be a system of excitatory neurons. Based on this assumption, Freud believed that when a person was worried or preoccupied with something, an excited neuron causing a dream would be the only way to release this nervous energy. Now it is known that this is actually not true; the nervous system is made up of both excitatory and inhibitory neurons. However, based on what was known at the time, this was a logical theory. (3). Furthermore, this theory supports the idea that it is the pattern of firing and not the type of neuron that is critical in the production of behavior. Although Freud never delves into the details of how the excitatory neurons are firing, he does not explain dreaming by specific neurons but rather, their activity. However, one question that his theory does not answer is why repressed feelings have to be carried out in the form of a dream and during sleep? Why can't the person instead express their desires during wakefulness in some other disguised way? Perhaps moving to the next important theory of dreaming, we can develop a less wrong theory of dreaming.

In 1977, two influential men, Hobson and McCarley, developed yet another dream theory called the Activation Synthesis Model of dreaming. This model was meant to outright refute Freud's earlier psychoanalytic model. In laymen's terms, this model explains that the brain stem blocks motor and sensory neurons causing a flood of firings to the forebrain. Dreaming occurs because the forebrain tries to make sense of random firing of the brain stem. Furthermore, they suggest that dreams have nothing to do with emotion since they are merely triggered by sensory and motor aspects of bodily activity. (1). Most dreams are thought to occur when the pons sends signals to the thalamus, which then relays these signals to the cerebral cortex. (4). The function of the thalamus is to recognize sensory stimuli and relay sensory impulses to the cerebral cortex. The cerebral cortex is responsible for intelligence, memory, and the detection and interpretation of sensation. The thalamus and cerebral cortex are located in the forebrain, which is viewed as a more advanced structure (5). . Therefore, if these advanced structures are deciding how to interpret these random signals, doesn't this make the consequential dream not random? After all, just like we learned that the pattern of firing neurons are crucial to behavior, perhaps it is the structure or pattern of the story that is crucial to the dream.

Recently, there has been some evidence that dreams also occur during non-REM sleep, as well. (6). However, dreaming differs greatly depending upon the sleep stage the person is in. Specifically, a study by McNamara found that dreams where one is angry or emotionally aggressive towards another person were common in REM sleep but never occurred in non-REM sleep. (7). These differences may be key to understanding that dreams are not simply a result of random firing. Furthermore, it has been found that many dreams are linked to the ventro-medial frontal quadrant, which is the part of the brain that is responsible for wanting and seeking. This could possibly support Freud's theory, in that dreams are linked and perhaps motivated to our inner desires.

Furthermore, it is evident that sometimes the changes in brain (the dream) can later cause changes in behavior. For example, a mother has a bad dream about her children needing help and she wakes up and checks on her kids. Therefore, is it so far off to believe behavior can cause changes in the brain (i.e. the dream)? Perhaps Hobson and McCarley did not prove Freud wrong but rather made Freud's theory less wrong by explaining the actual physiological processes that lead up to dreaming as a breakthrough to the Id. After all, dreams have been shown to have coherence and have many similarities to people and events that occur in wakefulness and Hobson and McCarley's theory alone only offers the explanation that this is due to chance. However, if chance is the only reason for dreams, why is it that we dream of ourselves so often, if it is purely an unemotional stimulus coming from motor and sensory impulses. (8).

References



1) Dreaming: Function and Meaning , An essay of the two major dream theories and finding a middle ground.

2) On Dreams , an essay written by Aristotle about dreams.

3)The World of Dreams Reexamined , a helpful website on the Serendip web site.

4) Brain Basics: Understanding Sleep , a basic guide to what occurs during sleep

5) Online Learning Center: Health Psychology a>, a glossary of brain functions

6) American Psychoanalytic Association, A helpful article on the current scientific stance on REM sleep and dreams.

7) Metareligion: "Study Disputes Randomness of Dreams" , an interesting write-up of a study done on REM and non-REM dreams.

8) Dream Research.net: The purpose of Dreams, , a site that talks about why dreams happen.


Meditation and the Brain
Name: Erin Deter
Date: 2005-02-22 09:12:30
Link to this Comment: 13123

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Meditation seems to be the newest craze for those seeking a more healthy and balanced lifestyle. Just a simple search of the internet and one can find countless centers across the nation, and even the world, that teach meditation and praise its beneficial results. With all the hype surrounding meditation, one might ask the following questions: what is meditation, where did it come from, and in what ways, if any, does meditation affect the brain?

The definitions for meditation are countless, however the present mainstream idea is that meditation is a process through which one realizes self-awareness (1). This is achieved by relaxation of not only the physical self, but the mind as well, leading to a state in which a person can reach new levels of awareness (2).
From a historical and religious perspective, meditation was first practiced by the Buddha, a man who left his powerful family in Nepal to seek enlightenment and understanding of human suffering (3). The Buddha finally reached enlightenment after six years of practicing meditation, and soon began teaching others the way of enlightenment, which evolved into the Buddhist religion (4).

Meditation has taken on a new role in modern society, however. It has since moved away from its religious context, and has been commercialized into mainstream living. It is even used in some forms of therapy, due to its philosophical nature (1). The possible benefit of using meditation in therapy is that it promotes a focus on the self; to solve problems by looking inside oneself, understanding emotions, and teaching patience (1). These benefits, however, are not well studied for their efficacy in the clinical therapeutic setting, however popular they might be (1).

In recent years, researchers have tried to tackle the scientific aspect of meditation to investigate whether meditation creates any physical changes in a person, in addition to spiritual affects. There have been many studies already completed to test whether, and in what ways, meditation affects the brain. These studies have yielded interesting results for the brain's role in meditation.

The most common finding among researchers is that meditation can change the way one's brainwaves behave. For example, many studies compare the brains of Buddhist monks, who are highly trained in meditative practices, to a control group that does not have any formal training in meditation (5,6). The participant's brains are monitored by electroencephalogram during the process of meditation. This enables researchers to observe the participant's brainwaves during the act of meditation (6). These studies demonstrate that those who are practiced in meditation not only have a higher resting baseline rate of gamma brain waves compared to those with no training, but also show more gamma wave activity during mediation (6). This gamma wave activity is referred to as neuronal synchrony, and has underlying importance in such brain functions as conscious perception, learning, working-memory, and attention (5,6).

From these findings, it has been suggested that meditation actually allows the brain to practice mental abilities, and it is this practice that actually changes the neuronal connections in the brain (5). Another finding from these studies suggests that most of the increased brain activity occurs in the left prefrontal cortex, which has been shown to play a role in affective regulation, such as emotion and happiness (5).

While it seems that meditation affects the brain in very specific ways, it also may play a role in the body's immunity towards disease. One studied found that after eight weeks of meditative training, participants had produced more flu antibodies than those participants who had not been given training in meditation (7).

The scientific findings provide a fascinating insight into the way in which the brain can be shaped and altered due to mental practice, but is there a danger in trying to understand meditation in scientific terms? After all, science cannot account for such philosophical notions as mind and soul.

It seems that from a historical perspective, the religious and philosophical aspect of meditation was the most important role of meditation itself; the need to understand the injustices of the world by looking inside oneself for enlightenment was the purpose of meditation. What happens when the underlying philosophical basis for meditation is taken away? Does meditation still have its fundamental positive properties?

Perhaps the increased brain activity is not a benefit of meditation itself, but a by-product. It is possible that the true positive effects of meditation are seen in the mind or soul, and cannot be scientifically tested. It is possible, too, that deconstructing the concept of meditation into something that can be scientifically tested is detrimental to the practice itself. While these questions may never be answered, they are important questions to ask to help understand the relationship between science and philosophy.

References

1)Meditation: Concepts, Efficacy, and Uses in Thearpy by Alberto Perez-De-Albeniz and Jeremy Holmes, Taken from International Journal of Psychotherapy, March 2000, v.5(1).

2)Meditation, Thiaoouba Prophecy website

3)An Introduction to Buddhism, Shippensburg University website.

4)History of Buddhism

5)Meditation Gives Brain a Charge, Study Finds, The Washington Post Newspaper website.

6)Long-term meditators self-induce high-amplitude gamma synchrony during mental practice, Proceedings of the National Academy of Sciences of the United States of America webiste

7)Brain Scans, Blood Tests Show Positive Effects of Meditation, Center for the Advancement of Health website.


Connections Between Antidepressants, Drugs, and Se
Name: Christine
Date: 2005-02-22 09:32:04
Link to this Comment: 13124

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


The common situation that comes to mind when one tries to imagine a seizure is an unresponsive person writhing in convulsions on the floor. Still, there are many different types of seizures that have been diagnosed through the years. Although seizures are commonly associated with epilepsy, there are many other factors which can induce a seizure. Seizures can result from head injuries, narcotics, medications, brain tumors, and high fever, to name a few. (1). Certain antidepressants, including a medication called Wellbutrin (chemical name: bupropion), have been known to cause seizures in some individuals. (5). When it comes to ingested medications, an important question to ask is, "Do the benefits of the medication outweigh the risk of a seizure?"

The system of chemical signaling between neurons or nerve cells in the brain gives clues as to why seizures occur. Neurotransmitters, or chemical signals, bind to a receptor on the neuron. These neurotransmitters alter the voltage of the cell, which changes the activity level of the neuron. (3). In order for the signal to be transmitted, enough signals must accumulate to bring the voltage of the neuron up to the "threshold of activation." Everyone has their own particular threshold of activation, which is a measure of how much stimulation it takes to make the neurons activate. (2). The threshold for each individual is determined by his or her genetic makeup, but the threshold can be changed by outside factors. Once the signal meets the particular threshold, a nerve impulse is initiated. (3). This nerve impulse travels down the axon, which is a nerve fiber that protrudes from the neuron and conducts signals to other neurons. This is also known as neuron firing. The space between the end of an axon on one neuron and the receptor on the next neuron is called the synapse. Presynaptic neurons send signals to postsynaptic neurons. (3).

The threshold of activation is similar to the seizure threshold, which is the minimum amount stimulation needed to cause a seizure. (1). Often due to genetics, some people have a low seizure threshold, so a minor stimulation may produce a seizure. Often, epileptic patients suffer from a low seizure threshold. In people with a more "normal" seizure threshold, the stimulation needs to be much more severe. (1). A person has a seizure because their neurons fire uncontrollably after being stimulated to a point at or above their seizure threshold. (1). A seizure is a change in behavior which is due to electrical activity in the brain. Some sufferers experience convulsions and unconsciousness, depending upon the type of seizure. Epilepsy is when the individual has recurrent seizures. (4).

Wellbutrin is an antidepressant which increases the levels of the neurotransmitters dopamine, serotonin, and norepinephrine. (5). Common antidepressants called SSRIs (selective serotonin reuptake inhibitors) concentrate on increasing serotonin at the synapse. Wellbutrin is different in that it is called a dopamine reuptake blocking compound because it primarily affects dopamine. (5). Reuptake is a process where neurotransmitters are released into the synapse, bind to the receptor on the receiving neuron so that it may activate, and then are sent back to the original neuron. (6). The antidepressant compounds bind to the receptor on the presynaptic neuron so that the neurotransmitter will not be transported back to the original nerve cell. Reuptake inhibitors allow the neurotransmitters to stay in the synapse longer so that they can be recognized by the postsynaptic receptor repeatedly and therefore increase their effects and levels in the synapse. (6). Since dopamine is a compound which is said to increase pleasure, it makes sense that a taking a dopamine reuptake blocking compound might make a person "feel better." (7). The problem is that if these signals are constantly firing because they are uninhibited, the seizure threshold can become lower, which can cause a seizure. (1).

The relationship between antidepressants and narcotics and their similar ability to cause seizures was surprising. Cocaine, for example, is also a dopamine reuptake blocking compound. (8). In fact, Wellbutrin has been used to gradually wean addicts off of cocaine. (10). Similarly, bupropion is also known as Zyban, which is a medication to help people stop smoking. (9). It would seem that Wellbutrin is similar to a low dosage of cocaine. Cocaine is a leading cause of seizures for the same reason that antidepressants can cause them. (9). The narcotic also raises serotonin and norepinephrine levels, though as with Wellbutrin, dopamine is the neurotransmitter that is primarily affected. (8). It makes sense logically to believe that many types of psychological medications would be comparable to narcotics because they often both have the general effect of making the user feel better. Still, it is notable that psychiatrists often don't explicitly state the similarity between narcotics and certain medications, which would be useful information in the case of Wellbutrin because it also has the some of the same adverse side effects as cocaine.

Wellbutrin is said to only cause seizures when there are complications, such as previous neurological defects, a medication overdose, or taking Wellbutrin with other drugs. (11). If we look at the basic causes of seizures, however, it is relatively easy to have a complication. The seizure threshold can be lowered by problems such as sleep deprivation, low-blood sugar levels, metabolism, anxiety, and exhaustion. (1). If combined with Wellbutrin, a seizure could result. Medication overdoses occur with Wellbutrin even when it is taken as prescribed because the brain metabolizes the medication too quickly in some people. The neurons begin firing at a rapid rate all at once which causes an overwhelming amount of electricity in the brain. SSRIs target serotonin more than dopamine, so the side effects are not the same and seizures are not as much of a risk. (11). SSRI side effects occur because this medication floods the brain with serotonin. The overabundance of serotonin interferes with the activity level of other neurotransmitters, including those which control hormones for sexual desire. (6). SSRIs are known to cause nausea, diarrhea, headache, sexual dysfunction, and dizziness. (11).

Deciding whether or not to take a medication because of its side effects is a choice that is made on an individual basis. In the case of seizures, the decision is even more important because a seizure is potentially life threatening, especially if the sufferer is driving a car at the time of the attack. When it comes to chemicals that affect the brain, patients should be informed that it is possible that compounds with similar effects might actually work in the same way. Rather than downplaying the similarity between narcotics and antidepressants, physicians should research the validity of this argument in order to help the patient to understand what it is that they are ingesting. Having experienced a seizure due to medication, I can say that for me, the benefits did not outweigh the side effects.


References

1) Behavior Modification for Epilepsy: raising the seizure threshold, website about the seizure threshold

2) Nervous System, explains the causes for seizures

3) Campbell, Neil A. and Reece, Jane. B. Biology. San Francisco: Benjamin Cummings, 2002.

