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Full Name:  Emily Anne Lewis
Title:  Music, Happiness, and the Brain
Date:  2006-02-18 14:40:02
Message Id:  18190
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Have you ever come home after a long, hard day and turned on music to
de-stress? Do you associate music with different types of emotions (i.e. "I listen
to Green Day when I'm angry.")? Do you find it impossible to sit still while
listening to a certain type of music? Have you ever wondered why this happens?
So have I.

Ask most people to listen to music in a fast tempo and they will probably
say that it makes them feel happier, recall happy memories, and/or make them
want to dance. Give the same people slow music in a major key, and they will
say, most likely, that it makes them relax, that such music is good for meditation.
On the same line, slow music in a minor key makes people feel sad and possibly
recall sad memories. If most people are asked to listen to dissonant music in a
fast tempo, their most likely response will be fear.(1) To a certain degree,
dissonance is dependent on culture, but there is a theory that dissonance sounds
abrasive to listeners of any culture. Studies have demonstrated that babies as
young as four months old react negatively to dissonant music. (2)

For any piece of music, the way it is experienced by each listener is often
entirely different. One could hear Saint-Saens The Dying Swan (a slow piece for
solo cello) and literally picture the swan and it expires, while another could be
picturing the time she danced to the piece for a ballet class or the time she
played it for an audience. Either way, this piece is very moving and paints a
graphic picture for the listener. However, for the listener picturing the poor swan,
the reaction and memory associations would be very different than for the dancer
or the cellist.

It is a fact, as much as facts can exist, that the right kind music releases
endorphins. This causes relief of pain, and if there is no pain, happiness,
pleasure. (3) It has also been shown that music can induce sleep by convincing the
brain to release melatonin. This can be seen visibly in listeners to whom a
relaxing piece of music is being played. For many people, music that has an
intrinsic feeling of pleasure associated with it can cause a listener to become
motivated to do something. (4) These pieces have no other memories attached to
them, but, interestingly, when they are played, the areas of the brain that are
stimulated are those that are also stimulated by food, sex, and drugs. This could
imply that there is a connection between these things and the way that music is
processed by the brain.

What is it that makes music so intensely powerful? We may never really
know. As much as we can quantify the responses the brain produces when we
listen to music, we cannot yet explain why they happen.

1)Exploring the Musical Brain (2001) Scientific American

2)Biology and Music: Enhanced: Music of the Hemispheres

3)"Music on the Brain" (2000)

pleasurable responses to music correlate with activity in brain regions
implicated with reward and emotion." (2001)"

5) Jourdain, Robert. Music, The Brain, And Ecstasy : How Music Captures Our Imagination. Harper Paperbacks, 1998.

Full Name:  Nancy Evans
Title:  Phantom Limb: Hey, it beats a Parasitic Head.
Date:  2006-02-20 00:34:35
Message Id:  18215
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine glancing at your wristwatch for the time only to realize it is not there--the wrist, that is. Or hoisting yourself out of bed in the morning to discover no leg to support your weight. For amputees who experience feeling in their missing limbs, the sensations may not be as acute as described above; however, such accounts, for example the man who insists "I have a splinter in my toe" despite the absence of said toe, beg the question "what could be more eerie as pain emerging from a body part that does not exist" (2). But for the 50-80 percent of amputee victims who report 'phantom limbs', this unnerving (no pun intended) scenario is all too familiar. Symptoms range from itching to intense pressure and were aptly illustrated by one website as having the muscles of the leg twisted into a soft pretzel while simultaneously being struck by lightning and stabbed with a saber, all while floating above a lit candle (2).

A second, though no less eerie question, is inherently neurobiological: how does the brain function so as not to register the missing limb? Can it be that the brain creates a perception that is not true to reality? Or, in other words, "what is 'me' might not necessarily be" (4).

In order to begin to explain the phenomenon of phantom limbs, it is necessary to gain a general understanding of the organization of the brain as it relates to various parts of the body. As determined by V. Sussman in 1995, phantom limb sensations in the part of the brain called the sensory cortex (1). The sensory cortex bears a sort of map of the rest of the body, organized in a 'topographic' manner so that each part corresponds to a specific section of the body, thus earning the map the name "homunculus" or "little man" (1). Sensations originate in various body parts and make their way to the brain for recognition by the homunculus. Thus, according to Richard Sherman, a pinch on the left index finger tip stimulates a location on the homunculus representing the left index finger tip (2).

This is all well and good if every part of the body and its corresponding portion of the homunculus is in full operation. However, following an amputation the direct relationship between left index finger and homunculus is interrupted. As a direct result the brain changes, too. The brain has been noted to alter over a lifetime based upon various experiential factors. For example, blind Braille readers are found to have an increased corticol representation for their index fingers (3). Much the same 'plastic' effect of the brain is at work in the creation of phantom limb sensations.

According to Toni Ray in his article "Helping Phantom Limb Pain", when the body loses an appendage, the brain compensates for the signals it is no longer receiving by rewiring nerve impulses in the sensory cortex to travel down "previously untraveled pathways" (1). To think of this in terms of the 'little boxes' we discussed in class, we determined that very few inputs to the nervous system originate from sensory neurons (i.e. a pinch on the index finger). The lack of an index finger does not shut down the pathways from the finger to the brain, it merely prevents sensory neurons from doing their work. If signals are created inside the nervous system, as we know they are, they can still run along the same nerve paths to the homunculus and the resulting sensation may seem to originate in the missing finger. Thus, Sherman concludes, the brain has no way of actually knowing that the finger tip is not present (2).

This explanation via little boxes is supported by the monkey experiments performed by Merzenich. Merzenich found that by amputating the index finger of a monkey, within a month the cortical neurons could receive inputs from the back of the hand (4). These studies suggested that neurons within the homunculus rewired themselves to pathways that were only exposed once the original pathways were destroyed via the amputation of the finger. Therefore, the reorganization of the sensory cortex can be attributed as producing phantom limb sensations (4).

Treatments of phantom limbs are as intriguing as the condition itself. According to Sherman, success rates for curing phantom limbs have historically been dismal, with only about one percent of treated sufferers obtaining lasting relief for longer than one year (2). Different symptoms of phantom limbs can be treated individually. For instance, cramping limbs respond well to treatments for cramping in the remaining limb, even if the pain is not felt in that limb. Sufferers who report burning often respond well to increasing blood flow in the remaining limb. Both of these treatments suggest a rewiring of the homunculus so that treatment in one location--the remaining limb--corresponds to feelings in the phantom, or missing, limb.

Most interestingly, it seems the brain can be beaten at its own game. If the sensory cortex believes, due to inputs, that the limb exists some treatments bank on the notion that it can be fooled visually in quite the same way. Using a method called the Mirror Virtual Reality Box, the missing limb is visually simulated using mirrors in order to give the appearance of the phantom limb realized. Oftentimes, participants report a lessening of the tension and pain as if they are actually moving and stretching the missing appendage (3).

Phantom limb sensations provide the unique experience in which the brain might be able to conceptualize its own deception. Which is, to say the least, a disarming possibility.

Full Name:  Nancy Evans
Title:  Phantom Limb: Hey, it beats a Parasitic Head.
Date:  2006-02-20 00:36:19
Message Id:  18216
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine glancing at your wristwatch for the time only to realize it is not there--the wrist, that is. Or hoisting yourself out of bed in the morning to discover no leg to support your weight. For amputees who experience feeling in their missing limbs, the sensations may not be as acute as described above; however, such accounts, for example the man who insists "I have a splinter in my toe" despite the absence of said toe, beg the question "what could be more eerie as pain emerging from a body part that does not exist" (2). But for the 50-80 percent of amputee victims who report 'phantom limbs', this unnerving (no pun intended) scenario is all too familiar. Symptoms range from itching to intense pressure and were aptly illustrated by one website as having the muscles of the leg twisted into a soft pretzel while simultaneously being struck by lightning and stabbed with a saber, all while floating above a lit candle (2).

A second, though no less eerie question, is inherently neurobiological: how does the brain function so as not to register the missing limb? Can it be that the brain creates a perception that is not true to reality? Or, in other words, "what is 'me' might not necessarily be" (4).

In order to begin to explain the phenomenon of phantom limbs, it is necessary to gain a general understanding of the organization of the brain as it relates to various parts of the body. As determined by V. Sussman in 1995, phantom limb sensations in the part of the brain called the sensory cortex (1). The sensory cortex bears a sort of map of the rest of the body, organized in a 'topographic' manner so that each part corresponds to a specific section of the body, thus earning the map the name "homunculus" or "little man" (1). Sensations originate in various body parts and make their way to the brain for recognition by the homunculus. Thus, according to Richard Sherman, a pinch on the left index finger tip stimulates a location on the homunculus representing the left index finger tip (2).

This is all well and good if every part of the body and its corresponding portion of the homunculus is in full operation. However, following an amputation the direct relationship between left index finger and homunculus is interrupted. As a direct result the brain changes, too. The brain has been noted to alter over a lifetime based upon various experiential factors. For example, blind Braille readers are found to have an increased corticol representation for their index fingers (3). Much the same 'plastic' effect of the brain is at work in the creation of phantom limb sensations.

According to Toni Ray in his article "Helping Phantom Limb Pain", when the body loses an appendage, the brain compensates for the signals it is no longer receiving by rewiring nerve impulses in the sensory cortex to travel down "previously untraveled pathways" (1). To think of this in terms of the 'little boxes' we discussed in class, we determined that very few inputs to the nervous system originate from sensory neurons (i.e. a pinch on the index finger). The lack of an index finger does not shut down the pathways from the finger to the brain, it merely prevents sensory neurons from doing their work. If signals are created inside the nervous system, as we know they are, they can still run along the same nerve paths to the homunculus and the resulting sensation may seem to originate in the missing finger. Thus, Sherman concludes, the brain has no way of actually knowing that the finger tip is not present (2).

This explanation via little boxes is supported by the monkey experiments performed by Merzenich. Merzenich found that by amputating the index finger of a monkey, within a month the cortical neurons could receive inputs from the back of the hand (4). These studies suggested that neurons within the homunculus rewired themselves to pathways that were only exposed once the original pathways were destroyed via the amputation of the finger. Therefore, the reorganization of the sensory cortex can be attributed as producing phantom limb sensations (4).

Treatments of phantom limbs are as intriguing as the condition itself. According to Sherman, success rates for curing phantom limbs have historically been dismal, with only about one percent of treated sufferers obtaining lasting relief for longer than one year (2). Different symptoms of phantom limbs can be treated individually. For instance, cramping limbs respond well to treatments for cramping in the remaining limb, even if the pain is not felt in that limb. Sufferers who report burning often respond well to increasing blood flow in the remaining limb. Both of these treatments suggest a rewiring of the homunculus so that treatment in one location--the remaining limb--corresponds to feelings in the phantom, or missing, limb.

Most interestingly, it seems the brain can be beaten at its own game. If the sensory cortex believes, due to inputs, that the limb exists some treatments bank on the notion that it can be fooled visually in quite the same way. Using a method called the Mirror Virtual Reality Box, the missing limb is visually simulated using mirrors in order to give the appearance of the phantom limb realized. Oftentimes, participants report a lessening of the tension and pain as if they are actually moving and stretching the missing appendage (3).

Phantom limb sensations provide the unique experience in which the brain might be able to conceptualize its own deception. Which is, to say the least, a disarming possibility.

1)Phantom Limb Pain



Use 4)Phantom Limb Disorder

Full Name:  Courtney Moore
Title:  Mood Foods
Date:  2006-02-20 10:50:58
Message Id:  18222
Paper Text:
<mytitle> Biology 202
2006 First Web Paper
On Serendip

The latest national epidemic can't be cured with antibodies or prevented with immunization-it's depression, and it's sweeping the country. The National Institute of Mental Health estimates that nearly ten percent of the country suffers depression each year (8), and predicts further increases in the near future. The causes of depression are unclear at best and certainly highly controversial, but the latest technology invariably links mental illness with neurochemical levels. Neurotransmitters such as serotonin, norepinephrine, and dopamine are chemical messengers in the brain that affect emotions, behavior, and thought, and are therefore immediately associated with depressive disorders (9). In response to this information the medical world has responded with a host of pharmaceutical treatments designed to affect neurochemical levels with the ultimate hope of restoring a "normal" balance. However, these chemical treatments are often even more controversial than the dysfunction they are purported to treat, causing a range of detrimental side effects while exhibiting questionable efficacy: "anti-depressant medications, such as Prozac, are used to mimic or interfere with our natural biochemical processes, but there are problems with these. Individuals respond very differently to the exact same medication, so finding the right one is often by trial-and-error. Also, because they are synthetic as opposed to natural chemicals, these medications have a variety of side effects associated with them," potentially creating problems even more threatening than the initial complaints (4). In light of this, certain groups of health care professionals emphasize the plenitude of chemicals we consume or to which we are exposed on a daily basis, which may significantly affect neurochemistry. Natural chemicals found in food products, for example, may alter neurotransmitters in such a way that depression is either caused or relieved. These "mood foods" may therefore be considered one possible treatment for depressive disorders.

To explore depression one must explore the very notion of the brain, and the connection between the brain and nutritional factors is a central contribution to brain activity. "The brain is basically a chemical factory that constantly produces dozens of neurotransmitters, such as serotonin and dopamine, which act as messengers to start, continue or stop biochemical processes" (4). The nutrients garnered from food intake are the building blocks for these processes, thus explaining the link between food and mood. Complex carbohydrates and nutrients such as folate, magnesium, niacin, selenium, and tryptophan are particularly influential on brain processes, and thus may be used to decrease symptoms of depression (7). For example, many of the B-vitamins are associated with brain functioning, such as vitamin B6, which is vital in the formation of many neurotransmitters. High levels of vitamin B6 occur in cauliflower, watercress, spinach, bananas, okra, onions, broccoli, squash, kale, kohlrabi, Brussels sprouts, peas and radishes, and a deficiency of vitamin B6 often results in agitation, irritability, depression, and impaired intellectual function (6). Zinc may actually function as a brain neurotransmitter, hence low levels of zinc may result in irritability, anger, poor memory, reduced intellectual function, impaired immune function, and an inability to deal with stress. Similarly, copper is involved in the process of converting dopamine to norephinephrine, and an excess of this nutrient can lead to over stimulation and ultimately depression.