4) Seizures and Epilepsy: Hope Through Research, details causes and types of seizures

5) Wellbutrin etc. (Bupropion), explains how Wellbutrin works

6) Selective serotonin reuptake inhibitor, uses of SSRIs

7) Dopamine, effects of dopamine on the brain

8) Cocaine, relationship between dopamine and cocaine

9) The Real Facts About Wellbutrin/Zyban a.k.a. Bupropion, harmful effects of Wellbutrin

10) Bupropion, uses for Wellbutrin

11) Wonderful Wellbutrin?, side effects from antidepressants


Acupuncture: An Alternative Way to Treat Pain
Name: Shu-Zhen K
Date: 2005-02-22 09:49:28
Link to this Comment: 13125

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Living in America has taught me that common medical problems can be relieved with over-the-counter or prescription medicines. Pain relief comes in a pill. Or does it? Even if the pain subsides for the moment, the side effects from taking the pain killers may be unbearable for certain people, resulting in more problems than the medication seem to solve (1). An example of this is aspirin, which has been linked to gastrointestinal problems. Oxycontin has proven to be a dangerous painkiller for doctors to prescribe because of its addictive qualities. More recently the much publicized pain killer Vioxx, a cox-2 inhibitor, was taken off the market due to an increase in cardiac risks, which is correlated with taking this drug (2). Cox-2 inhibitors prevent inflammation by blocking the cox-2 enzyme from producing a chemical message that indicates pain to the brain (3). There are ongoing discussions about whether other cox-2 inhibitors should be taken off the market.

However, many people still experience pain despite taking such medications. This is why many Americans seek alternative methods and medicines to hopefully find an effective way to ease their pain with minimum side effects, such as acupuncture. When it comes to pain relief Western medicine is not meeting its demands from patients with chronic pain. Is acupuncture an effective alternative to taking pain medications?

Acupuncture, a traditional Chinese medical technique, has been used for many centuries by the Chinese to treat all types of disease and pain. This technique inserts very thin metal needles into specific points in the body. The needle will pierce the ski, but the patient should not be in pain (8). It is believed that the body contains about 500 acupuncture points connected to the 14 main meridians or channels (4). Certain acupuncture points are used to treat specific locations of the pain. For instance, acupuncture points on the thumb, knee and wrist are used to treat headaches (8).

To understand this ancient technique, one must grasp the concept of "chi". Traditional Chinese medicine is rooted in the idea that "chi", or energy, flows through all living things, including the human body. A disruption in chi, caused by an imbalance of ying (negative energy) and yang (positive energy), is the origin of illness and disease. Acupuncture brings ying and yang back into balance by unblocking the chi and restores the body to a healthy state (4). The concept of chi is not mentioned in any modern medical textbook, but for centuries, traditional Chinese medicine has based their system of diagnosis and treatment on the idea of keeping the chi in equilibrium.

Many studies have shown that acupuncture is an effective way to treat pain. One study reported patients experience less pain and more mobility when receiving regular acupuncture treatments than patients receiving fake treatments (5). Another similar study showed that acupuncture was an effective treatment for knee and back pain (6). However, it is still unclear how this technique actually works. Because traditional Chinese medicine is not based on a modern understanding of the human body, there are many people who are skeptical about acupuncture. Nevertheless, mounting evidence reveals that acupuncture can bring about pain relief. With all the medical advances taking place in Western medicine, a 2000-year-old technique for treating pain is making a comeback.

Even though no definitive answer is available at this moment, there are theories on how acupuncture might work. Studies have shown that acupuncture stimulates the nervous system to release natural pain killers such as endorphins, thereby reducing the pain experienced by the person (7). Another idea is that acupuncture blocks the sending of electrical impulses to the nervous system, thus preventing pain (4). When an outside stimulus is detected by sensory neurons, a pain message in the form of electrical impulses is sent to the spinal cord. The spinal cord then processes the information and sends it to the brain. A person is believed to experience pain when the message is relayed to the brain (1).

Acupuncture may also work through the placebo effect by leading the patients to believe that their pain is being treated (4). However, as mentioned previously, many studies have ruled out the placebo effect by giving both fake and real acupuncture treatments (5). Even if for some cases people with chronic pain get relief due to the placebo effect, why should they be discouraged from receiving acupuncture? Whether it is the placebo effect or actual benefits from the acupuncture treatments, people with chronic pain are getting the relief that they did not find while taking medications.

However, this does not mean that anyone seeking pain relief should try acupuncture. Although many people have found pain relief through acupuncture, there are just as many people who did not. Pain relief from acupuncture may be transient and individual results will vary. Usually a series of acupuncture treatments are necessary before any sign of pain relief happens (4). As with any medical treatment or medication, acupuncture will not likely dissipate the pain in one treatment. Immediate pain relief from an acupuncture treatment has been reported by only a few people (8). It may take many more treatments and lots of patience before any effect is noticeable.

Many people are willing to try acupuncture since there seems to be relatively little side effects to the treatments. However, there have been reports of punctured organs, broken needles, and allergic reactions to needles that were not surgical steel. Acupuncture needles should be made of solid metal and sterile when used (8). These reports are most likely due to treatments received from unlicensed acupuncturists, but in America, there are licensed physicians and non-physicians that practice acupuncture. This treatment should be discouraged for pregnant women because of the possible stimulation of increased levels of labor inducing hormones that can result in premature labor and miscarriage (4). The undesirable side effects in pregnant women receiving the treatment provide additional evidence that the body is reacting to acupuncture.

There are always risks involved with any medical treatment and the patient should assess each of these risks before deciding on the best method. Given that acupuncture is still used extensively in China and the side effects from western medicine, this treatment should be an option of which patients with chronic pain should be aware. Although a medical explanation of how acupuncture works is still in development, much research supports the fact that acupuncture brings about pain relief for many people. The question should not be on how acupuncture works, because people living with chronic pain today are looking for relief. I believe the medical community should make an effort to provide patients with all the viable options. Acupuncture is an effective method of pain relief as studies have shown. The unanswered question of why acupuncture works will be interesting for researchers to continue exploring. A new way of thinking about pain may come about from its discovery.

References

1) Pollack, Andrew. "The Search for the Killer Painkiller." New York Times. 15, Feb. 2005: F1.

2)MSN Health and Fitness, article about pain killers

3)Wellmed, LLC, information about cox-2 inhibitors

4)The Skeptics Dictionary on Acupuncture, information on acupuncture

5)Infotrac Onefile, database found in the Bryn Mawr College website

6)MSN Health and Fitness, article about study done on acupuncture

7)health.ivillage.com, study done on acupuncture

8)HealthLink Medical College of Wisconsin, information about acupuncture


Gender Bender: The Brains Role in Transsexuality
Name: Yinnette S
Date: 2005-02-22 09:49:45
Link to this Comment: 13126

Concepts that transcend the binary norms our society places on gender have been around for centuries, but have only recently been considered for scientific exploration; the truth is that the gray area which today is transsexualism, existed way before it had an actual name. Historically societies all around the world made sense of this internal conflict that affects approximately 1 in 10,000 of the male population and 1/3 of the female population1. In societies dubbed, "primitive," people who experienced these kinds of gender complexities within their own lives had significant roles in their communities as shamans or as other types of leaders who inherently had a different sense of the world and were as a result thought to be gifted because of their abilities to exist as two selves simultaneously. Historically the Greek Gods Hermes and Aphrodite were beings that when in regards to sex and gender also had an ambiguous gender identity. We could go through history and pick out countless accounts which describe men and women who because of their ambiguity were and were not part of their respective societies; considered holy individuals in some cases and in other cases, depending on time period and cultural practices, considered threats to society. Today because of advancement of technology transsexualism today has taken on a new meaning but in many ways it is still confined within some social stigmas of the past.
The question of nature versus nurture is constantly debated when considering the construction of gender identity and its effect on transsexualism. Some scholars argue the cause of this state of being solely deals with nature and the surrounding environment of the individual. Yet there are others who argue that Transexuality is directly linked to the brain and the effects that hormones have on it during the stages of prenatal development. Data has been collected in support of the belief that sex hormones play a key role in the development of the child and his or her sex, and therefore, in his or her gender identity. Sex hormones also impact the child's tendencies, attitudes, and learning which can in many ways explain the feelings shared by transsexuals. According to Pfaffin, "girls exposed prenatally to unusually high levels of androgens have more masculine and less feminine interests..." (P. 12)
This prenatal hormonal environment has also been thought to affect the actual physical structure of the lower brain. Parts such as the hypothalamus, and according to some researchers, the organization of the cortex1 in transsexuals is structurally different than the brains of people with whom they share the same sex. In 1995 a team of researchers in the Netherlands headed by, Dick Swaab studied the differences in the brains of homosexual men, heterosexual men and women, and six male to female transsexuals. Their findings gave evidence in support of the idea that the brain structures found in the male to female transsexuals were exactly like the ones found in the women studied, despite the fact that physically these male to female transsexuals resembled males in all other physical ways. "They found that a tiny region known as the central region of the bed nucleus of the stria terininalis (BSTc) was larger in men than in women. The BSTc of the six transsexuals was as small as that of women, thus the brains of the transsexuals seem to coincide with their conviction that they are women". The result supports the hypothesis that gender identity stems from an interaction between the developing brain and sex hormones which leaves us with an interesting question when in regards to the environment and its role in this type of gender expression. If the actual brain structures of these people are of the wrong sex then the environment can only play a very minimal role in the type of behavior that is exemplified through these people's actions and choices. In the end the brain structures are different regardless of environmental factors that affect the person after they are born. I think that in this case nature weighs a bit heavier than nurture.
The Brain=Behavior model fits in this case. In essence the structure of the brain has been altered as a result of hormonal changes and these changes allow for a radical and noticeable change in behavior. The reality is that many times these behaviors are internalized by the people who are experiencing them unfortunately because many of our societies continue to shun this ambiguous gender expression of gender. It is acknowledged however, that there is still a lot more research that needs to happen so as to determine better ways to understand the transsexual community.

Websites/Sources:
1) Transsexuality: An Introduction
http://www.gendertrust.org.uk/showarticle.php.aid3
2) Hormones & Behaviour, Lecture 6: Hormones & Brain Structure/Function
http://psych.unn.ac.uk/users/nick/hormoneslec06.htm
3) The transexual brain
http://www.genderweb.org/~janet/znature.html
4) Cohens-Kettenis, Peggy T. Friedman Pfafflin
2003 Transgenderism and Intersexuality in Childhood and Adolescence:
Making Choices. Thousand Oaks, CA: Sage Publications.


Vagus Nerve Stimulation and the Mystery Behind It
Name: Emily Trin
Date: 2005-02-22 09:51:06
Link to this Comment: 13127

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Epilepsy is a chronic disorder of the central nervous system, in which nerve cells of the brain produce abnormal pattern of neuronal activity. These imbalanced electrical signals are carried by the nerves, or communicating highways between the brain and the body, to specific peripheral cells and can cause disturbing behaviors, sensation, memory, thought, and emotions. One of the more severe symptoms that are generally used to characterized epilepsy is periodic convulsive seizures (1). Many new treatments for epilepsy over the years are aimed toward treating these recurring seizures and they include medication, surgery, non-drug therapies, and also the ketogenic diet. One treatment, however, that stands out from the rest is called vagus nerve stimulation (VNS). Even though this treatment helps many people with epilepsy, it is still a very controversial treatment since doctors are still puzzled at how the stimulator prevents seizures.

The vagus nerve stimulation is used to treat many different types of epileptic seizures, thus it is important to have an understanding on the types of seizures that are associated with the disorder. Epileptic seizures are usually brought forth by sudden discharges of excess electrical activities within the nervous system and can be classified as generalized or partial seizures. Generalized seizures have more serious effects than partial seizures because the abnormal electrical signals of the nerve cells occur in many diffuse regions of the brain (1). One type of generalized seizure is tonic-clonic seizure, in which muscles alternate between contraction and relaxation, and so some patients may lose bowel or urinary control. Tonic-clonic seizures usually last about 2 to 3 minutes, after which the patients remain unconscious and later awaken to confusion, fatigue and severe headache (1). Absence seizures are also another type of generalized seizures in which the patients suffer for a short cessation (30 seconds) of physical movement and loss of attention that occur around 50 to 100 times a day. Partial seizure, unlike generalized seizure, occurs very often in epileptic patients and is caused by neuron disorders in a particular region of the left or right side of the brain. Simple partial seizure, or Jacksonian epilepsy, is one type of partial seizure in which patients do not lose consciousness but experience jerking movements, confusion, hallucinations, strange thoughts, and extreme reaction toward smell and taste. Complex partial seizure, also a subtype of partial seizure, occurs in the temporal lobe or the region of the brain near the ear. Patients with this type of seizure experience a loss of the ability to make judgments, involuntary behaviors, and also loss of consciousness. Before the actual occurrence of the seizure, patients will experience aura or warning signs, which include feeling of warmth, hallucination, and also repetitive movement (6). There are other seizures that are not related to generalized or partial seizures, and they include atonic seizures, clonic seizures, and myoclonic seizures. The vagus nerve stimulating treatment, however, is more directed toward treating generalized and partial seizures since these types of seizures are often seen in epileptic patients.

The vagus nerve stimulation (VNS) device, or more commonly known as the "pacemaker for the brain", sends regular pulses of electrical energy to the brain by stimulating the vagus nerve. An incision along the outer left side of the chest is made for the implantation of the VNS battery-powered device. In the lower part of the neck, another incision is made in order for the stimulator wire to wind around the vagus nerve. The VNS device is programmed by the neurologist to deliver mild electrical stimulation to the vagus nerve according to the patient's individual needs (1). For instance, some of the typical settings on the device are stimulation amplitude, stimulation frequency, and pulse width. These settings can easily be altered by using a programming wand and a computer. Before a seizure attack, many patients may experience auras or warning signs. The neurologist can easily stop the seizure before it happens by passing a magnet over the device to give it an extra dose of electrical stimulation to the vagus nerve. In order to be considered as a VNS candidate under the American Academy of Neurology, the patients must be over 12 years old, are not suitable for major surgery, and also have partial seizures that cannot be resolved by using medication (6). Some complications that can arise with the VNS procedure include shortness of breath, sore throat, coughing, nausea, and vomiting. These complications can easily be reduced by decreasing the intensity of the stimulation to the vagus nerve by the VNS device.

The idea that the VNS device can reduce seizures seems unfeasible and inconceivable at first glance (before reading the article) because I did not see how stimulating the vagus nerve and the structure itself have anything to do with seizures. The vagus nerve, or pneumogastric nerve, is one of the 12 pairs of cranial nerves and originates in the brain and passes through the neck and thorax into the abdomen. It supplies motor and sensory function to the ear, tongue, larynx, diaphragm, heart, pharynx, stomach, and esophagus (7). All of the important structures that the vagus nerve targets are outside of the brain region and so the vagus nerve did not seem to be related to seizures except for the single fact that the vagus nerve has its origin in the brain. Thus, I wonder if stimulating the vagus nerve will affect other structures that are connected to the vagus nerve? Furthermore, I did not see the mechanism or pathway through which the vagus nerve stimulator works to condition the brain to respond better to interruptions in the functioning of the brain. Does the electrical stimulation from the device destroy the abnormal electrical pattern produced by the neurons, or does it modify the imbalanced electrical signals back to the normal state again?

However, after reading the article "Vagus Nerve Stimulation", I saw that it does provide much solid evidence to support a strong connection between the vagus nerve and seizures (2). For instance, vagal stimulation resulted in changes of the EEG because of the responses from the thalamus and also the ventroposterior complex. The EEG also showed that low frequency stimulation to the vagus nerve can cause synchronization, while high frequency stimulation results in desynchronization (1). In 1988, Penry, Wilder, and Ramsay performed the first VNS device implantation into a human being. There were about 15 people who volunteered for the experiment, and the result showed that seizures were reduced around 50% There has not been a precise model that can describe the action of the VNS to reduce seizures. Researchers, however, discovered that the VNS has the ability to target the medulla, locus cerules, hypothalamus, cingulate gyrus, and amygdala (3). Some of them believe that the VNS reduces seizure in several ways. For instance, VNS causes more GABA and glycine in the brain to be released, which in turn will cause an increase in the threshold for seizure. Action potential will not be created and so there is no current flowing down the axon. Other theories state that the VNS influences the reticular activating system to decrease the cortical epileptiform activity. Another theory claims that the VNS causes changes in the cerebellum, blood flow in the brain, thalamus, and the cortex, which then can activate inhibitory structures in the brain to decrease the seizures activities (2).

Researchers have yet to find out the complete pathway in which stimulating the vagus nerve can cause a decrease in seizures. Thus, vagus nerve stimulating treatment is still under heavier scrutiny from the public and the health industries. Furthermore, there have not been many long-term studies on the side effects of having continuous stimulation to the vagus nerve. I feel, however, that having the vagus nerve subjected to the continuous stimulation might not be a good idea because of the connection between the vagus nerve to other structures. The vagus nerve represents a box in the "boxes inside boxes" model, and so this box is connected to many other boxes like the amygdala .If the vagus nerve is damaged due to the strong electrical stimulant from the VNS devices, other structures around it will also be damaged in the process.

References:
1)Epilepsy, History and Treatments of Epilepsy
2)EMEDICINE on Epilepsy
3)What is Epilepsy
4)The Foundation of Epilepsy
5)VNS Therapy
6)Epilepsy
7) Web Md


Handedness: Biological or Socio-Cultural?
Name: Catherine
Date: 2005-02-22 10:10:26
Link to this Comment: 13128

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Handedness is marked by the preference of one hand over another for fine motor tasks, especially writing. Usually, only one hand is considered dominant, however, there are individuals who exhibit the ability to use both hands equally (ambidexterity). It is generally the case that most people are right-handed, with left-handed people constituting approximately 2% to 30% of the population, depending on the criteria used, with the median estimate of about 10%. (2). Is this propensity to use the right hand genetic, or does it result from socio-cultural pressures?

Firstly, the preference for one hand over another is most likely the effect of brain lateralization. The human brain is divided into two hemispheres (right and left) connected by the corpus callosum. The hemispheres are contra lateral, meaning the left-brain controls the right side of the body and vice versa. (4). Different skills and abilities are associated with the two hemispheres; basically, the brain is compartmentalized, relegating specific abilities to one location. The "information" necessary to perform various tasks is stored within the brain. This is dependant on surface area: the greater the surface area, the greater "storage space." Since writing and other fine motor skills require "storage space," it is logical that these abilities are usually restricted to one hemisphere rather then having the same information stored in two places. For this reason, humans prefer one hand over the other; when this information is stored in the right brain, the individual displays a tendency to use the left hand (the reverse is also true). However, it should also be noted that just because people usually prefer one hand as opposed to the other, fine motor skills are not exclusively associated with that hand (i.e. right-handed people are capable of playing instruments, such as the violin, which rely on motor skills of the left hand). (4). Therefore, an individual will prefer to use one hand (especially for writing), but is still capable of using the other for other fine motor tasks.

Given that the brain is compartmentalized, many scientists believe there is a genetic basis for handedness. "Dominance" of one hemisphere over the other could be passed down through DNA (specifically, some alleles may be "coded" for handedness). "In humans, the inheritance of handedness fits well one-locus models where one allele causes right-handedness and another left- or right-handedness at random." (3). Thus, according to this model, handedness is determined by what is "coded" on the allele. Since one allele is specifically programmed for right-handedness, but the other can be programmed for either, right-handed people outnumber left-handed people because of a greater probability of having an allele coded for right-handedness. The percentage of right-handed people in the general population (~70 95%, depending on the criteria used) further affirms the assertions of this genetic model. Furthermore, since left-handed people are statistically more prone to diseases, handedness does indeed appear to be influenced by genetics. Statistically, left-handed people are more likely to be dyslexic, schizophrenic, have Crohn's disease, ulcerative colitis, and mental disabilities. (1). Since left-handed individuals are afflicted with these genetic disorders with greater frequency, it suggests that there may be a genetic basis for handedness. However, some assert that this increased frequency of diseases among those with left-hand dominance suggest that this is due to some sort of "trauma" during gestation or birth. "It could be that this early trauma is also the trigger behind health problems linked to left-handedness. Coren points to two famous left-handers, Presidents Bill Clinton and George H.W. Bush, as evidence. Both had histories of birth stress and have health issues from Clinton's severe allergies to Bush's Graves' disease." (1). Thus, the increased frequency of disease may be the result of genetics, or perhaps the result of "trauma" during gestation. However, if left-handedness truly were genetic, then why could some individuals switch from writing with the left hand to the right hand?

Some individuals have switched hand "dominance" due to socio-cultural pressures. Left-handed individuals were at one point considered evil, or even communist, for being left-handed. (2). In fact, the English language demonstrates this bias against lefties. The word "sinister," meaning evil or wicked, comes from the Latin word "sinistra," meaning left. This derivative alone shows the societal connection between "left" and "evil." Due to this societal belief, many left-handed individuals were forced to switch and use the right-hand instead. (2). Furthermore, there is a higher percentage of left-handed people in "permissive" societies than in "restrictive" ones. (5). This further reinforces the idea that handedness is susceptible to socio-cultural pressures, and in fact, may be changed. Therefore, it is possible that the human brain in malleable, meaning that it can be "rearranged" so that coordination of certain skills, like writing, can be switch from right brain to left-brain. Furthermore, humans seem to be the only species to demonstrate "population-level handedness," meaning that humans overwhelmingly seem to prefer right to left. (5). While some animals do indeed exhibit a preference for one hand/paw to another, they do not seem to have "population-level handedness." (5). This further suggests societal pressures may determine handedness (for, if it were purely genetically based, animals would probably exhibit the same "population-level handedness").

In conclusion, while handedness does appear to have a genetic basis, it is also influenced by socio-cultural pressures. The propensity to use the right hand demonstrates a left-brain "dominance," whether or not it is genetically imposed. Much is still unknown as to why an individual is right or left-handed, and further exploration is necessary before a definitive explanation can be offered. There is also the question of ambidexterity how does the brain of an ambidextrous person differ from that of a left-handed or right-handed individual? Is ambidexterity genetic, or culturally influenced, or neither?

References


1)The Left-Handed Advantage, ABC News Article


2)Gauche, Left-Handers in Society


3)The Evolution of Brian Laterization: a game theoretical analysis of population structure, Genetic basis of handedness


4)Lateralization of functions in the vertebrate brain: A review, Lateralization in the human brain as compared to other vetebrates


5)Do scientists understand why there are so many more right-handers than left-handers? Do other primates show a similar tendency to favor one hand over the other?, Handedness in humans and primates


Where does my English come from?
Name: Ayumi Hoso
Date: 2005-02-22 10:19:21
Link to this Comment: 13129

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


YOUR TEXT. REMEMBER TO SEPARATE PARAGRAPHS WITH A BLANK LINE (OR WITH

, BUT NOT BOTH). REFERENCES (IF ANY) GO IN A NUMBERED LIST AT THE END (SEE BELOW). TO CITE A REFERENCE IN THE TEXT, USE THE FOLLOWING AT EACH NEEDED LOCATION:
(YOUR REFERENCE NUMBER).

References

SUCCESSIVE REFERENCES, LIKE PARAGRAPHS, SHOULD BE SEPARATED BY BLANK LINES (OR WTIH

, BUT NOT BOTH)

FOR WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY

REFERENCE NUMBER)NAME OF YOUR FIRST WEB REFERENCE SITE, COMMENTS ABOUT IT

FOR NON-WEB REFERENCES USE THE FOLLOWING, REPEATING AS NECESSARY

REFERENCE NUMBER) STANDARD PRINT REFERENCE FORMAT

Almost seven years have passes since I came to the U.S. Although I came to the U.S without knowing much English especially how to speak it, I became an advanced ESL speaker over years. I communicate with people in English, I write papers in English, I read textbooks in English and I even dream in English. When I go home and speak Japanese, my native language, I drop many English vocabularies in the sentences. This shows that I feel very comfortable with English. However, it is still far away from being perfect and my struggles continue in many situations. I have begun to think that it is nearly impossible to write, speak or understand like a native speaker. "Will my English ever get closer to the native level?" This has been a question I have been wondering for a long time. Though I feel comfortable using English everyday, I sometimes feel weird and unnatural about speaking English. I can speak Japanese without thinking whereas I still need to remind myself of grammatical rules with English. There must be a language property within the brain, but I wonder if I use same parts of brain when I use Japanese or English. If I do, how do I differentiate to use two languages? If I do not, where does my English come from? Are there any differences between bilinguals who learn multiple languages in the early age and who learn later? Does the second language acquisition of age matter? I need to know how our language process takes place within the brain as well as its relationship to the brain. Also, it is important to mention the concept of critical age. Through my research, I found that there have many various theories of where the second language takes place within the brain as well as lab researches utilizing the recent technology. The research tends to result more heavily on the possibly of using a different part of brain between the first and the second languages these days, but there has not been a single answer found yet.

Within the brain, there are two areas called Broca's area and Wernicke's area. About 97% of people equip Broca's area and Wernicke's area only in the left hemisphere of the brain, and they are the areas that we think our language process takes place (1). Broca's area has properties of verbal production of language including speech patter, grammar and syntax, whereas the Wernicke's area has a property of understanding of what the words mean. According to the experiments with many children and the way they acquire the native language, Asher concludes that "comprehension comes before speaking" (2). Considering the functions of Wernicke's area and Broca's area, this conclusion shows that Wernicke's area has to "light up for along period of time before the circuitry of the left brain in Broca's area flickers on" (2). Also, in order to speak either after reading or hearing, the information is transmitted in a order of Wernicke's area, Broca's area and then Primary Motor Cortex(1). Thus, our language system is located mostly in the left hemisphere of the brain and we usually process the language through Wernicke's area to Broca's area by sending information.

One thing that becomes important to consider is what we often hear, "critical period" for language acquisition. An example of Genie has been one of the most famous researches that prove the possible existence of critical period for language acquisition. Genie, who spent her childhood life in a closet without verbal communication until the age of 13, never developed the adequate level of language. There have been many researches and we have associated the inability of acquiring a language with the plasticity and lateralization of the brain. Many scientists came to conclude that after the ages between two to twelve, the brain "appears to lose its plasticity for learning language" (3). Because somebody missed the period when the brain is still flexible enough to adopt much information including the language system, the left hemisphere of the brain does not possess it. Counting in the existence of critical period as well as the plasticity of the brain, it is not very practical to believe that people can successfully acquire the second language and reach the native speaker level, because the native language has been in the left hemisphere of the brain for a long time. Learning a language means "habituating the body and nervous system to new patterns" (4). If plasticity really does diminish after the critical period, how hard it is for the new language that is learned after the critical period to come into the left hemisphere of the brain where the native language system resides.

Many researches have looked at the brain differences between monolingual speakers and bilingual speakers. Recently, the research has also been paying more attention to the differences between bilinguals who learn the second language at the early age of their lives and bilinguals who learned at the later age. This also helps to explain the importance of the critical period and plasticity of the brain.

One of the hypotheses is that bilinguals who learn their second language at a later age process the second language through the right hemisphere of the brain whereas "early bilinguals" process the left hemisphere (3). The role of the right hemisphere of the brain has been paid attention. However, more researches have been done, and it seems that the right brain have a significant role in second language acquisition only in the early stage, but not in the later stage (5). It means that initial process of acquiring the language is done within the right hemisphere of the brain whereas leaning involves with the left hemisphere of the brain. However, these researches have not looked further yet and they have not asked where the second language is being processed within the left hemisphere of the brain, either a same area where the first language system exists or a different area.

The recent researches often utilize the high technology. The 1997 research done by Kim, Relkin, Lee and Hirsch has shown one of the most interesting findings through MRI. In their research, they conducted a study with six early bilinguals and six later bilinguals, who are all fluent with the second language. They look at the activity of the brain while they ask the speakers to talk to themselves in one of their languages while looking at various pictures. What they found out from this research was that the early bilingual's activity of both languages were located in the same region of Broca's area whereas the activity of the later bilingual was located in a separated region of Broca's area though it was adjacent to where the first language is processed (6),(7). They also found that the activity showed only in one region with Wernicke's area with both in their first language and the second (6), (7). According to these two hypothesis, we can presuppose that the second language acquired in the later age is processed in a different place from their first language is processed. Maybe the initial acquisition part involves with the right hemisphere of the brain, but when people learn and get used to the language, the second language starts to be processed in the close region to where the first language is processes, usually in the left hemisphere of the brain.

If it is the case that the first language and the second language which is acquired after a particular age are processed in the different parts of the brain, how much room is there for the improvement of the second language? It is probably not easy to say that there is a big space for an improvement to reach the same level as the first language, because the second language cannot fit into where our first language is, thus we cannot provide the best environment for the language acquisition. However, if the MRI research is right and the difference in activity between the two languages is not found in Wernicke's area, we can still assume that it is possible to learn the semantics property of the second language. Also, the activity difference in Broca's area means that the grammar and syntax properties may not be something that we have a control over.

There have been more researches going on in this field, and this finding might not the final result. Also, the improvement of the second language learned after puberty has some variations among people depending on the similarity of sounds and the syntax system between the first language and the second language. At this moment, I am content to suppose that my English processor resides in a different place from Japanese. If the research is right, my English never shares the residence with Japanese since I started learning English at a later age. After this research, something new puzzles me. If the bilinguals can process two types of language in the same area, I wonder if they ever get confused. Is it possible for human to acquire two or more languages perfectly and maintain both languages at the same level? I would like to know more about the language system and the brain.


WWW sources


1)Thinkquest website,The Brain and Communication

2)TPR website ,Organizing Your Classroom for Successful Second Language Acquisition

3) Dr. Loretta Kasper's ESL 91 on the web, Language Acquisition in Humans

4) Bryn Mawr Library Search , practical linguistics/ A sensible theory of Language by
Childs, Marshall R. The Yomiuri Shimbun, 4/11/2003

5)Stephan D Krashen's webpage , Second Language Acquisition and Second Language Learning

6) The University of Missouri-Columbia website , Bilingualism Comes in Different Ways

7)University of Washington website , Second Language Learning.