Essential fatty acids (EFAs) are critical in brain development and nerve transmission, and imbalances of EFAs can hence lead to depression, aggression, or a number of additional extreme feelings or behaviors (4). It is thought that they affect fats in the brain, perhaps by making membranes more resilient and easing the flow of neurotransmitters (6), which would involve affect depressive disorders. Fatty acids can be found in avocados, ground flax seeds, raw nuts and seeds, almond or peanut butter, soy nuts, dark green veggies, deep-water fish, extra virgin olive oil, flax seed oil, and other pure properly processed oils. The Pfeiffer Treatment Center, which specializes in nutritional therapy for depressive disorders, has observed that most victims of depression fall into one of five biochemical classes: high histamine, low histamine, pyroluria, high copper, and toxic overload. Using food-based treatments, and cater their treatments based on this sort of diagnostic. The Treatment Center performed an outcome study of 200 depressive patients: 92% reported improvement, with 60% reporting major improvement and 32% reporting partial improvement. Additionally, after beginning nutritional therapy roughly two-thirds of the Pfeiffer patients reported that their antidepressant medications were no longer necessary (4).

Depression has additionally been associated with a high intake of caffeine, but there is some question as to whether caffeine consumption incites depression or depressed individuals tend to turn to caffeine to boost their mood (3). Refined sugar is also said to aggravate depression, but it is difficult to ascertain what sugars can be constituted as healthy and necessary, and what sugars ought to be avoided. While the combination of caffeine and refined sugar is purported to be even worse for depression than either substance consumed alone, the same dilemmas apply to this assumption.

Some professionals offer a "psycho-nutritional model" suggesting that depression and other mood disorders are diseases of energy production (5), linking depression to hypoglycemia and other sugar-related disorders. Hypoglycemia, while rarely recognized as a medical "illness," is characterized by unstable blood sugar levels, which feed the brain inadequately and consequently cause excess stress hormones to flood the body (5). This model would indicate depression as a nutritional disorder, instigated by excess or deficient blood sugar levels. Most cells require about 2 million molecules of energy (ATP) per second to fuel biochemical reactions inside the cell, and this energy is entirely derived from glucose in our food. In the absence of this energy, the brain cannot synthesize neurotransmitters such as serotonin, norepinephrine, or dopamine that normally bring about feelings of happiness and relaxation (5). Therefore blood sugar levels would seem to have a direct and vital impact on mood and mental health, and nutrition cannot be ignored in the battle against depression.

Depression exists as an enigma-it stems from a range of causes and manifests in a variety of symptoms. There are scores of treatments yet, as in the case of most mental "illnesses," no single and reliable "cure." Pharmaceutical medications attract many sufferers with the appeal of a simple and successful treatment, but in truth these treatments are fickle and fallible, and may even be dangerous to the patient. Nutritional therapy therefore offers an alterative method of understanding and treating depression, providing a more holistic view of the patient and therefore catering to both the physical brain and the mental self.

1) "Depression a Nutritional Disorder," , posted by Jurriaan Plesman

2)"Dealing with the Depths of Depression," , By Liora Nordenberg

3)Holistic health remedies, Information on treating depression holistically

4)"Nutrients and Depression: Food for Your Mood" , by Constantine Bitsas, Executive Director Health Research Institute and Pfeiffer Treatment Center

5) "Depression a Nutritional Disorder" , By Jurriaan Plesman

6) "'Mangia, Mangia!' -- Certain Foods Fight Depression,", Harvard University study: posted March 25, 2005

7) "Online holistic health advice" , Food remedies for depression

8) National Institute of Mental Health on depression

9) Medical Terminology , Information on neurotransmitters

Full Name:  Perrin Braun
Title:  Two Heads Are Better Than...?
Date:  2006-02-20 11:26:41
Message Id:  18223
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

One would think that the Oprah Winfrey Show would be an unlikely venue to explore issues of neurobiology, but one particular episode that featured "medical miracles" caught my attention. The show described in great detail a thirteen-hour operation in which Egyptian doctors successfully performed a revolutionary procedure on an infant who suffered from one of the rarest forms of birth defects. Manar Maged was treated for craniopagus parasiticus—meaning that she had a conjoined twin that was connected to her at the upper left side of her skull, sharing an integral blood vessel. This type of defect occurs when an embryo begins the process of splitting into twins, but fails to complete the splitting process when one of the twins fails to fully develop in-utero. The weight of the extra head was preventing Manar from being able to freely move, in addition to creating problems with blood circulation.

However, Manar's twin had never developed a body below her neck and was therefore not able to survive independently of Manar, although the twin was still able to smile, blink, and exhibit some reflexes. In order to separate Manar's 'parasitic head,' the surgical team carefully separated her brain from that of the conjoined twin and disconnected the blood flow to the extra head. A similar surgery was performed in the Dominican Republic, in which a second conjoined twin failed to develop a body, but the operation ended in the deaths of both twins.

There are several issues of both science and morality which arise from the case of the parasitic twin. Although the twin wasn't able to sustain independent life, she was certainly cognizant of her surroundings and exhibit 'human' emotions. Footage from the show even shows the conjoined twin to be sucking on a pacifier while Manar's attention was focused elsewhere. There was absolutely no uncertainty that Manar would have died if her twin had not been removed, but Egyptian religious authorities have argued that the twin was indeed a distinct human being and therefore had its own separate soul. Following the burial of the head, the Maged family named the second twin Islaam in order to grant her dignity and distinguish the twin as a separate human life, but some people have argued that killing the twin, despite the fact that the operation was intended to save Manar's life, was problematic in that doctors were toying with fate. In this sense, this issue is akin to that of abortion, which poses uncertainties regarding the definition of what it means to be living. The parasitic twin was certainly conscious of its surroundings and exhibited behavior that resulted from external stimuli. She was most definitely aware of her environment, making her intentional death even more problematic.

Another problematic subject that arises involves the brain = behavior debate. In the case of the Maged twins, the two children shared the left side of the brain, while the right side of Manar's brain was joined with the right side of her twin. From one perspective, it can be said that since our existence is essentially defined by the physicality of our brain, the twin was parasitic twin was indeed functional in the sense that it contained the neurons that are necessary to exhibit reflexes and facial expressions. Yet, the twin had no body below the neck and therefore had no complete nervous system of its own. If the brain is entirely dependant on the nervous system and the brain = behavior, the subject of whether or not the twin could be described as a separate human entity is in question.

If we can define behavior as having reflexes and possessing a higher consciousness, the twin does exhibit some form of behavior, but where would her sense of self be? Since the conjoined twin did not have a body, one might assume that her I-function might have been located in her brain. However, this assumption becomes a problem when you take into account that the twins shared internal organs, in addition to a part of the brain. Might it be possible that the twins shared an I-function and they were therefore co-dependant on each other in terms of their identity? To date, Manar is thriving and doctors are still monitoring her progress to see whether or not her brain has been damaged by the separation. She is able to move her limbs with ease and her brain has regained activity. Since her conjoined twin was removed in infancy, she will not remember ever having an extra head and will develop into her own I-function as she gains more cognition of her surroundings. What remains to be seen, is how Manar's conception of her self will progress as she grows—if she will think of herself in terms of her dead twin or as a completely independent life.