Creutzfeldt-Jakob Disease
Name: Bridget Do
Date: 2005-02-22 11:11:50
Link to this Comment: 13130

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


Transmissible spongiform encephalopathies (TSE) are infrequent, incurable brain conditions that have affected sheep and goats since around 1730 when their presence was first described by farmers in Britain and Europe. The disease in sheep was called Scrapie, and has never been found in any other species. It was the only TSE on record for almost 200 years until the discovery of human TSE, Creutzfeldt-Jakob disease (CJD), was made by scientists in Germany in 1920. In 1985, the first instance of bovine spongiform encephalopathy (BSE) was discovered to have caused the fatalities of several cows in the United Kingdom, and the "Mad Cow Disease" outbreak began (7). Until the discovery of variant CJD, the varieties of TSE which affected the different species appeared to be related through their symptoms, but unable to be transferred between species (4).

TSE is characterized by the appearance of the brain which has been contaminated by a form of TSE. Under the microscope, the brain is revealed to be full of holes and resembles a sponge. It was originally thought that a virus or bacteria caused the condition, but the virus or other organism has never been able to be isolated, nor has it been affected by any prescribed medications which usually have an impact on viruses and bacteria. It is believed that prion proteins, a normal form of protein found in animal cells, can mutate into an infectious form that starts a chain reaction, thus causing other prions to morph and clump together. These aggregates are believed to lead to the neuron loss and other damage to the brain as can be seen in affected animals. How this damage occurs exactly is still unknown. It is very difficult to spread TSE, most specifically CJD because it cannot be transmitted through air or casual contact, and in no instances has a patient who has received blood transfusions contracted CJD from a blood donor ((1).

A wide variety of physical and neurological symptoms occur when a human has been infected by CJD. They do not include a fever or any flu symptoms, and can easily be confused for other neurological disorders such as Alzheimer's or Huntington's disease. Early symptoms include the impairments of memory, judgment and thinking, behavioral changes, lack of coordination, impaired vision and visual disturbances. Victims may also suffer depression, insomnia and unusual sensations (5). Later, mental impairment becomes progressively more severe, and the patient experiences involuntary muscle jerks, blindness, weakness of extremities and hallucinations. Eventually, the person who suffers from CJD loses the ability to move and speak and enters into a coma (1).

Diagnosing CJD is a very trivial task, because there is no single test which can confirm the presence of the disease unless the patient is deceased. The presence of CJD cannot be confirmed without a brain biopsy or autopsy after the victim has passed away. When a neurosurgeon removes a portion of the patient's brain to be studied in a biopsy, there is a chance that an infected portion of the brain will not be isolated and therefore CJD will go undiagnosed. A biopsy is considered a risky procedure, and because there is no treatment for CJD even if it is diagnosed, the procedure is usually discouraged. If a doctor believes a patient to be suffering from CJD, he or she can only be sure of ruling out other treatable brain disorders such as encephalitis or chronic meningitis. This can be done by performing standard diagnostic tests such as a spinal tap, an electroencephalogram (EEG) or with magnetic resonance imaging (MRI). Frequently, CJD will go undiagnosed until the patient dies and an autopsy is done ((1).

There are four types of CJD, the most recent of which, variant CJD, was discovered in 1994. Iatrogenic CJD is the least common form today. It is transmitted accidentally during medical or surgical treatments such as neurosurgery, cornea transplants, human dura mater implants and the use of human cadaveric growth hormone (hGH) and human pituitary gonadotrophin (hGNH). Cases of iatrogenic CJD are identified chiefly from the patient's recent history of such a procedure. Genetic CJD is the variety that affects five to ten percent of CJD cases. In this form, the sufferer inherited an abnormal gene. These cases are most easily identified if a family history of the disease has been recorded. Variant CJD (vCJD) is believed to be caused by ingesting food contaminated with the BSE agent. Aside from few cases found in France, Ireland, Italy and the USA, this strain of CJD has been confined to the United Kingdom. The most common form is sporadic CJD (sCJD). SCJD accounts for 85 percent of CJD cases and has been found in every country in which it has been tested for. For sCJD to occur, it is believed that the prion mutates spontaneously to the abnormal form, resulting in the disease (6).

There are subtle differences between the forms of CJD. The age of onset is on average between 50 and 75 years old. Sufferers of variant CJD, however, are on average 27. Those diagnosed with sporadic CJD most often affects middle-aged and elderly persons. The gestation period of the two forms is also quite different. Variant CJD cases have may take a year or more to take full effect. Sporadic CJD usually has a duration period of a few months, or in some cases, only a few weeks. There are several exceptions to each of these generalizations, however, so they cannot be used to categorize the two types of CJD (6).

As was previously stated, there is no treatment or cure for CJD. Scientists all over the world are searching for an answer to the fatal disease. In San Francisco it was reported in 2004 that a 20-year-old female who was diagnosed with vCJD and treated in a pioneer drug trial recovered fully from her condition. Two likely candidates for the treatment of CJD are quinacrine and pentosan polysulphate (PPS). Both are being further investigated as remedies for CJD sufferers, but must still undergo a great deal of research before they can be prescribed (3).


References

1)Creutzfeldt-Jakob fact sheet, general information on CJD

2)Monthly Creutzfeldt-Jakob disease statistics, chart of CJD diagnoses, deaths

3)Potential treatments for Creutzfeldt-Jakob disease, an essay on possible cures for CJD

4)20/20Hindsight, an essay on BSE

5)Creutzfeldt-Jakob disease fact sheet, more general information on CJD

6)The National Creutzfeldt-Jakob disease surveillance unit, resource from the UK

7)BSE - bovine spongiform encephalopathy "mad cow disease", resource from University of Chicago at Urbana-Champaign


Why Are Humans Vulnerable to TBI (Traumatic Brain
Name: Jasmine Sh
Date: 2005-02-22 11:36:29
Link to this Comment: 13132

<mytitle>
Biology 202, Spring 2005
First Web Papers
On Serendip


After a recent family member's loss due to what doctors call brain death, I started to question whether or not the brain is truly safe. After billions of years of evolution, one would think that humans have evolved into a present, ideal state of being. With current technological innovations, doctors are also more capable of curing and treating patients for sustained and prolonged life. However, despite the extensive medical attention which can be provided for patients, there is always a limit to our own bodies' capacities and threshold for maintaining life. As I mentioned above, my uncle recently passed away due to a traumatic fall from a flight of stairs. The traumatic brain injury (TBI) that he suffered caused his brain stem to cease functioning, and this, in turn, made him brain dead. Before this incident occurred, I never truly understood the fragility that comes with life and living in our own bodies. As I said before, doctors can only do so much to sustain our lives when injuries occur. But how come our own bodies, specifically our brains, have been created to be so susceptible to traumatic brain injuries in the first place? And how can one truly define brain death as opposed to the "body's death"?

According to a source, "The brain is the hub of the central nervous system and controls all bodily functions and processes," (4). More important than the actual brain is the brain stem, which is at the base of the brain and continually carries signals from and to the body. By sending these signals, the brain stem controls our consciousness, fatigue levels, heart rate and blood pressure. Thus, if the brain stem ceases to function, due to bleeding, swelling, bruising and tearing of brain tissue (from a traumatic brain injury), an individual can enter a state of coma (unconsciousness) because he or she can no longer control the body. Coma is defined as "damage to the brain's thinking and life support centers," (5). Thus, the brain stem can be considered as the body's life support center because it does control consciousness, our heart rate and blood pressure! (5).

So now that we understand why an individual can get brainstem damage and enter comas, we should know how these damages occur in the first place. "Traumatic brain injury (TBI) is sudden physical damage to the brain," (2), which is the leading cause of death for persons under the age of 45 in the United States. TBI occurs most commonly due to motor vehicle accidents, falls, or sports injuries! (3). Because of the high number of fatalities due to TBI, there is no doubt that our brains are extremely susceptible to both penetrating head injuries and closed head injuries, (or that people are engaging in more risky behavior these days.) Penetrating injuries are caused by damage occurring along the route that a particular object has taken into or through the brain. Closed injuries occur when there is a certain blow or pressure against the head, damaging the interior of the brain (1). Both can cause either primary damage (fractures, hematoma, and lacerations) or secondary brain damage (edema, epilepsy, increased intracranial pressure) (1).

While the dangers associated with penetrating injuries are obvious (such as a gunshot wound), many people do not understand the severity of closed-head injuries. They are not aware that the brain continues to move after the skull hits a stationary object and becomes still. The brain's continued movement inside the skull causes bruising, bleeding, or damaged nerves on the inside of the skull, all of which lead to more severe problems like increased intracranial pressure, hemorrhaging, and brain stem dysfunction (2). In the most severe TBI cases, the abundant brain swelling and intracranial blood pressure put an enormous amount of added pressure on the brainstem (the part of the brain that controls consciousness), causing the brainstem to cease functioning and the individual to become brain dead and fall into a permanent coma, (as explained above) (2).

Then why, might we ask, is the human brain so susceptible to TBI and other brain injuries? First of all, we must always remember that "While the brain is by far the most complex object on earth, it is soft and vulnerable with a consistency of firm pudding," (3). The human brain, because it is so soft, can be vulnerable to TBI in many ways. First of all, the cerebral cortex can easily be bruised when the head or brain comes in contact with hard objects. Secondly, the gray matter can also easily suffer from diffuse axonal injury. (Because the brain has nerve cells in the grey matter that send signals through their axons to the white matter, sudden impact to the brain causes the axons of the nerves to twist or become damaged so they can no longer transport the necessary signals) (3).

Thirdly, some of the resulting types of brain injury are: Edema (swelling, which increases the intracranial pressure and prevents oxygenated blood from entering the brain,) Hematoma (Blood clot formed by tissue injuries,) or Hydrocephalus (when blood gets into the cerebrospinal fluid and inhibits fluid "absorption sites," enlarging the ventricles and adding extra pressure in the brain (3).

Ultimately, once these irreversible damages occur to the brain stem, individuals are considered brain dead. Because the brain stem controls breathing, blood pressure, heart rate, and consciousness by sending signals to the rest of the body, damaged brain stems can no longer send signals to the rest of the body to make it function. Brain stem death, in general, can be caused by: TBI, brain hemorrhaging, thrombosis of blood vessels, cerebral anoxia, or brain tumors (7).

However, although brain stem dysfunction is a necessary condition for determining brain death, how can one truly distinguish death between one's body, and one's brain? While doctors today can maintain the functioning of our vital organs such as our heart and lungs for long periods after the brain has ceased working, ultimately, without those mechanical supports, the body itself would give out. The individual has reached a point where the "life-maintaining centers of the brain stem tissue" have stopped working, giving him/her a dead brain but viable body (if sustained through medical equipment) (6). In other words, once the dead brain cells cease functioning and regenerating, the brain can no longer control the body, and the body, without medical help, will eventually give out (7). But how long can one really sustain a body through hospital machines and ventilators? And when is it time to let go? To make these questions easier to answer and handle, laws have been passed, stating that once brain death has occurred, the individual being cared for is legally dead.
So how do you actually check for brain death? To do this, doctors must make sure that the following symptoms exist in patients: no electrical activity in the brain, no blood flowing into the brain, and the absence of the functioning of the brain stem (7). Doctors check if these symptoms exist by checking if: the patient's pupils don't respond to light, the patient doesn't breathe on their own, natural eye movements do not exist, the patient has no gag reflex, the patient doesn't respond to pain, or if the patient's eyes do not move when cold water is poured into the ears (8). In other words, brain death is "the irreversible loss of all function of the brain," (7).

However, even if an individual is brain dead, how come hospitals can not keep patients on life support? Why is it that the end of brain function creates death, even if the body continues to work on machines? Don't our bodies continue functioning with medications if we have severe medical problems? Then why can't the machines be considered "medications" that sustain life? The reason for this phenomenon is the human's extraordinary reasoning capacities. Lawmakers and doctors have come together to distinguish brain death as actual death due to the reasoning that if the brain doesn't work, the rest of the body can not work on its own. This point makes sense if we consider that "behavior can be operationally defined as the net sum of muscle and gland activity both of which constitute the output of neural function," (9). Thus, from a neurobiological perspective, if the neural function (brain stem function) ceases, our behavior ceases to exist, and thus, we become brain dead. This is in accordance with current laws used to distinguish brain death. At that stage in life, humans are only carrying out the life processes (i.e. "behaving") with the help of machines. Because the brain stem can't function, individuals can no longer control their own actions. As a result, they eventually become brain dead.

In sum, it seems as if the human brain is truly not a safe place because it is so vulnerable to traumatic brain injuries. Also, because the human brain is such a complex region, any small laceration or contusion can create devastating and long-lasting damage. With regards to the controversial issue of brain damage, I now have a better understanding as to how one can determine brain death and distinguish it from the body's death. In connection with our course material, I have truly come to understand that the brain does equal our behavior. As with brain damage and death, if the brain does not work, our behavior ends and we are considered dead. Thus, brain activity determines our behavior! From my research and new understanding of this topic, I advise people today to be extra cautious with their daily activities and to truly comprehend the fragility of the human brain and life.


References


1) American Speech-Language Hearing Association , has good information about traumatic brain injury.

2) National Institute on Deafness and Other Communication Disorders , has good information about classification of brain injuries.

3) Brain Injury Information and Medical/Legal Advice , has information about different types of brain injuries and on legal information about brain death and injury.

4) Online Neurology Channel , an overview of TBI information.

5) Brain injury Resources Center , has good information about comas and brain death.

6) Neurology and Brain Death , explains brain death.

7) What Is Brain Death? , explains brain death in detail.

8) Institute of Child Health, Brain Stem Death , explains brain stem death.

9) Klemm W. R., and Robert P. Vertes, eds. Brainstem Mechanisms of Behavior. New York: Wiley-Interscience, 1990.


But It Just Feels So Good! On the neurobiological
Name: Katherine
Date: 2005-02-23 01:03:51
Link to this Comment: 13152

<mytitle> Epics tales of passion and punishment construct the foundation of our collective human consciousness. Even as children, we are fed stories detailing terrible transgressions and the decisive action inflicted in response to these said offenses, and by the popularity of these examples we are encouraged to feel a degree of righteous satisfaction when the "bad guy" is punished. Contemporary cinema provides ample support for this social norm, as is demonstrated by the following monologue from the opening scenes of director Quentin Tarantino's film, Kill Bill Vol. 1. The speaker, known to the audience only as the Bride, has just awoken from a coma and is intent on exacting punishment on those who wronged her:

Looked dead, didn't I? Well I wasn't, but it wasn't for lack of trying, I can tell you that. Actually Bill's Last bullet put me in a coma. A coma I was to lie in for five years. When I woke up ... I went on what the movie advertisements refer to as a Roaring Rampage of Revenge. I roared and I rampaged and I got bloody satisfaction. In all, I've killed 33 people to get to this point right now. I have only one more. The last one. The one I'm driving to right now. The only one left. And when I arrive at my destination...I'm gonna Kill Bill. 1)Bergen International Film Festival.

Despite the comically horrendous violence utilized to exact revenge upon the offenders, one has to admit feeling a certain degree of satisfaction when she enacts her revenge and is reunited with the daughter torn from her womb. But where does this feeling come from? Why is it okay to commit several murders for the purpose of satisfying ones personal yearning for vengeance? Is this solely an issue of our social and cultural upbringings, or can the answer find its roots across all people, in the very biology of our respective selves?

In respect to these questions, I would like to call to your attention a recent Swiss study concerning "The Neural Basis of Altruistic Punishment" (2004). Authored by scientists Dominique J.-F. de Quervain, Urs Fischbacher, Valerie Treyer, Melanie Schellhammer, Ulrich Schnyder, Alfred Buck, and Ernst Fehr, the study organized men into anonymous pairs of two (A and B) and instructed them to play a laboratory-devised game of money exchange. In one series, Player A was given the option of keeping a sum of 10 Money Units or giving it to Player B, knowing that the money received by Player B in this exchange would in fact be four times the original amount. Player B, in turn, had the option of keeping a total sum of 50 Money Units or returning half (25 MU) to Player A, thus assuring that both players enjoyed equal wealth. If Player B chose to keep the total amount of money, leaving Player A with none, then Player A was given the option of punishing Player B; sometimes, the reprimand was strictly symbolic, while in other situations, experimenters deducted a sum of money from Player B's total. In each case, Player A had one minute to consider whether or not to penalize Player B; during this time, scientists employed a positron emission tomography (PET) to scan Player A's brain for neurological activity. 2)Science Magazine. PET scans of Player As brain during the one minute deliberation period demonstrated increased activity in the dorsal striatum, an area of the brain associated with the processing of rewards and feelings of satisfaction and enjoyment. This activity was only found when a real penalty was inflicted; in situations where the punishment was only symbolic, scientists did not find similar stimulation of the dorsal striatum. 3)Scientific American.

So, what does this all mean? What is the significance of these PET scans? The researchers originally hypothesized that by initiating an exchange with the gift of a sum of money to an anonymous partner, Player A must trust Player B. In return for this trust granted to him by a complete stranger, Player B would, according to social norms governing fairness and interdependence, reward Player A by returning half of his money so that both share equal investments and rewards from the exchange. Thus, in cases in which Player B keeps all of the money, he transgresses these norms governing social behavior, thereby wronging Player A. 2)Science Magazine. As the scans show, when given the opportunity to punish Player B for breaking these commonly accepted standards, Player A experienced psychological redress. That is, in these situations, revenge actually felt good! 3)Scientific American. To this, Dr. de Quervain comments,"These findings reflect the everyday experience that some people are willing to invest much more than others in punishing norm violations." 4)MSNBC Stories from Science.

De Quervain's observation may in fact be better understood when one considers that in all situations, both Players in the exchange remained anonymous and therefore acted as complete strangers. This could account for why Player A felt comfortable and in fact derived pleasure from inflicting "altruistic punishment," or action against a stranger who had broken a social code of behavior. Possibly, he acted not necessarily for himself, but rather out of "altruistic interests" for the good of humanity, collective society, rather than his individual self. Had Player B been a friend or acquaintance, the scans of Player A's brain activity may very well have produced different results. But, that is for another experiment to reveal.

To return to our discussion of Player As brain activity while he deliberated punishing the Player who broke his trust, it should be noted that another area of the brain simultaneously experienced heightened activity. This area, called the prefrontal cortex, generally comes into play when weighing the costs and benefits of a choice. In the case of Player A, his prefrontal cortex became activated while he compared "the satisfaction derived from punishment against the monetary cost of punishing." In fact, the scientists also found that as the cost of punishment increased, the satisfaction garnered decreased. 5)National Geographic. This weighing of options indicates a rational process that is important to remember in this discussion. Upon first glance, it seems quite bestial or "uncivilized" that a human being would feel pleasure from inflicting pain. However, as the scans of the prefrontal cortex indicate, the brain plays host to continual struggles. Though the findings are so new that any conclusive research expanding upon this study have yet to be published, it is possible that if Player A and B were to engage in a similar exchange, but in this instance, removed from anonymity, Player A's prefrontal cortex may indicate increased activity as Player A weighs the pros and cons of inflicting a penalty on a friend or punishing a transgressor of social norms.

In light of these startling findings, what is one left to think? Surely, the results of this study ring true to many if not all, but this is just one report, and there are many questions left unanswered. How/would the results be different if they included women? Given the evolutionarily differing roles of men and women in a community, would the regions of women's brain associated with conflict resolution and group cohesion be activated? Also, this study was conducted using a presumably Swiss population sample. How, if at all, would the results change, if scientists were to apply this experiment to cultures that were more individually-based? In such cultures, social norms would presumably be less important to the identity of the society and the well-being of others. If this is true, would Player As of this sample experience less activity in their dorsal striatum? And finally, to return to the original example of "the Bride," who exacts revenge on over 30-people, there is no possibility of scanning her fictional mind in order to better understand the processes of her behavior. However, she serves as a good, modern day example of an old, familiar archetypethat of the avenging warrior, determined to punish, and in fact, enjoy punishing, those who wronged her.


Investigating the Neurobiology of Consciousness
Name: Patrick We
Date: 2005-02-23 13:40:09
Link to this Comment: 13162

<mytitle> In looking at the source of consciousness, we must first decide how to define consciousness. I believe that one logical way to do this is to see consciousness as a spectrum, ranging from states of heightened awareness to states of drowsiness, sleep, and coma (1). This interpretation of consciousness is employed by today's scientists and its origins go back to William James, who was one of the first to delve into questions concerning questions of conscious and unconscious states (2). When thinking about consciousness, we realize that consciousness can vary significantly depending upon the amount of attention we owe a particular process. We can control how we focus our attention when we try to recognize a face in a crowd, memorize new vocabulary words, or play an instrument.

Now that we have a working definition of what consciousness is, we must determine how we will go about identifying it in the brain. One place to start is to locate what has been called the neuronal correlates of consciousness (NCC). That is, to find the neurons that are responsible for processes that are directly involved in conscious activities (3). An example of a process that would be highly correlated with consciousness is vision. Vision is used for recognition, a common process in our conscious lives. We use visual recognition to read, determine where to move, recognize familiar faces, and so on.

Work has been done to establish a biological account for the distinction between perception and awareness. While attempts to locate the NCCs responsible for this distinction have been done, further investigation is needed to map the differences. Some reports believe that the barrier lies in the complexity of the part of the brain where NCCs are thought to be (4). Others have found limitations in the kinds of subjects that can be tested on. Animals such as monkeys have been used because their brains are similar to human brains and because scientists can control their experiments by intentionally damaging certain parts of the brain to gain insight about the functioning of it. However, since animals cannot describe what they are experiencing, it is difficult to determine if the targeted brain area is affecting their motor visual processes or their experiential visual processes (3). There is also the possibility that NCCs are not static and that any neuron can take on the function of a NCC at any place (in the neocortex) at any time (3).

While NCC mapping is still in stages of infancy, certain areas of the brain that are thought to contribute most to consciousness have been identified. Research has found that in those areas of the brain, neuromodulating occurs, a process by which chemicals affect the speed of cortical neurons synapses. Neuromodulating requires more time than a regular synapse would take thus, some believe it is there that consciousness occurs (1). These approximately one second intervals account for the extra time it takes to think about and perceive the process that is occurring. It is also interesting to note that as a conscious task is repeated, the synaptic connections between the cortical neurons occur more easily, and in parallel, the task takes less concentration to do. This could suggest a biological account of the economy of consciousness: the more I do something, the easier it becomes, and the less concentration I must spend on it to do it. While this brings us a step closer to understanding how neurons work in the systems that seem to give rise to consciousness, there are still problems to deal with.

Above, we laid the foundations for the time gap it takes for thinking to occur, but we inferred that the time gap was somehow associated with consciousness, without finding a direct accounting of it. Similarly, any mapping of NCCs could explain which neurons make consciousness possible, but it would fail to explain how they do so. David Chalmers has criticized the NCC approach to finding consciousness because he believes that such an approach can only solve part of the puzzle. In looking at a process that is associated with consciousness, we are merely explaining a cognitive function. That function can be explained using a mechanistic model, but it fails to relate that model to conscious awareness (5). Koch and Crick have a theory that neural oscillations occurring at 40 hertz bind and integrate information in such a way that makes consciousness possible (6). However, this theory, while a good account of the binding of information, still fails to explain why the bound material is experienced as conscious experience (5).

Chalmers' puts forth a theory that since the traditional reductive method of explaining consciousness has failed to answer the hard questions, a non-reductive theory should be employed. There are several scientific findings that have required non-reductive methods of explanation. For example, when electromagnetic fields were first discovered, the language used to account for a theory of physics had to be expanded. He believes that if we take experience as a fundamental, we can accomplish more to account for consciousness, as it relates to the rest of the world (5). A set of psychophysical principles that would supplement physical principles would help to explain the consciousness in a way that would be shed more insight on it than current reductive theories do. Chalmers' principles of structural coherence, organizational invariance, and the double aspect theory of information would create a new definition of consciousness that could be expanded to a number of entities that previously would not be considered conscious.

His third principle of the double aspect theory of information suggests that information consists of two parts: information states and information space, in which the former is embedded in the latter (5). This would mean that information has two aspects: a physical and a phenomenal, or experiential. If we say that information has an experiential aspect, then the binding of information through 40-hertz oscillations in neurons could give an account of consciousness. However, this would also imply that a thermostat could have experience and consciousness at some very basic level (7).

Chalmers seems to be looking for a silver bullet that will explain consciousness immediately, without having to search for something new. While there is a certain allure to his theory, it seems to be too easy. While it would help account for the gap between NCC behavior and consciousness itself, it does not explain why information is experiential.

Whether or not we want to grant a thermostat consciousness is not an issue to be taken lightly. His hypothesis means that a computer, which has great capacity to process information, has consciousness on some level. Granted, that the human nervous system is more complex and processes more information than any computer to date, but it would seem that if one were complex enough, perhaps a supercomputer, it could have a consciousness equal to, or even superior to our own. Perhaps if it is true that information is experiential, then it could be the patterns and structures that give rise to consciousness. There may not be a missing or unmapped biological element we have not accounted for, but rather a physical pattern of information that gives rise to consciousness, by virtue of the pattern and not the substance. This, however, would seem to be a reductionist theory, if it were possible to reduce consciousness to a pattern of information. The difference between a reductionist approach to this possibility and a non-reductionist approach is the proof. Reductionists would require an account of how the pattern of information gives rise to consciousness while the non-reductionist would take this on faith.

I think that either is a distinct possibility, but I find myself more skeptical of the non-reductionist approach to this matter. While electromagnetic fields required a new vocabulary for physics, it is the kind of simplistic, 'take it as fundamental' thinking that reinforced the notion of a geocentric universe for so long (8). Furthermore, I am skeptical of Chalmers' jump between physical and experiential information. Such a jump requires further explanation and evidence to make it a strong and convincing theory.

I began this research as open to both reductionist and non-reductionist possibilities. However, I am more skeptical of the non-reductionist theory, despite the difficulties that the reductionist approaches have faced. I believe it is far too soon to discount the reductionist approach as being unable to bridge the gap between neural behavior and consciousness. Given what I have seen, I believe that further research into NCCs will reveal more about how consciousness is created by the brain.

References

1) Roth, Gerhard. "The Quest to Find Consciousness". Scientific American (2003).

2) William James on Serendip; a resource on William James' work, written by Eugene Taylor of Harvard University Medical School.

3) Crick, F. and Kock, C. "Some Thoughts on Consciousness and Neuroscience", The New Cognitive Neurosciences. Cambridge: MIT, 2000. pp 1285-1294.

4) Perception Without Awareness; a paper by Fred Dretske of NYU.

5) Chalmers, D.J. "Facing up to the Problem of Consciousness", Explaining Consciousness, The 'Hard Problem'. Cambridge: MIT, 1997. pp 9-30.

6) Crick, F. and Koch, C. "Toward a neurobiological theory of consciousness", Seminars in the Neurosciences (1990), 2, pp. 263-75.

7) Chalmers, D.J. "The Puzzle of Conscious Experience". Scientific American (2002).

8) Can Neurobiology Teach us Anything about Consciousness?; a paper against non-reductive theories of consciousness, by Patricia Smith Churchland of University of California, San Diego.


God on the brain
Name: Elizabeth
Date: 2005-02-24 00:13:35
Link to this Comment: 13200

<mytitle>
(1)

As a Unitarian Universalist, but more importantly as a human, I search to understand my place in the universe. Sometimes this is through looking at the vastness of the night sky, but usually, or at least on those days that are cloudy, the search is through religion; namely, the entity of God. People from time immemorial have had some sort of religious practice, whether it was sacrificial or if they had multiple gods, there has always been a sense of something larger than ourselves. However, if our lives can be described in one sense as the summation of all our sensory inputs and thoughts through the brain, then does that make a religion just another output of our minds?

In more recent years, scientists have started to take on this question and study it through neurobiology and the brain structure. Doctors and scientists looked at people with epilepsy, specifically temporal lobe epilepsy, for they are known to have deep religious experiences during the seizures. Dr. Vilayanur Ramachandran, who headed the experiments at the University of California at San Diego found that those with temporal lobe epilepsy, in comparison to normal patients, were more responsive to religious words and images (2). "Spiritual experiences are the inevitable outcome of brain wiring," said [Andrew] Newberg. "We believe that the human brain has been genetically wired to encourage religious beliefs" (3). Dr. Newberg and the late Dr. Eugene d'Aquili worked on tracing the parts of the brain dealing with religion through nuns and monks during prayer. They studied the gray matter of the brain by using a single positron emission computed tomography (SPECT), which allowed them to detect the areas of the brain that received more blood during the religious experience, where more blood usually equates more activity. Their results indicated that there was "increased activity in the frontal lobes, the attention area, and decreased activity in the posterior superior parietal lobe" (3). The frontal lobe activity should not surprise most people simply because it is the area that is commonly associated with the higher mental activities and specifically with humans.

However, the surprising result of this study was the decreased activity in the posterior superior parietal lobe, or what is called the orientation association area (OAA). This area of the brain, "which must constantly generate a clear, consistent awareness of the physical limits of the self in order for us to function," (3) may also allow humans to "transcend material existence and acknowledge and connect with a deeper, more spiritual part of ourselves perceived of as an absolute, universal reality that connects us to all that is" (4). Newberg and d'Aquili further hypothesized that the process of deafferentation, which is when a brain structure is somehow deprived of sensory input, may be responsible for the experience of a unitary state with a higher being or larger group (3).