Works Cited

"Baby stable after second head removed." 21 Feb. 2005. Reuters Limited.
10 Feb. 2006. .

"The Two-Headed Baby Miracle." The Oprah Winfrey Show. ABC. 19 May 2005.

Full Name:  Claude Heffron
Title:  The Correlation Between Death Row Inmates and Schizophrenia
Date:  2006-02-20 13:31:35
Message Id:  18226
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Since I was very young and began to hear talk of the death penalty, I always intuitively believed that most people who commit crimes that are punishable by death are not normally functioning people. Scientific research supports my early belief that there is some kind of link between violent criminal behavior and mental illness. Of mental illnesses, paranoid schizophrenia seems to be one of the most prevalent among death row inmates. Schizophrenia influences the features of the brain, which causes schizophrenics to behave in ways that are seen as deviant by the rest of the population. While many researchers maintain that there is no connection at all between violence and schizophrenia, they often concede that schizophrenic patients are more likely to abuse alcohol and drugs, which often contributes to violent behavior (10)National Institute of Mental Health,).

Schizophrenia has been labeled one of the ten most debilitating diseases by the World Health Organization (12)Amnesty International). The 1% of adults who suffer from schizophrenia may experience "positive symptoms" such as hallucinations, delusions, thought disorders, or disorders of movement; "negative symptoms" like speaking infrequently, an inability to sustain activities, or a lack of pleasure; and "cognitive symptoms" including short attention spans, poor executive functioning, and difficulty with memory (10)National Instititute of Mental Health).

An Australian study on schizophrenia declares that schizophrenics are three to five times more likely to commit violent crimes than non-schizophrenics. In contrast, another study over a thirteen year period reveals that fewer than .2 percent of schizophrenics committed murder (9)Schizophrenia Daily News Blog). This evidence shows a correlation between death row inmates and schizophrenia, but it cannot be assumed that schizophrenia necessarily causes people to exhibit criminal behavior.

Causes of schizophrenia are attributed mainly to genetics, but environmental influences are also factors in the development of this disorder (10)National Instititute of Mental Health). So what exactly makes schizophrenics different? The National Institute of Mental Health proclaims that imbalances in neurotransmitters, specifically dopamine and glutamate are observable in schizophrenics (14)Schizophrenia is a Brain Disease). People with schizophrenia have distinctly different features in their brains when compared to non-schizophrenics. For one thing, they have 25% less gray matter, when measured in volume, than non-schizophrenics in the frontal and temporal lobes of the brain. According to certain studies, schizophrenics also have enlarged amygdalas and enlarged lateral ventricles (5)Schizophrenia). In a study at King's College of London, researchers found that the difference in brain size that is evident in schizophrenic patients was even more pronounced in those schizophrenics with a history of violent behavior (1)Brain Info).

Given what is known about the differences in the brains of schizophrenic patients, it is possible to hypothesize that features of the brain could contribute to the violent criminal behavior that is occasionally demonstrated by schizophrenics. Various methods, such as CAT scans and MRI imaging, show that there is a decreased frontal lobe size in schizophrenic patients. This can certainly explain why schizophrenics have difficulty focusing and difficulty with memory. The frontal lobe also has numerous effects on personality, and deficiencies in it could potentially result in abnormal behaviors such as irritability or aggressive acts (13)Psychopathology of Frontal Lobe Syndromes), including violent criminal acts.

One notable effect of smaller temporal lobes in schizophrenics is the inability to classify things. Malfunctioning temporal lobes can lead to memory, mood, and drive problems (14) Schizophrenia is a Brain Disease ). Furthermore, it is possible that schizophrenics' ineptitude with classification could make understanding the difference between "right" and "wrong" or legal and illegal very challenging.

Lateral ventricles distribute cerebral spinal fluid throughout the brain, distributing nutrients, ridding the brain of wastes, and cushioning the brain (2) Brain and Behavior: Lecture 2). The reason that schizophrenics have enlarged lateral ventricles, and the effects of this feature are largely unknown, but as with all parts of the brain this region is very likely to effect behavior.

The New York Academy of Sciences theorizes that the unusually small size of the amygdala in schizophrenic patients may help explain their disorder (11)New York Academy of Sciences). They theorize that this characteristic of the amygdala may lead to fear and anxiety, potentially causing paranoid behavior. Another variation in the limbic system is a high concentration of both D3 and D4 (dopamine) receptors that could be a cause of schizophrenics' inability to inhibit and express emotions (4)Serendip).

People with mental illnesses are much more likely to use or abuse alcohol or drugs. In fact, as much as 50% of the mentally ill population suffers from a substance abuse problem (5)Schizophrenia). There are several possible reasons why schizophrenics are likely to end up abusing substances. Some use alcohol or drugs to reduce anxiety and fear. Another explanation is that social stigmatization can force the mentally ill into economic situations that put them in frequent contact with substance abusers.

The link between schizophrenia and violence is not universally agreed upon. Some scientists do not believe that the mentally ill are any more likely to commit violent crimes than the general population. Others have found much anecdotal and statistical evidence indicates that a link between mental illness and criminal behavior does exist.

Schizophrenia may be the most dominant in the news, but people with all different types of mental illness and brain trauma often end up on death row. Dr. Dorothy Lewis of New York University did a study of juvenile convicts and found that of 14, all 14 had experienced brain trauma, 12 had been abused by their parents, and five had been sodomized by relatives (6)Death Penalty Info). ACLU reports that since 1983, at least 60 mentally ill people have been executed, although this most likely reflects serious underreporting as quite a number of mentally ill prisoners do not disclose this information (7)American Civil Liberties Union).

A good example of anecdotal evidence indicating a link between schizophrenia and violence is the case of James Blake Colburn. Colburn was executed in 2003 in Texas. A paranoid schizophrenic who also suffered from post-traumatic stress disorder, James Colburn had a long history as a drug user and had attempted suicide several times. He seems to have been having a hallucination when he claimed in court to have heard voices telling him that the way for him to get back into prison was to murder someone. Colburn was sedated for his trial, convicted, and sentenced to death (12)Amnesty International).

Assuming that brain and behavior directly influence one another, it is inhumane to execute mentally ill criminals. People with brains that are far different from those of the majority of the population can be expected to exhibit very different behaviors, including the ability and desire to commit violent crimes. The National Alliance for the Mentally Ill states that "the death penalty is never appropriate for a defendant suffering from schizophrenia or other serious brain disorders" (12)Amnesty International). The American Psychological Association also actively lobbies against the death penalty on the basis that it is unfairly applied to the mentally ill (8)American Psychological Association). People who cannot categorize things, such as right and wrong, experience delusions and hallucinations that tell them to murder, or people that have difficulty inhibiting their emotions, abuse substances as a result of mental illnesses, and are paranoid cannot be held to the same standard of responsibility as the rest of population. On this basis, it is unjust to apply the death penalty to the mentally ill.

Works Cited

1) Barkataki, I., V. Kumari, M. Das, P. Taylor, and T. Sharma. "Volumetric Structural Brain Abnormalities in Men with Schizophrenia or Antisocial Personality Disorder." Brain Info. 6 Feb. 2006. Institute of Psychiatry, King's College London. 15 Feb. 2006 .