Why would humans block certain signals in order to lose their sense of self in a highly competitive world? This really does not work in conjunction with evolution and survival of the fittest if we all feel a connectedness to each other. People do have to access this event through a ritual of some sort, namely prayer or meditation in this case, so that we all are not walking around in a state of connecting bliss. Perhaps it is some way that the brain has evolved to flood it with a euphoric feeling of floating in the web of others instead of rigidly controlling the self, something akin to a brain holiday. On the other hand, if "mystical prayer and sexual bliss use similar neural pathways," then the reasoning behind this process could have a basic function in the brain. (3) It is true that two of the most basic systems, the arousal and quiescent systems, are involved in religious activity (3). This explains why religion is so popular if the nerves that are excited are the same as those that are excited for sexual arousal. If it feels good, why stop doing it? Does that then make religion innate, or at least faith in something larger? If the source for our religious feelings lies within us in the brain, then does that necessarily mean that we are "believers" whether we want to be or not? I believe that the key here is the ritual of prayer or meditation. Without this key element to trigger the brain to feel a connectedness, which would be a conscious decision at an individual level, then the "faith" lies untouched. It is nice to believe that at some level, we can feel like we are in a greater group than just ourselves.

What does this mean for organized religion? Obviously, religion is a touchy subject for many people and these are highly controversial bits of information. Not being of an organized religion that takes a stand one way or the other in recognizing a god, I can see that finding a "God part" of the brain could cause trouble for many people. It could mean that the way they had conceived of God and what they had learned their whole lives was being repudiated. It reduces a whole belief system into a few nerves. On the other side, I think it is nice to know that "God" could be with each of us, all the time. Just because there is the capacity to believe in something does not mean that you do or that the something you can believe in is defined. There is a vast difference between a feeling of connection to something greater and a religion.

The other thing to keep in mind about these findings is that they may not even be the "God part" of the brain. It could just be that the part of the brain recognized as the "God part" has just been associated with religion because of the cultural construct that religion is good. The people tested by Newberg and d'Aquili were obviously happy with their religions, otherwise they would not have devoted their lives to it. Perhaps it was simply a happy part of the brain that has been identified, which religion happens to work into. Certainly if the neural pathways of the religious experience and the sexual experience are similar, then pleasure has something to do with it. Those with temporal lobe epilepsy may be able to describe their experiences in terms of sexual bliss as well as religious bliss. Neurotheology, as the field is now being called, is still quite new and the field is advancing every year. There may be more methods of evaluating processes in the brain coming soon, if we can ever truly understand all the complexities of the brain.

References

Card, Orson Scott. Xenocide. New York: Tor Books, 1991; page 335.

2)"'God spot' is found in the brain" Steve Connor, LA Times, 29 October 1997.

3)"Exploring the biology of religious experience" Rich Heffern, National Catholic Reporter.

Newberg, Andrew and Eugene d'Aquili. Why God Won't Go Away. New York: Ballantine Books, 2001; page 9.

Albright, Carol and James Ashbrook. Where God Lives in the Human Brain. Naperville, Illinois: Sourcebooks, 2001.

6)"Religion and the Brain" Religion and Ethics Newsweekly, 9 November 2001.


Connections Between Antidepressants, Drugs, and Se
Name: Christine
Date: 2005-02-25 20:17:55
Link to this Comment: 13228

<mytitle>
(1). Certain antidepressants, including a medication called Wellbutrin (chemical name: bupropion), have been known to cause seizures in some individuals. (5). When it comes to ingested medications, an important question to ask is, "Do the benefits of the medication outweigh the risk of a seizure?"

The system of chemical signaling between neurons or nerve cells in the brain gives clues as to why seizures occur. Neurotransmitters, or chemical signals, bind to a receptor on the neuron. These neurotransmitters alter the voltage of the cell, which changes the activity level of the neuron. (3). In order for the signal to be transmitted, enough signals must accumulate to bring the voltage of the neuron up to the "threshold of activation." Everyone has their own particular threshold of activation, which is a measure of how much stimulation it takes to make the neurons activate. (2). The threshold for each individual is determined by his or her genetic makeup, but the threshold can be changed by outside factors. Once the signal meets the particular threshold, a nerve impulse is initiated. (3). This nerve impulse travels down the axon, which is a nerve fiber that protrudes from the neuron and conducts signals to other neurons. This is also known as neuron firing. The space between the end of an axon on one neuron and the receptor on the next neuron is called the synapse. Presynaptic neurons send signals to postsynaptic neurons. (3).

The threshold of activation is similar to the seizure threshold, which is the minimum amount stimulation needed to cause a seizure. (1). Often due to genetics, some people have a low seizure threshold, so a minor stimulation may produce a seizure. Often, epileptic patients suffer from a low seizure threshold. In people with a more "normal" seizure threshold, the stimulation needs to be much more severe. (1). A person has a seizure because their neurons fire uncontrollably after being stimulated to a point at or above their seizure threshold. (1). A seizure is a change in behavior which is due to electrical activity in the brain. Some sufferers experience convulsions and unconsciousness, depending upon the type of seizure. Epilepsy is when the individual has recurrent seizures. (4).

Wellbutrin is an antidepressant which increases the levels of the neurotransmitters dopamine, serotonin, and norepinephrine. (5). Common antidepressants called SSRIs (selective serotonin reuptake inhibitors) concentrate on increasing serotonin at the synapse. Wellbutrin is different in that it is called a dopamine reuptake blocking compound because it primarily affects dopamine. (5). Reuptake is a process where neurotransmitters are released into the synapse, bind to the receptor on the receiving neuron so that it may activate, and then are sent back to the original neuron. (6). The antidepressant compounds bind to the receptor on the presynaptic neuron so that the neurotransmitter will not be transported back to the original nerve cell. Reuptake inhibitors allow the neurotransmitters to stay in the synapse longer so that they can be recognized by the postsynaptic receptor repeatedly and therefore increase their effects and levels in the synapse. (6). Since dopamine is a compound which is said to increase pleasure, it makes sense that a taking a dopamine reuptake blocking compound might make a person "feel better." (7). The problem is that if these signals are constantly firing because they are uninhibited, the seizure threshold can become lower, which can cause a seizure. (1).

The relationship between antidepressants and narcotics and their similar ability to cause seizures was surprising. Cocaine, for example, is also a dopamine reuptake blocking compound. (8). In fact, Wellbutrin has been used to gradually wean addicts off of cocaine. (10). Similarly, bupropion is also known as Zyban, which is a medication to help people stop smoking. (9). It would seem that Wellbutrin is similar to a low dosage of cocaine. Cocaine is a leading cause of seizures for the same reason that antidepressants can cause them. (9). The narcotic also raises serotonin and norepinephrine levels, though as with Wellbutrin, dopamine is the neurotransmitter that is primarily affected. (8). It makes sense logically to believe that many types of psychological medications would be comparable to narcotics because they often both have the general effect of making the user feel better. Still, it is notable that psychiatrists often don't explicitly state the similarity between narcotics and certain medications, which would be useful information in the case of Wellbutrin because it also has the some of the same adverse side effects as cocaine.

Wellbutrin is said to only cause seizures when there are complications, such as previous neurological defects, a medication overdose, or taking Wellbutrin with other drugs. (11). If we look at the basic causes of seizures, however, it is relatively easy to have a complication. The seizure threshold can be lowered by problems such as sleep deprivation, low-blood sugar levels, metabolism, anxiety, and exhaustion. (1). If combined with Wellbutrin, a seizure could result. Medication overdoses occur with Wellbutrin even when it is taken as prescribed because the brain metabolizes the medication too quickly in some people. The neurons begin firing at a rapid rate all at once which causes an overwhelming amount of electricity in the brain. SSRIs target serotonin more than dopamine, so the side effects are not the same and seizures are not as much of a risk. (11). SSRI side effects occur because this medication floods the brain with serotonin. The overabundance of serotonin interferes with the activity level of other neurotransmitters, including those which control hormones for sexual desire. (6). SSRIs are known to cause nausea, diarrhea, headache, sexual dysfunction, and dizziness. (11).

Deciding whether or not to take a medication because of its side effects is a choice that is made on an individual basis. In the case of seizures, the decision is even more important because a seizure is potentially life threatening, especially if the sufferer is driving a car at the time of the attack. When it comes to chemicals that affect the brain, patients should be informed that it is possible that compounds with similar effects might actually work in the same way. Rather than downplaying the similarity between narcotics and antidepressants, physicians should research the validity of this argument in order to help the patient to understand what it is that they are ingesting. Having experienced a seizure due to medication, I can say that for me, the benefits did not outweigh the side effects.


References

1) Behavior Modification for Epilepsy: raising the seizure threshold, website about the seizure threshold

2) Nervous System, explains the causes for seizures

3) Campbell, Neil A. and Reece, Jane. B. Biology. San Francisco: Benjamin Cummings, 2002.

4) Seizures and Epilepsy: Hope Through Research, details causes and types of seizures

5) Wellbutrin etc. (Bupropion), explains how Wellbutrin works

6) Selective serotonin reuptake inhibitor, uses of SSRIs

7) Dopamine, effects of dopamine on the brain

8) Cocaine, relationship between dopamine and cocaine

9) The Real Facts About Wellbutrin/Zyban a.k.a. Bupropion, harmful effects of Wellbutrin

10) Bupropion, uses for Wellbutrin

11) Wonderful Wellbutrin?, side effects from antidepressants


CSF Leaks and Spontaneous Intracranial Hypotension
Name: Flicka Mic
Date: 2005-02-26 14:50:19
Link to this Comment: 13236

<mytitle>
Spontaneous Intracranial Hypotension (SIH) is a condition where a patient gets postural headaches due to a leak of the Cerebrospinal Fluid (CSF) in the spinal membrane. (1) What happens is that the leak causes low CSF pressure within the nervous system, and thus causes a constant string of headaches to the patient. The problem with SIH is that it is very hard to diagnose and there is not a great deal of information on why it occurs. In 1995, a study showed that only one in fifty-thousand people in Minnesota had SIH. It also showed that SIH was more common in women than in men, and that the condition usually developed while the patient was between 40 and 60 years old. (5) When first researching this condition, my two main questions were: Why does it develop and can it be cured? In order to answer these questions, one must first examine how CSF runs through the body and the specific symptoms of SIH.

Cerebrospinal Fluid is formed in ventricles of the brain. It moves through the ventricles and leaves the brain at the base, underneath the cerebellum.(2) Then, the fluid moves into the spinal cord and the nerves, and finally returns to
the brain. Throughout this time, the CSF is moving through a membrane, called the dura that surrounds the brain and spinal cord. The condition of Intracranial Hypotension (IH) develops when a rupture occurs in the membrane. Thus, the CSF leaks out of the dura, causing a dislocation of the brain downward and "pressure on pain-sensitive structures."(5) IH can develop as a result of brain surgery, spinal surgery, or any major trauma to the head. (3) However, as in the case of SIH, the rupture can sometimes occur spontaneously. In other words, there is no known cause for the rip in the dura. Some doctors speculate that the spontaneous tear is due to the initial weakness of the dura, or a traumatic event that went undetected; however there is not a great deal of information on this subject.(5)

The principal symptom of Spontaneous CSF leaks is headaches. The headaches only occur when the patient is upright, and gradually disappear when the patient is lying down. In most cases, the headaches gradually increase from the moment the patient wakes up in the morning. However, in other cases the headaches are quick and severe. The acuteness of the headaches varies in each case, which affects how quickly the condition is diagnosed. Some of the related symptoms of SIH are a loss of hearing, tinnitus, vertigo, stiffness of the neck, nausea, and even vomiting.(5)

Since the primary symptom of SIH is constant and severe headaches, it is often misdiagnosed. Unfortunately, misdiagnosis can increase the painful treatment for other conditions that imitate SIH (such as Chiari malformation) as well as the possibility for
early treatment. In a study done by Dr. Wouter I. Schievink between 2001 and 2002, he found that 94% of patients who had SIH were initially misdiagnosed when they visited a doctor about their symptoms.(4) Some of the common treatments due to misdiagnosis included craniotomies (surgical incisions in the skull) and cerebral arteriographies (a procedure that uses an injection of dye and x-ray images to examine arteries in the brain). More than half the number of cases of SIH has been reported in the last decade.(5) Therefore, because SIH is so often misdiagnosed, it is not likely that there has been a drastic increase of the condition, but rather that more cases of it are being correctly diagnosed.

In some cases of SIH, the condition disappears as spontaneously as it appeared. Mild cases can be cured through a general increase in fluids, especially caffeine, and lots of rest. However, more serious cases will require a procedure called the epidural blood patch. This is a procedure where autologous blood is injected into the patient's lumbar spine. The blood travels through the spinal cord, finds the rupture in the dura, and clots the rupture. Success of the epidural blood patch in patients with IH can usually be determined immediately after the procedure. If it is not successful, the procedure can be repeated several times with a larger amount of blood injected (no more than 30 ml) and in many cases can lead to a permanent closing of the torn dura. (5)

However, in more severe cases of Spontaneous Intracranial Hypotension, the epidural blood patches that are injected into the lumbar spine are ineffective. At this point, an effort to locate the exact position of the rupture in the membrane can be made and then another epidural blood patch may be performed at that location.(5) This location-specific procedure is more effective than a regular epidural blood patch, and should cure the condition. However, there are a few cases where even this procedure is not successful. Further procedures to resolve the issue include an injection of fibrin glue into the specific location of the rupture and (in the most persistent cases) even surgery, both of which seem to cure the condition.(5)

In conclusion, Spontaneous Intracranial Hypotension is a very rare type of a Cerebrospinal Fluid leak, but unlike other types, it does not occur due to any specific traumatic event or surgical procedure in the nervous system. Although there is not much
information on the possible causes of SIH, it is suspected that an intrinsic weakness of the spinal membrane or an abnormality of the brain structure causes the rare condition. The symptoms of SIH are so small and so common, that it can often be misdiagnosed. Therefore, the condition of SIH, although thought to be very rare, is probably more likely than one might think. So how can someone prevent SIH? Is there anything a person cando to prevent the rupture of the dura? Unfortunately, there is no clear answer because very little information exists as to the primary cause of the tear. All one can really do is avoid brain surgery or any head trauma that could trigger the onset of regular IH. Hopefully, as more observations are gathered about Spontaneous Intracranial Hypotension, the causes of it will be identified and the ways to help prevent it will become more apparent.