2) Christoff, Kalina. "Brain Structure and Function I." Brain and Behavior: Lecture 2. 31 Jan. 2005. Stanford University, Department of Psychology. 15 Feb. 2006 .

3)Claxton, Nathan S., Shannon H. Neaves, and Michael W. Davidson. "Rat Brain Tissue Sections: Lateral Ventricles." Olympus FloView Resource Center: Confocal Gallery. 2006. Florida State University. 15 Feb. 2006 .

4) Frederickson, Anne. "The Dopamine Hypothesis of Schizophrenia." Serendip. 1998. Bryn Maw College. 15 Feb. 2006 .

5) Hatfield, Agnes B. "Dual Diagnosis: Substance Abuse and Mental Illness." 1993. 15 Feb. 2006 .

6) Mansnerus, Laura. "Damaged Brains and the Death Penalty." Death Penalty Info. 21 July 2001. Death Penalty Information Center. 15 Feb. 2006 .

7)"Mental Illness and the Death Penalty in the United States." American Civil Liberties Union. 31 Jan. 2005. 15 Feb. 2006 .

8) "Resolution on the Death Penalty in the United States." APA. 2001. American
Psychological Association. .

9)"Schizophrenia Daily News Blog." Schizophrenia Daily News Blog: Crime and Schizophrenia. 27 Apr. 2005. 15 Feb. 2006 .

10) "Schizophrenia." NIMH: Schizophrenia. 19 Oct. 2005. National Institute of Mental Health. 15 Feb. 2006 .

11)"The Amygdala: The Mind's "Emotional Engine" Focus of 2002 Conference Conference Set for March 24-26 in Galveston, Texas." The Amaygdala: The Mind's "Emotional Engine" 24 Mar. 2002. New York Academy of Sciences. 15 Feb. 2006

12) The Execution of Mentally Offenders: Summary Report." USA: The execution of mentally offenders- Summary Report. 2006. Amnesty International. 15 Feb. 2006

13) Thimble, Michael H. "Psychopathology of Frontal Lobe Syndromes." Psychopathology of Frontal Lobe Syndromes. Sept. 1990. 15 Feb. 2006 .

14) Torrey, E. Fuller. "Schizophrenia is a Disease of the Brain." is a Brain Disease. 15 Feb. 2006 .

Full Name:  Danielle Marck
Title:  Finding the Perfect Mate: Male Pheromones and Female Attraction
Date:  2006-02-20 14:27:57
Message Id:  18227
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The process of finding a mate is a series of conscious and unconscious determinations made by the brain and body of the organisms seeking to reproduce. While men and women both emit and are affected by pheromones, females unknowingly respond to these chemical signals when searching for a partner. Most females swoon over the looks of handsome men, with defined muscle and beautiful symmetrical facial features, but fail to realize that attraction does not solely revolve around physical attributes: "it's not how you look on the outside but what's on the inside that counts". Perhaps this statement holds a scientific truth.

While looks might appear as the most important factor at the start of any relationship, what drives strong emotional feelings are a series of chemical signals being emitted by the male. These chemical signals, or pheromones, interact with specific sites in female nostrils to cause intense emotional feelings. These sites include a series of vemeronasal organs (VNOs) that process pheromone signals from men and connect directly to a part of the brain that manages basic drives and emotions. 1) Smell: The Forgotten Sense The pheromones act as emotional stimuli and carry an array of markers that can identify a particular male's major histocompatibility complex (MHC), or a cluster of genes that play an important role in immune function. 1) Smell: The Forgotten Sense To respond to continuously changing environmental selection pressures, the MHC and pheromone signals, work effectively with female mate preferences to ensure a diverse selection of allele combination for future progeny. The MHC influences both body odors and body odor preference in human females to ensure the production of genetically diverse offspring.

Pheromones themselves share similarities with odorants, or those chemicals detected by the body as odors, but both simple odors and pheromones stimulate different pathways within the brain. The difference between normal odorant signals and pheromone signals lies in the responses elicited by the brain. Odorant signals result in sensations of smell while pheromone signals trigger a characteristic behavior or psychological response. 2 ) Pheremones: What's in a name? Pheromones are processed by the vomeronasal system or accessory olfactory system, in the brain, which uses a specialized structure in the nose, the vomeronasal organ, to receive chemical signals. On the other hand, normal odor signals interact directly with the main olfactory system. 2 ) Pheremones: What's in a name? > In 1985 researchers at the University of Colorado isolated the VNOs within human nostrils and coincidentally VNOs connected directly to part of the brain responsible for drives and emotion by stimulation of the hypothalamus in the cortex of the brain. 1) Smell: The Forgotten Sense

The pheromones originate in the apocrine glands of the skin located in the axillae of the armpits and pubic region. 1) Smell: The Forgotten Sense > In humans the apocrine glands are focused in areas around the face, chest and wherever body hair exists and become activated after puberty, a time focused on finding a mate. 3) The World of Skin Care In male sexual maturation, the apocrine glands produce steroidal secretions derived from testosterone, as andorstenone (male sweat exposed to oxygen) and androstenol (fresh male sweat). 4) Male Pheromones and Sexual Attraction As a result, pheromones act as hormones or chemical messengers that are transported outside of the body to evoke responses in another. 5) Social Issues Research Centre

Current research suggests that influences of the MHC alter body odor, and male body odor preferences in females. Pheromones work with MHC specific cites as cues to persuade certain human mate choices. 1) Smell: The Forgotten Sense Recent studies support the theory that the MHC acts as a genetic marker of relatedness that prevents inbreeding and thus the exposure of deleterious allele combinations. The MHC consists of a large cluster of genes located on the short arm of Chromosome 6. 6) MHC-Dependent mate preferences in humans The MHC contains many base pair polymorphisms which allow for distinct individual immune defenses, and may define the chemical differences that are distinguishable among male pheromones. 7) The Majorhistocompatability Complex

Female attraction to male specific pheromone secretions, that represent differing immune identifiers, prevents producing multiple progeny with similar MHC loci. The diverse MHC among offspring of female mammals leads to diverse allele combinations that can in turn lead to a more diverse immune function. Through the discouragement of non-random mating, this specificity leads to a decrease in effective population size which changes the distribution of allele frequencies in the next generation. By choosing opposite allele types in the MHC the female is ensuring the energetic investment made by her nine month gestation period will result in a viable and healthy offspring. In mice, pregnant females that come in contact with male mice that contain similar MHC loci as the fathering male can spontaneously abort the fetus. 6) MHC-Dependent mate preferences in humans The spontaneous abortions are the cause of mother investment to the progeny and preventing the selective process. The great diversity of MHC loci and immune function result in a diverse heterogeneous society and thus allow heterogeneity to be promoted through sexual selection. If people of similar MHC loci mate then the offspring would be at a selective disadvantage due to a lack of diverse immune defense. By the spontaneous abortions, as seen in mice, the mother is eliminating the duplication of multiple equal MHC loci.

The question still remains as to what happens if the female has defective VNOs and cannot effectively identify a male with differing MHC loci. In this case the cycle of heterogeneity fails and perhaps the large percentage of immune dysfunctional individuals can attribute their deficiencies to defects in female mate choice. Perhaps these defective progeny as well inherit the defective VNO trait and add to the large genetic variability of immune diseases. This indicates a defective strain in the cycle of heterogeneity among individuals. Perhaps the complexity of relationships is out of individual control and remains under the harsh grip of chemical signals and input pathways.

Works Cited

1) Woronczuk, Julia and Medwid, Stephanie, and Neumann, Laura, and Eshelman, Sarah. "Smell and Attraction". Smell: The Forgotten Sense. January 22, 2006

2) Elia T. Ben-Ari. Pheremones: What's in a name?. Biological Sciences, Vol. 48, No. 7. (Jul, 1998),pp. 505-511

3) Dr. John Gray. The World of Skin Care. January 22, 2006.

4) Thorne, Frances and Neave, Nick and Scholey, Andrew and Moss, Mark, and Fink, Bernhard. Male Pheromones and Sexual Attraction. Neuroendocrinology Letters 2002.<>

5) Rationis,Vox. "Sexual Attraction". Social Issues Research Centre. January 28, 2006<>

6) Claus Wedekind; Thomas Seebeck; Florence Bettens; Alexander J. Paepke. MHC-Dependent mate preferences in humans. The Royal Society : Biological Sciences, Vol. 260, No. 1359 (Jun. 22, 1995), 245-249.

7) RT. "The Majorhistocompatability Complex". January 24, 2006.

Works Consulted
Gale Peter Largey, David Rodney Watson. The Sociology of Odors. The American Journal of Sociology, Vol. 77, No. 6. (May, 1972), pp. 1021-1034. <>

Erik E. Filsinger, Richard A. Fabes. Odor Communication, Pheromones, and Human Families. Journal of Marriage and the Family, Vol. 47, No. 2.(May, 1985), pp. 349-359.Stable URL:

Full Name:  Stephanie Pollack
Title:  Schizophrenia: From Nash to Neurotransmitters
Date:  2006-02-20 19:34:48
Message Id:  18230
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The disease schizophrenia often causes people to think of Russell Crowe's character John Nash in the film A Beautiful Mind. Schizophrenia is a serious mental disorder, which affects about one percent of the human population (1). Like most victims of schizophrenia, the brilliant mathematician John Nash, developed the disease in his early adulthood (2). The onset of schizophrenia in early adulthood establishes that brain development remains underway during this period. However, John Nash's genius is uncharacteristic of schizophrenics; most are of average intelligence, and often experience a declining IQ as the disease progresses (1). Schizophrenia impacts not only the victim, but all those around him. The schizophrenic often has trouble holding a job and leading a normal, independent life, frequently having difficulty dealing with the challenges of daily living (2).

Usually, the symptoms of schizophrenia are severe at the start of the disease and then continue "to worsen and improve in cycles known as relapses and remissions" (8). Schizophrenia varies in its severity and can be categorized into four classes: Paranoid schizophrenia, Disorganized schizophrenia, Catatonic schizophrenia and Undifferentiated schizophrenia (8). Paranoid schizophrenia is the most common form and causes sufferers to believe they are being persecuted and to hear imaginary voices (7). These delusions and hallucinations are examples of positive symptoms, or symptoms absent in people without schizophrenia (8). Negative symptoms, or the lacking of particular normal behaviors in people with schizophrenia, include antisocial behavior and poor personal hygiene (8).

Presently, treatments for schizophrenia blend therapy with prescription medications (antipsychotics) which help to alleviate the more stereotypic symptoms of the disease, such as paranoid delusions and hallucinations (2). Electric shock treatment, an older method of treatment, is rarely used today (8). Drugs that treat schizophrenia work to manipulate the expression of symptoms "by neuroreceptor antagonism." (3)

Recent studies have shown that schizophrenia can be a precisely diagnosed disease with evident "changes in brain structure and function" (2). On average, schizophrenics tend to have smaller brains than their normal counterparts (1). Aside from size, individuals with schizophrenia have anatomically distinct brains from unaffected individuals, raising the question of whether changes in brain structure cause schizophrenia or if schizophrenia causes changes in brain structure. Schizophrenics "have abnormalities in the prefrontal, temporal, and anterior cingulate regions" of the brain, which are areas that help direct cognition and emotion (2). Additionally, memory loss brought on "by lesions of the frontal lobe... [is] evident in schizophrenia and may account for the cardinal symptoms of disorganization in thinking, planning and expressing thoughts" (2).

Scientists have come to realize that no one part of the brain is solely responsible for schizophrenia. Schizophrenia, like normal behavior, involves the combined effort of the entire brain, and the interruption of normal function results from the interactions of multiple brain regions (1). Schizophrenia is a complex disorder that is believed to have a genetic basis. The disease is not caused by a single gene defect, rather it is polygenic, or brought about by multiple genes acting together (6). This genetic predisposition is combined with environmental factors to yield the disorder. Such environmental factors include "obstetric complications, intrauterine abnormalities, and viruses" (2). Polygenetic forces may account for the wide range of symptoms across schizophrenic patients (1).

Interestingly, the drug amphetamine mimics the symptoms found in schizophrenic patients in normal individuals (5). Additionally, when schizophrenic patients are given amphetamine, their schizophrenic symptoms often worsen (5). Consequently, amphetamine must interact with neurotransmitters in the brain to elicit such similar symptoms. Researchers have been on the hunt for which neurotransmitter in particular gives way to schizophrenic behavior.

Dopamine is an important neurotransmitter in the central nervous system and its receptors are linked to "a number of neuropathological disorders such as Parkinson's disease and schizophrenia" (3). The "dopamine theory" suggests that the symptoms associated with schizophrenia are correlated with "excess dopamine release in important brain regions" (1). Therefore, an increased level of dopamine receptors in schizophrenic patients can be used to help diagnose the disease (3). The dopamine hypothesis can be extended to the limbic system, which directs emotion and cognition (4). These areas of behavior are clearly altered in those suffering from schizophrenia. The limbic system "is richly innervated by noradrenic and dopaminergic neurons", and thus demonstrates how malfunctioning dopamine receptors can influence schizophrenic behavior (4).

Although this evidence is quite convincing, new data has indicated that the neurotransmitter glutamate may play a more active role than that of dopamine (1). Glutamate can be found in nearly all areas of the brain and would be a better candidate to explain schizophrenia's variety of symptoms (1). While glutamate is important in signaling all over the brain, dopamine's significance is confined to only certain parts of the brain (1).

Clearly, the intricacies of the roles of neurotransmitters in the brain are not yet fully understood. Continued research in this area will lead to the development of more effective drugs to combat the devastating disease of schizophrenia.


1) Javitt, D.C. & Coyle, J.T., Decoding Schizophrenia, Scientific American, January 2004, Vol. 290 Issue 1, p48-55.