References

1)Abstract of two cases by T.A. Rando and R.A. Fishman, general information on SIH

2)Discovery Health: CSF leak, general information on Cerebrospinal Fluid leaks

3)University of Maryland Medical Center, general information on Cerebrospinal Fluid leaks

4)Archives of Neurology, Abstract of a study on the Misdiagnosis of SIH

5)Medscape: Spontaneous CSF leaks, A review by Dr. Wouter I. Schievink


Causes of Depression: Internal or External?
Name: Anna Tomas
Date: 2005-02-28 23:41:05
Link to this Comment: 13320

<mytitle>
One of the most frustrating questions regarding the states of happiness and depression is whether internal or external factors are responsible for these psychological states. When we are depressed, is it because of the genetic build up of our brains? Or is it because of a negative environment? Based on the declaration of Emily Dickinson, "The Brain - is wider than the Sky/ -For - put them side by side /- The one the other will contain/ With ease - and You beside" insisting that brain = behavior and only internal factors can be responsible for depression. Can there be absolutes? Can we declare that either genetics or the environment is solely responsible for the psychological well being of a person? The lines between normalcy and clinical depression are constantly blurring and evolving. Further, depression has become one of the most significant mental conditions of our time. By the year 2020, it is predicted to be the second most debilitating condition, after heart disease (1). The increasing instances of depression, due to the changing standards for clinical depression, and the idea that brain = behavior have lead me to believe that there are no absolutes; that depression and happiness are caused by both internal and external factors. I will attempt to support this argument by examining evidence provided by The Science of Happiness: Unlocking the mysteries of mood by Stephen Braun, and the January 17 2005 edition of Time Magazine "The Science of Happiness".

Stephen Braun's research provides ample evidence to support Emily Dickinson. By studying antidepressants and their activities in the brain, he suggests that brain does equal behavior and that depression is caused by genetics instead of one's surroundings. Antidepressants, such as Prozac, are ultimately successful, although they can take up to a month to become effective (2). The reason for this time lapse in between administering these drugs and their effect is because these drugs stimulate the growth of dendrites in the brain, a process that can take several weeks. The growth of dendrites increases the flow of information between neurons, thus increasing the versatility of the brain and decreasing the chances of depression (2). Because neurons store information, they cannot be "renewed" because people would suffer from a constant memory loss (2). So "old" neurons continue to exist and "new" ones grow. The growth of these neurons allows the brain to send more information effectively, which in turn leads to more parts of the brain, including the pleasure centers, to be stimulated. Thus a person's behavior or mood can be altered by manipulating the way the brain functions. Braun also examines the work of Richard Davidson, neuroscientist of University of Wisconsin at Madison, who researched the importance of the front of the human brain: the prefrontal cortex. Based on his research the prefrontal cortex is largely responsible for our emotions "abstract reasoning, complex analysis, and foresight" (2). The prefrontal cortex is divided in two. The left half functions as a behavioral approach system. It forces the "outward" behavior of people (2). This is what encourages people to go forward in pursuit of happiness and survival. On the other hand, the right prefrontal cortex is the half that is responsible for inhibitory behavior. It is the right side that is in control of the "flight or fight" thought processes (2). This side of the prefrontal cortex that prevents us from running into oncoming traffic, or to react to stress. If the left side is more active, the person is viewed as happier, eager to learn and take advantage of opportunities. Whereas increased activity on the right side of the brain usually leads to a more introverted individual. According to Braun and Davidson, antidepressants are actually responsible for stimulating more electrical activity in the left prefrontal cortex as well as for the stimulation of neuron growth (2). Therefore, a person can have a more active left prefrontal cortex, making them less apt to be depressed, because of the genetic build up of his or her brain. According to this research of antidepressants and their effects, it is safe to assume that genetics are indeed responsible for depression. If the brain's activity can be manipulated by chemicals, and this manipulation results in the change of psychological state, then Emily Dickinson is right about the brain equaling behavior, and genetics are responsible for depression and happiness.

However, in a special edition of Time magazine from this past January 2005, an alternate argument was made. According to researcher David Lykken, people are actually in control of their psychological state "It's clear that we can change our own happiness levels widely up or down" (6). Psychologist Martin Seligman proposes that we are in control of reaching our ultimate happiness capacities by following these components: pleasure, engagement and meaning (7).. This means that we are in control of achieving happiness by pursuing personal pleasures, by engaging in relationships with those surrounding us, our activities and professions, and by applying our knowledge and skills to serve others (6). The Centers for Disease Control and Prevention support Seligman's ideas of pleasure, engagement and meaning leading to happiness. In a report titled "Marital Status and Health: United States, 1999-2002", it was proven that married couples are less likely to suffer from psychological disorders than are single people (5). Therefore individuals benefit psychologically from engaging in a relationship with another. A neuroscience professor from Stanford, Brian Knutson, researches our control over our happiness by using MRI. By studying the brain activity of people who were informed they would be winning money, he noticed activity in pleasure centers of the brain. The levels of activity depended on the amount of money won as a prize (4). His findings suggest that is the idea of feeling good that can induce brain activity and therefore happiness. If this is true, then situations in our environment can frequently induce happiness. For example, if we associate massages with feeling good, then the idea of receiving a massage will make the subject feel happy before actually having the massage. Clearly, Knutson's ideas were instigated by the work of Pavlov and his dogs (4). If we associate certain experiences and situations with being happy, and that in turn makes us happy, then we are indeed formed by our environments and experiences.

In conclusion, I believe that both internal and external factors affect psychological states. There are discrepancies in both arguments. For example, in researcher David Lykken's studies, although the majority of subjects supported the theory that genetics are responsible, 8% of the 4000 subjects reported that external factors (marriage, social status, money) effected their happiness. Despite being a small percentage, evidence that external factors are responsible exist. Further, there are those who take up to eight years to recover from the loss of a spouse (or the loss of a source of engagement) (6). On the other hand, there are those who do not become ultimately happier after winning the lottery (3). Somehow the end result of depression or happiness is achieved by a combination of environmental and genetic factors. Whether one can become depressed by the environment without inherent genetic factors has yet to be seen. More research must be done on depression and its causes not only for curiosity's sake, but for the sake of developing the "perfect" cure for depression. However the idea of the "perfect" antidepressant is another story and possibly another web paper.

Reference List:
1)Depression Learning Path , Major depression facts

2) Braun, Stephen. The Science of Happiness: Unlocking the mysteries of mood. John Wiley & Sons, Inc. New York. 2000.

3) Easterbrook, Gregg. "The Real Truth About Money." Time Magazine 17 January 2005.

4) Lemonick, Michael D. "The Biology of Joy." Time Magazine 17 January 2005.

5) Stein, Joel. "Is There a Hitch?" Time Magazine 17 January 2005.

6) Wallis, Claudia. "The New Science of Happiness." Time Magazine 17 January 2005

7)Reflective Happiness, About Happiness

Other Websites used for research:
http://www.thedoctorwillseeyounow.com/articles/behavior/depressn_5/

http://web.isp.cz/jcrane/IB/The_neurobiology_of_depression.pdf

http://www.nimh.nih.gov/publicat/depression.cfm#ptdep4

http://www.clinical-depression.co.uk/Depression_Information/facts.htm


Can Music Make you Smarter? Happier
Name: Georgia Gr
Date: 2005-03-02 14:06:06
Link to this Comment: 13343

<mytitle>
Different researchers performed a variety of studies (1)(2)(3)(4) where comparisons were made between the cognitive skill levels (what this means differs depending on the experiment, but some examples are IQ, language, social and spatial skills, and academic performance) of individuals before and then after music lessons. In all instances there was an observable, though not always dramatic, increase in cognitive skill level. For example, in a study performed by Dr. E. Glenn Schellenberg in Toronto, 144 six-year-old children were randomly separated into four groups and then evaluated for IQ and academic skills. For the duration of one year, the children either received singing lessons, piano lessons, drama lessons or no lessons at all outside normal school. When their IQ's and academic skills were reevaluated, the children in both kinds of music lessons demonstrated the greatest gains.(5) This appears to prove the Mozart Effect true, however, in similar experiments where the individuals being tested LISTENED to music rather than LEARNED it, no significant improvements were noted. This seems to imply that although none of the researchers were able to cite a specific aspect of music education that leads to the boost in intellect, LEARNING music requires mastering a number of skills that can contribute to overall intelligence. "For instance, musical training requires kids to pay attention for long periods, to read notation, to memorize extended passages, and to master fine-motor skills".(6) Therefore recent studies indicate that, contrary to popular opinion, it is learning music, rather than listening to it, that can lead to increases in intelligence.

That is not to say that listening to music does not have an effect on the brain, however. The majority of people have had some sort of emotional experience with music; that is, whether they were uplifted, saddened, excited or comforted, they have had an emotional response as the result of listening to music. In fact, recent experiments have shown that the region of the brain that is associated with food and sex is also stimulated when test subjects listen to music that they deem beautiful enough to give them 'chills'.(7) In other words, when an individual experiences a moment of euphoria, PET (positron emission tomography) scans show activity in the region of the brain associated with emotions. Music it seems, is capable of inducing such euphoric moments, or in other words is capable of triggering parts of the brain that cause emotions such as happiness.(8) This comes as no surprise to anyone who has ever been moved by a piece of music however, for the soothing and mood enhancing effects are easily felt. Perhaps it is this very phenomenon that is at the heart of the few remaining reports that supposedly show a link between listening to classical music and elevated intelligence. That is, the negative effects of stress on cognition are well documented, and music often has a soothing, brightening effect, which could counteract those negative effects. Therefore it would be possible to say that listening to music has a positive effect on cognition and IQ.

It seems then, that whichever method you choose to examine whether music influences the brain, the evidence points to music's having an impact on brain functioning. This leads to a number of other questions; for example, how a cultural phenomenon like music has come to have the same neurological effects as basic biological stimuli such as food and sex. Also, what does this imply about the nature of the brain (or the mind) in terms of how much of our cognitive ability is genetically determined, and how much is open to influence by internal as well as external factors. While recent studies may point us in the right direction regarding these and other important questions, there is still a lot of research to be done on the influences of music (and other factors such as meditation) on the brain.

Web References:
http://parenting-baby.com/Parenting-Baby-Music-Research/Music-Research.html

http://web.sfn.org/content/Publications/BrainBriefings/music_training_and_brain.htm

http://www.amc-music.com/musicmaking/thebrain.htm

http://www.educationthroughmusic.com/brainarticles.htm#Brain%20Alive

http://www.intelihealth.com/IH/ihtIH/WSIHW000/333/8014/334988.html

http://www.nature.com/cgi-taf/DynaPage.taf?file=/neuro/journal/v2/n4/full/nn0499_382.html

http://www.sciencedirect.com/science?_ob=ArticleURL&_aset=V-WA-A-W-C-MsSAYWA-UUA-U-AAAAZBDCYZ-AAUEWAYBYZ-EBZVBWBZC-C-U&_rdoc=4&_fmt=summary&_udi=B6V9F-45WYSNP-J&_coverDate=11%2F30%2F1994&_cdi=5897&_orig=search&_st=13&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=90bc5f1a3745ae7a84eb6eb82d49e673

http://www.sciencenews.org/articles/20040619/fob6.asp

http://www.thecurrentonline.com/news/2004/08/23/Opinions/Does-Music.Affect.Intelligence-704177.shtml?page=1

References

1)Society for NeuroScience, Brain Briefings page of SFN site

2)American Music Conference Research Page, A site dedicated to music and music education

3)The Current Online, University of Missouri-St. Louis Student Newspaper Online

4)Science News Online, Weekly newsmagazine covering research in all fields of science

5)The Current Online, University of Missouri-St. Louis Student Newspaper Online

6)Science News Online, Weekly newsmagazine covering research in all fields of science

7)Aetna Intelihealth, A subsidiary of Aetna Inc, a healthcare provider that works with Harvard Medical School to educate the public

8)Aetna Intelihealth, A subsidiary of Aetna Inc, a healthcare provider that works with Harvard Medical School to educate the public


Examining Homeopathy--1st paper for Neurobiology a
Name: Carly Frin
Date: 2005-03-10 23:01:57
Link to this Comment: 13450

<mytitle>

In the 19th century, Samuel Hahnemann of Leipzig, Germany found that quinine, a drug that caused symptoms of malaria when given to healthy people, actually could be used to treat malaria in people who had the disease. From that point on, small doses of drugs that produced the same symptoms of a certain disease were used to treat people infected with the disease.
(1) Such treatments were called homeopathic remedies. Remedies may be made from plant, mineral, or animal material, and sometimes chemical drugs. (4) The remedy is diluted with water and/or alcohol until just the essence of the remedy is left-- generally one part of the remedy to about 1,000,000,000,000 parts of water. (2) and (4)

There are three principles of homeopathy. They are:


1) Like cures like. (As in quinine being used to treat malaria.)


2) Minimal dose. (Remedy taken in dilute form.)


3) The single remedy. (One remedy used to treat all symptoms as one, which means symptoms do not usually reappear post-treatment.) (2)

Currently, homeopathy is "the second most widely used system of medicine in the world." (2) It is, however, a form of alternative medicine that is not given much attention in United States medical schools (1) though it has been growing in popularity over the past decade (2). Some physicians in Europe and Asia have been incorporating homeopathy into their treatments more frequently as they have come to recognize its benefits. (1)



Perhaps the reason homeopathy is not very popular is due to the fact that many people think it is just a placebo. However, homeopathy has been proven to work on individuals who are unconscious, infants, and even animals. Medical treatments that are similar to homeopathy include giving an allergy sufferer a small amount of the material she is allergic to, and vaccinations "where an impotent form of the virus is given to bolster the immune system against that particular virus." (2)



Homeopathy does not treat symptoms the way other forms of medicine do (for example, cough suppressants taken to "cure" a cough), because symptoms are the body's way of trying to bring itself back to full health. Homeopathy helps this process. In other forms of medicine, if a patient takes medication regularly, and then stops taking it, the symptoms will return because the medication she has been taking have been to suppress the symptoms, not to restore her to full health. A homeopathic remedy aims to restore a person to full health, thus, when she stops treatment eventually, the symptoms should not return. (3)



Homeopathy remains a controversial practice. Many doctors believe it is quackery, and there are groups and individuals who want to sue distributors of homeopathic remedies for false advertising and other crimes, and even to see homeopathic remedies banned. They believe there is insufficient evidence to support the effectiveness of these remedies. (8) Indeed, many studies have been done, but few have been able to prove any real difference in results between patients who were administered a placebo as opposed to a homeopathic remedy. (5) and (6)



Other questions and arguments over homeopathy are: [How] can such a tiny amount, to the extent of being unmeasurable, of anything actually have an effect of any kind? How can something that causes certain symptoms cure an illness that is responsible for these symptoms? Does a remedy need a thorough explanation or detailed evidence of how it works? Is it enough just to know that is does work, somehow? (7)



Those arguing for the benefit of homeopathy say that remedies are highly individualized in that they depend very much on the detailed specifics of each person and each aspect of their illness. They say as well that the kinds of experiments generally done to prove whether any non-homeopathic treatment works or not cannot be applied in the same way to homeopathy because a homeopath (a physician who administers homeopathic remedies) would try a different remedy if the first did not help the patient. (2) Also, there are other non-homeopathic remedies that work which have not been fully studied. (7)



I personally have used homeopathic remedies and know a doctor who advocates their use whole-heartedly. However, the questions above are ones that I myself have asked from the beginning. I tend to think that a remedy that is not harmful does not need thorough explanation if it is indeed working. Yet I do recognize that homeopathy must be more thoroughly examined if it is to become a more widely-accepted and widely-used treatment.