2) Workshop on Schizophrenia

3) A Peripheral Marker for Schizophrenia: Increased Levels of D3 Dopamine Receptor mRNA in Blood Lymphocytes

4) Schizophrenia: Elevated Cerebrospinal Fluid Norepinephrine

5) Phenylethylamine in Paranoid Chronic Schizophrenia

6) Schizophrenia: Genetic Tools for Unraveling the Nature of a Complex Disorder

7), Classification of Schizophrenia

8), Mental Health: Schizophrenia

Full Name:  Fatu Badiane
Title:  This is Your Brain on Drugs: An Inside Look at Addiction
Date:  2006-02-20 20:26:59
Message Id:  18232
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Neurobiology and behavior
Prof. Grobstein

The prevalence of addiction within our society ranges from movie stars dealing with a cocaine habit in the tabloids to the backyards of our home towns where adolescents get high off of prescription drugs. Although there is already much knowledge one the physical manifestations of addiction, there is also a hint of unfamiliarity when it comes to looking at the workings of the brain. Addiction, so far, has revealed to be a complicated change of the brain that can easily overwhelm a person's life. Current research has revealed that several intertwined pathways focusing on rewards and learning are the key players of this lifestyle.

These major pathways in the brain are quite different from the intial model of addiction, the opiate model. This model was developed by Abraham Wikler on the belief that it is drug withdrawal symptoms that drive the cycle of addiction. Withdrawal symptoms are physical side effects, such as shaking and nausea, and cravings addicts experience when their bodies are depleted of their usual intoxicants. Follow the mind set of the opiate model, it is the want to diminish the withdrawal symptoms that keeps addicts within their vicious cycle (2). According to Wikler, then, so long as the withdrawal symptoms, especially the drug craving, are under control it should be relatively easy to detoxify an addict. The millions of addicts and thousands of drug rehabilitation clinics, however, easily prove that this is not the case.

Wikler soon realized that his simple theory had two major holes: "One was that the model cannot explain why an addict would [take drugs] so regularly and in such a quantity to become physically dependent in the first place . . . [and how this theory can] account for relapse after subsidence of the withdrawal syndrome." (2).

The first hole in Wikler's theory is on the foundation of addiction itself. What is it that makes a person want to take a substance to the point of addiction? The key to this answer is reinforcement. Reinforcements are positive consequences that encourage a behavior to continue. In the case of drug dependence, that positive outcome is the high. The role of reinforcement and rewards in drug addiction was studied by Bozarth and Wise using rats. They "demonstrated that a single injection of heroin is reinforcing in drug-naïve rats, inducing a clear preference for the environment in which the effects of that drug were experienced." (2). The rats tested in this experiment easily become accustomed to the feelings of a drug after simply one dose and are even encouraged to seek more of it. It is possible that the first dose of heroine is all a person needs to feel the positive effects that encourage them to continue taking that drug. The bottom line of this idea is that reinforcement plays a big role in addiction. If drugs were unpleasant, people would not be encouraged to seek them and take them again and again.

The pathway in the brain that is responsible for these reinforcing effects is the mesolimbic dopaminergic pathway. Rewards, both natural (food, sex) and substance based (alcohol, opiates), are founded in this pathway. The pathway runs on dopamine, a common neurotransmitter that is known for its role in the pleasure pathway and drug addiction. Researchers are not exactly sure what mechanism dopamine plays in the mesolimbic dopaminergic pathway, but they have two hypotheses. The first believes that drug use heightens dopamine concentrations in the brain, which results in pleasure. This model gives the idea that drug usage creates a rush of dopamine in the brain. This rush produces a long lasting feeling of pleasure. The second theory is that drugs make the dopamine system more sensitive to dopamine. Drugs, then, increase the brain's responsiveness to dopamine and drug taking is basically keeping the brain's receptors sensitive to get that desired high. (1). But this still is not the end of the story. Dopamine makes one happy, but how does one remember it makes them happy? This is where the pathways of memory and learning come into play.

"The imbedding of the experience of substance use in tandem with the attendant conditioned environmental stimuli produces an "addiction memory" or "neural ghost". This neural ghost remains imbedded in the mesolimbic circuitry, particularly the amygdala – often outside of conscious awareness. Upon stimulation of the mesolimbic pathway, either by conditioned drug cues or by drug priming, the circuit is activated, inducing a desire, or wanting, for additional drug. The formation of the associations between salient stimuli and internally rewarding events is facilitated by stimulation of dopaminergic neurons." (1). A physical change takes place in the brain every time an addict gets high. A neural ghost becomes engraved in the mesolimbic pathway, particularly the part the runs through a region of the brain associated with memory, the amygdala. The activation of the mesolimbic pathway along with the memory creation of the amygdala create an effect called priming. Priming is a way of creating simple associations. These associations create an even stronger attachment to the drug than just the ordinary high. All of the people, places, and tools become wrapped in the brain as one entity that corresponds to getting high.

The way priming takes place between the drug-induced high and the environment where that high takes place is through a process known as Pavlovian classical conditioning. Classical conditioning is a theory of learning that says when two stimuli presented one after the other together the later stimulus will be able to induce a response without the earlier stimulus. For example a dog can be conditioned to salivate at the sound of a bell if it believes the bell signals food. Food on its own will cause the dog to salivate, but when the food is paired with the bell an association is made. The dog believes that the bell is a signal for it. In the end, it will salivate if only the bell is presented.

The conditioning hypothesis was tested by O'Brien, Ehrman, and Ternes. They did an "experiment in which withdrawal-inducing injections of the opiate antagonist naloxone were repeatedly given to methadone patients in the presence of distinctive cues. When a saline injection was subsequently given in the presence of the same cues, conditioned withdrawal symptoms were evoked." (2).This study looked at how distinctive cues can be paired with withdrawal syndromes. The methadone patients learned to associate the naloxone induced withdrawal syndromes with distinctive cues, such as a specific room for example. When they were given a placebo in that same room, the same withdrawal syndromes returned. The patients had come to associate that room with withdrawal. O'Brien et al. came to the conclusion that if certain stimuli can be associated with drug withdrawal then others can be associated with intoxication. This, in fact, is true; "in real-life situations experienced by opiate addicts, drug-related stimuli are repeatedly paired with both intoxication and withdrawal, leaving the possibility that drug-like responses could be conditioned to such stimuli in addition to, or instead of, withdrawal-like responses." (2). Drug addicts, therefore, have been trained to make associations between places, people, things and their drug of choice. They do not even need the physical drug infront of them for cravings to set in; even just seeing a familiar area where they enjoy get high can spark wanting for their drug. They cannot fully be freed from their habit if so many associations exist around them that enforce it. In order for these associations to take place, there is a learning process involved.

Just as dopamine is the main neurotransmitter in reward and reinforcement, glutamate is the primary neurotransmitter when it comes to learning and memory. "[As] the chief agent of fast neuron stimulation, glutamate is at the core of nearly all brain physiology and biochemistry and is central to the most sophisticated cortical processes. Glutamate receptors in the hippocampus appear to trigger the complex cascade of biochemical reactions that convert short-term memories into permanent ones, a process called long term potentiation." (3). Glutamate is the main player when it comes to memory. It is used in changing short-term memories to long term ones. When looking at an addict, one can see how glutamate would play a role in the addiction process. The associations that they make through conditioning, which was previously discussed, become more and more natural habit as certain areas, people, methods as hard wired into their brain with the help of glutamate. They learn, they remember, they know all the key players in their drug habit. Once this habit is built in, just like with any other process that humans learn, it is very hard to un-learn or un-remember it.