I am left with the following questions:


* How does homeopathy work to restore full health?


* To what extent does believing in any treatment, homeopathic or not, make the treatment work? (The placebo effect.)


* If it is so harmful to one's body to suppress symptoms as homeopaths or homeopathic advocates say, why are symptom-suppressing medications so widely used and accepted?


* What is health? Are we healthy when we want to be or believe ourselves to be healthy? How do our minds and/or brains serve to let us know that we are sick? Can we be sick without knowing itthat is, can our bodies be fighting a virus while our brain doesn't allow us to feel the effects of that fight?


* Do people who are more mentally fit (not sure how exactly to define this) get sick less? Is it possible that mental and emotional health dictate how often and to what extent we get sick more than physical health/fitness does?

References


1) encyclopedia.com, Search "homeopathy", Definition of Homeopathy.


2)abchomeopathy.com, All about homeopathy.


3) National Center for Homeopathy. How does homeopathy differ from conventional medicine?, One in a series of questions about homeopathy.


4) National Center for Homeopathy. What Are the Meds?), Another in a series of questions about homeopathy.


5) National Center for Complementary and Alternative Medicine, Q&A. Study results 1.


6) National Center for Complementary and Alternative Medicine, Q&A. Study results 2.


7) National Center for Complementary and Alternative Medicine, Q&A.


8) Homeopathy: The Ultimate Fake, Arguments against homeopathy by Stephen Barrett, M.D.


9) sciencedirect.com: The Faculty of Homeopathy., Patients' assessments of the effectiveness of homeopathic care in Norway: A prospective observational multicentre outcome study.


Ritalin Kids: A New Generation of Abuse
Name: Amelia Jor
Date: 2005-03-12 00:28:00
Link to this Comment: 13456

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The Sublime Experience
Name: Anna Katri
Date: 2005-03-21 13:28:26
Link to this Comment: 13758

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For starters, what is the sublime? Situations or locations, like Big Wave surfing, the Grand Canyon, finding out your pregnant, can be sublime in the sense that they provoke an extreme emotional reaction: exhilaration, overwhelming beauty, pain. The sublime, as a feeling or state of mind, differs. If there were a sublime spectrum, ranging from infinite to infinitismal, aesthetic experiences rank with little value besides the immediate. To be "stuck" in, or consumed by the sublime is an entirely different state of awareneness not in this universe, even though the physical state of being is in reality. Philosopher Edmund Burke specifically defines the sublime experience in his essay, "A Philosophical Enquiry into the Origin of Our Ideas of the Sublime and Beautiful," as the "strongest emotion" due to the element of terror. To be labeled a truly sublime experience, the presentation or object of circumstance must hinge on some modality of terror and pain. For Burke, the key word is astonishment, "that state of the soul, in which all its motions are suspended, with some degree of horror (1). Burke's definition relies heavily on the pain component because pain is stronger than pleasure. Human nature is to dwell on loss over the pleasure of gain. Even love, Burke argues, no matter how beautiful, is powerful enough to metamorphosize the mind and fully engross the senses, driving the body to do horrific things.

This definition of the sublime refers to a feeling or a state of mind characterized by internal discord rather than harmony, so what happens when the body encounters the opposite? Meditation often creates a sensation of oneness with the universe (8); the feeling of awe that accompanies revelation, even the sensation of weightlessness or floating in an epsom salt bath can play with the body's ability to perceive natural forces, such as gravity (9). Sublime experiences such as these are provoked by self-induced changes in stimuli, and not necessarily by external influences on the senses.

Thoreau describes boundaries between the self and nature, which when dissolved, help us to understand ourselves and our place in the world. I think the sublime experience lies somewhere in between the "intangible gap between consciousness and the material world" (2). . What if, when we enter the sublime, we are somehow caught in a zone between mental stratospheres? A sort of black hole in the brain. If the range of the sublime experience begins at infinite and extends to infinitismal, when we lose all sense of math and logic, are we somehow lost in the universe, vacillating between levels of strata, floating or vibrating in a space not yet defined in the brain? When the mind and body are unable to overcome a sublime experience, as Burke would define it, can it result in death? Is there on some level, something subliminal about being in a state of shock? Can a person be scared senseless?

What part of the brain is the sublime connected to? There are four different types of brain waves ranging from most activity to least activity: beta, alpha, theta, and delta. A beta brainwave state is characterized by an active mind, responsive to a task, whether in conversation with another person, or singing in a musical. The alpha state is has a slower frequency and tends to be a more relaxed state of mind. Theta waves are even slower than alpha waves, and indicate a deep state of mental relaxation, where the mind in a sense, detaches from the body's movements, and both can act independent of each other. Delta brainwaves have the slowest frequency and the highest amplitude on an EEG machine. Healthy delta brainwaves range from 1.5 cycles to 4 cycles per second, normal range is 2 to 3, but should you drop down to zero, the brain goes dead (3). When you fall asleep at night, you slowly descend from beta to alpha to theta to delta brainwave state. Although only one brainwave is predominant at a time, there are traces of the other three in the mix at any given moment.

The difference between brain waves is necessary in understanding two very different definitions of the sublime. I believe the sublime experience achieved during meditation takes place within the visceral part of the brain, the area where thoughts and ideas are born (8). The mind and body are only capable of achieving the level of astonishment Burke purports when actively, if not overly, stimulated by an object or through circumstance. In particular, the theta state is when the mind/brain is most disengaged, most open to mystical stimuli; whereas in beta state, the brain behaves with rapid-fire output, overly aroused by external stimuli, becoming unstable, and throwing the body into a state of anxiety and stress. In order to be scared senseless or utterly astonished and terrified by a sublime experience, I believe there must be an internal crossing over the mental threshold- to the extent that the brain is literally traumatized.

The theta state is the most elusive, mysterious and enlightening of all the brain wave states. Interestingly enough, when a person is depressed or has brain trauma, they tend to produce excessive theta brain waves. When a person begins to daydream, they are entering a theta brainwave state. In the theta state, the body is in a figurative, if not literal state of darkness. The theta state is one of the most difficult states to study as well because it is difficult to maintain (3), (4), (5). A sublime experience achieved through meditation is due to a self-induced change in brain wave frequency, where the individual actually concentrates intensely on settling down into a silent, yet fully awake state of awareness. When a meditator eclipses the highest strata of the human mind, they remain in possession of their own self-awareness and can control their detachedness from the external world. After a terrifying experience, it may be impossible for the brain, and thus, the body, to recover without the aid of neurotherapy or shock treatment. Although the theta state promotes the free flow of ideas, it is a state where "tasks become so automatic, you can mentally disengage from them", (3), (4), (5). Such as driving on the highway, your mind disengages from the task (although your eyes do not) and the brain permits itself to wander. When you have a "near death" experience, or are in a state of shock, I think your self plays in that black hole/area 51 of the mind, the place in between strata, where the body ceases to exist and the mind is in a trans-human state, unable to "see the light" and guide itself back to cognitive awareness.

In Burkian terms, in order to have a truly authentic sublime experience, the mind and body must be shocked or terrified into a state of total suspension. The problem is, very few people have such control over their mental state to recover from such a sublime experience. The brain is a very delicate, intricate system composed of neurons, axons, nerves, and lots of other stuff; but if you don't exercise your capacity to shift from different modes of sensing and interpreting the external and internal worlds in which you live, the brain cannot function in overwhelming situations. The key is to be aware, play with your brain, test the limits, because I think I've discovered there are none.

References

1) Edmund Burke Page, Everyone should read Burke's manifesto on the Sublime and the Beautiful, it's delightful and lovely in every way.

2) Thoreau Writings, The Naturalist Revolution! Make sure you read it Thoreaughly.


3) Brain Wave Functions, If you are totally clueless about the function of brain waves, explore these sites.

OR

4) Brain Waves and Biofeedback Science.

OR

5) Brain Waves (EEG).

6) Neurofeedback, What's the composition of thought? Check out this site to find out ways in which mapping the brain and understanding where imbalances occur can help you perform your absolute best.

7) Brain Sync, This site actually has links to other interesting articles regarding the mind/body connection. Wait! so there IS a connection after all!

8) Meditation Handbook, A really cool PDF about the mind, body, meditation, philosophy, and the divine experience with respect to many different religions. Totally enlightening to read.

9) Float Tanks, Ahhhh, the floating experience. After you read this, get in a tub or pool and pay attention to your body's response. Try to remember what it was like to float inside your mother's womb, experience the sublime!

10) Lucid Quest, These sites are kind of surreal, it's weird that there's a whole sect of people on a mission to achieve a sort of paranormal state of consciousness. Or wait, is that weird or scary? Maybe someday we'll shift our paranoia about guns, bombs, and war to the threat of mind terrorists. Make sure you read the disclaimer at the bottom of this site.

OR

11) Lucid Quest Link.


Ritalin Kids: A New Generation of Abuse
Name: Amelia Jor
Date: 2005-03-24 11:41:41
Link to this Comment: 13974

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Our parents view Ritalin as a way to calm their overactive children, which doctors and psychiatrists simply hand out when they are approached with a kid who is unable to maintain an extended attention span. It is considered a "quick fix" by many adults, not a potentially harmful, habit-forming drug. Parents are often unaware of the drug's dangers because a great deal of research has been ignored or kept quiet by pharmaceutical companies to promote sales (3). On the other hand, to college-aged and high school students it is just another drug that can be taken recreationally. Because it is prescribed, and not illegal, many people do not see an addiction to Ritalin as a "real" drug issue; many believe that one cannot become "addicted" to it because it comes from a doctor's office. It is harmful when abused, and people need to realize that.

The active ingredient in Ritalin, methlphenidate, was initially introduced to Switzerland and Germany in 1954. The drug, created by Leandro Panizzon in 1944, was named "Ritalin" after his wife Marguerite, whom he called Rita (1). When Ritalin was placed on the United States market in 1956, it was classified as a light psycho stimulant (or a central nervous system stimulant) in the same class as amphetamines; the pills were originally sold described as a new type of drug that "acts more carefully and longer than caffeine and amphetamines and does not involve habituation" (1).

Methlphenidate is prescribed for people with ADHD/ADD, and targets parts of the brain which are used for attentiveness and ability to follow directions. It is also supposed to aid in decreasing hyperactivity and aggressiveness (2). These psychotropic substances, which are primarily prescribed to children to help them with school and extracurricular activities, include such drugs as: Dexadrine, Dextrostat, Adderall, Desoxyn, Gradumet, and Cylert (3).

A person with ADHD should become calm and more focused after ingesting Ritalin, but adverse affects occur when those who do not have the disorder take it (4). In a normal person's dopamine (DA) pathway, a transmitting neuron releases the neurotransmitter dopamine, which then binds to dopamine receptors on the receiving neuron. This reception propagates an action potential in the receiving neuron. After this has occurred, the dopamine reuptake transporters (DATs) of the transmitting cell pump the dopamine back into the cell to be used again.

As the term "psycho stimulant" suggests, when the drug is taken, Ritalin initiates a series of chemical activities inside the user's Central Nervous System (one without ADHD). Once the bloodstream has picked up the amphetamines and they have been carried to the brain, the methylphenidate binds to the transporters used for the reuptake of dopamine into the presynaptic neurons. This binding blocks the reuptake of dopamine, causing its levels to rise within the synapses. When part of the brain called the nucleus accumbens contains large quantities of dopamine, a "high" sensation is emitted (5). The drug also reduces the "background" firing of neurons, allowing a clearer signal to be transmitted through the brain, decreasing distractions (6).

This mental high is very similar to that of cocaine, as are the adverse physical effects, which makes its abuse more easily understandable. The physical side effects include: increased heart rate, elevated blood pressure, dilated pupils, dry mouth, perspiration, appetite loss, insomnia, and nervousness (8). Longer term side effects can consist of strokes and seizures as well. There have also been several deaths attributed to Ritalin abuse (9). When Ritalin is prescribed, it is to be introduced to the body in slow, steady doses, which simulates the brain's natural dopamine production. Research has shown that addiction seems to occur when large, fast amounts of dopamine are rushed to the brain (7). Users have reported feelings of "superiority" as well as the ability to accomplish short term goals (8). The elevated concentration and emotional high that occurs when the drug is taken is the desired affect among abusers, and because of this "caffeine-like jolt" its abuse has become especially prevalent on high school and college campuses (4). One is five students at the University of Wisconsin admitted to taking Ritalin recreationally (without a prescription) (8). Students have said that it helps them get their work done more efficiently and keeps them awake when they need to study late at night. One of the primary issues surrounding Ritalin abuse is its availability. It is not a street drug that one has to purchase from a dealer in an alley at night. It could be found in one's own medicine cabinet; users often take the pills from siblings or friends who have prescriptions.

The most common ways Ritalin is abused is by taking the pills orally or crushing and snorting them. People have also been known to dissolve the tablets in water and then inject the fluid into themselves (7). Because of the rates of observed abuse, distribution of Ritalin is now strictly controlled in pharmacies, federal law prohibits doctors from including refills with prescriptions, and doctors are not even allowed to call in orders of it (4).

Because the brain is physically altered when Ritalin abuse has been prolonged, the user cannot consciously command him/herself to stop wanting the drug. The number of dopamine receptors in the brain does not return after a long period of time, causing the user to develop a tolerance. This makes it especially difficult to treat the individual, but the best way to do so is through drug counseling. Ritalin has been on the market long enough to conduct studies on its effects. Clearly, there are quite a few negative aspects of its prescription, so the question remains as to whether or not it should be taken off the market to prevent these effects and should patients on it should be treated for ADHD with psychotherapy alone?

Sources

1. http://translate.google.com/translate?hl=en&sl=fr&u=http://www.hypsos.ch/presse/novartis.htm&prev=/search%3Fq%3Dleandro%2Bpanizzon%2Britalin%26hl%3Den%26lr%3D

2. http://www.drspock.com/article/0,1510,4506,00.html

3. http://www.breggin.com/Ritalinprnews.html

4. http://www.freerepublic.com/forum/a39fca5b129fd.htm

5. http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/D/Drugs.html

6. http://www.udel.edu/chemo/teaching/CHEM465/SitesF02/Prop26b/Rit%20Page5.html

7. 7. http://www.nida.nih.gov/Infofax/ritalin.html

8. 8.http://flatrock.org.nz/topics/drugs/wanna_feel_good.htm

9. http://www.healthysource.com/add.html





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