In addition, " [neuroscientists] of all sorts have paid intense attention to a crucial link in this chain, an intracellular signaling chemical called cyclic adenosine monophosphate (cAMP), because it turns genes on and orders them to make some very consequential proteins. These proteins help form new synaptic connections between neurons – the basis for long-term potentiation." (3). Glutamate is an extracellular signaling chemical. It is an external switch to the cascade of events that occur within a neuron. The second half of the story lies inside nerves cells, neurons, with cyclic adenosine monophosphate (cAMP). cAMP controls the activation of genes found in all cells. When cAMP is activated it instructs the formation of proteins which creates new connections between neurons and leads to long-term potentiation, or the transfer of information from short-term to long-term memory.

To put everything all together, dopamine controls the high a person feels every time they take their drug whether it is caffeine, methamphetamine, or ecstasy. Dopamine makes that person feel good through the various interactions that drug has with the dopamine pathway, the mesolimbic dopaminergic pathway. The connections made between the drug and other important environmental cues are learned and then put into memory through the help of glutamate. Lastly, it is cAMP that solidifies the long-term memory connections between neurons that turn drug use into full blown addiction.

Addiction is not simply the struggle between withdrawal symptoms as was previously believed. Addiction is a change in the brain, a physical change in the brain, as a result of a behavior. It is interesting to look at addiction in this new light and to understand that all of the intertwined pathways discussed in this paper may only be the surface. There is so much more to addiction, and other behaviors in general, and their affect on the brain. One of the main debates currently taking place in the field of neurobiology is whether the brain is behavior. This is to say that all behaviors, in essence, start in the brain. This equation can also be seen in reverse when it comes to addiction, that behaviors, in essence, can and do change the brain.

Works Cited

1) Adinoff, Bryon. (2004). "Neurobiological Process in Drug Reward and Addiction." Harvard review of psychiatry. 12 (6). 305 – 320.

2) Lyvers, Michael. (1998). "Drug Addiction as a Physical Disease: The Role of Physical Dependence and Other Chronic Drug-Induced Neurophysiological Changes in Compulsive Drug Self-Administration." Experimental and Clinical Psychopharmacology. 6 (1). 107 – 125.

3) Powledge, Tabitha M. (1999). "Addiction and the Brain". BioScience. 49 (7). 513 – 519.

Full Name:  Rachel Freeland
Title:  Multiple Sclerosis
Date:  2006-02-20 20:42:12
Message Id:  18233
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. "In multiple sclerosis, the body incorrectly directs antibodies and white blood cells against proteins in the myelin sheath, which surrounds nerves in the brain and spinal cord" (1). This causes inflammation and injury to the sheath, disrupting or slowing nerve impulses and leaving areas of scarring (sclerosis). The disruption of nerve signals causes a variety of symptoms that can affect vision, sensation, cognitive abilities, and body movements (2). "Multiple sclerosis is classified according to frequency and severity of neurological symptoms, the ability of the CNS to recover, and the accumulation of damage" (6). The four classifications of MS are primary progressive MS, relapsing-remitting MS, secondary progressive MS, and relapsing-progressive MS.

The exact cause of MS is still unknown. However, it is speculated that MS is an autoimmune disease, which means that the immune system mistakenly attacks its own body, in this case, the myelin sheaths of the nerves. It is also unclear whether viruses or infectious agents play a role. In addition, other physical or emotional stressors may be a contributing factor.

The disease usually manifests itself in young adulthood; most people experience their first symptoms between ages 20 and 40. Multiple Sclerosis is approximately three times as common in women as in men. The course of the illness is enormously variable, ranging from death in less than a year, to little disability even after 50 years. "However, the majority, after an initially relapsing and remitting course, enter a phase in which there is continuous deterioration superimposed on which may be acute exacerbations of neurological deficit" (3). Exacerbations can last days, weeks, or even months.

At this time, there is no specific test for MS. Therefore, the diagnosis is primarily clinical, based on medical history, physical and neurological examination, blood tests, MRI, spinal tap, and neurological tests. However, in order to be diagnosed with MS, the patient must exhibit at least two separate sites of central nervous system damage and have a history of at least two episodes of neurological disturbance of the kind encountered in MS.

Treatments for MS vary considerably. "There is no cure for MS, but there are two types of treatments: those that modify the immune system to suppress the disease, and those that improve the symptoms of MS" (2). Examples of these types of treatments are immune modulators, steroids, cholinergic medications, antidepressants, physical therapy, speech therapy, occupational therapy, and exercise. A healthy lifestyle is encouraged, including good nutrition, adequate rest, and relaxation. "Attempts should be made to avoid fatigue, stress, temperature extremes, and illness to reduce factors that may trigger an MS attack" (4).

Due to the unknown origins of the disease and the inability to cure it, doctors are constently looking for new treament options. It is important to examine any abnormalities of function in patients with MS. One such abnormality found is the hyperactivity of the hypothalamo-pituitary-adrenal axis (HPA axis). It is believed that the dysregulation of the HPA axis reflects a disturbance of negative feedback at the level of the hypothalmus or pituitary gland. The overacitivity of the HPA system may contribute to the pathogenisis of the disease and its normalization may be beneficial (5).

During an exacerbation, active peptides and cytokines, secreted by the immune system, exert various effects on the HPA axis, for example, increased secretion of ACTH and cortisol during acute inflammtory reactions (5). Hyperresponsiveness of the HPA axis is due to diminished corticosteroid receptor function. Chronic hypersecretion of cortisol leads to a desensitization of immune cells toward the effects of corticosteroids, making steroid medication for acute relapse less effective (5). "Recent evidence suggests that in aged rats, hypercortisolism is a crucial factor limiting the proliferation of neural stem cells in the hippocampus, and that reduction of corticosteroid levels restores normal formation of neurons even in adult mammals" (5).

It has also been found that hyperactivity of the HPA system is associated with major depression. Successful treatments with antidepressants (such as MOA inhibitors) are associated with normalization of HPA hyperactivity because they increase glucocorticoid receptor messanger ribonucleic acid in the hypothalamus. A higher number of glucocorticoid receptors improves the disturbed feedback regulation of the HPA system. Due to the ineffectiveness of corticosteroids alone, it has been found that moclobemide (an MOA inhibitor) combined with corticosteroids will normalize the dysregulation of the HPA axis that's exhibited in patients with MS.

1)Mayo Clinic, information about Multiple Sclerosis
2)Aetna InteliHealth, information about Multiple Sclerosis
3) McDonald, W. & Ron, M. Multiple Sclerosis: The Disease and Its Manifestations. Philosophical Transactions: Biological Sciences, Vol. 354, 1615-1622.
4)Medline Plus Medical Encyclopedia, information about Multiple Sclerosis
5) Bergh, F., Kumpfel, T., Grasser, A., Rupprecht, R., Holsboer, F., & Trenkwalder, C. Combined Treatment with Corticosteroids and Moclobemide Favors Normalization of Hypothalamo-Pituitary-Adrenal Axis Dysregulation in Relapsing-Remitting Multiple Sclerosis: A Randomized, Double Blind Trial. Journal of Clinical Endocrinology and Metabolism, Vol. 86, 1610-1615.
6)Neurology Channel, information about Multiple Sclerosis

Full Name:  Christin M. Mulligan
Title:  Schizoaffective Disorder: The Journey Back from Crazy...
Date:  2006-02-20 21:14:49
Message Id:  18234
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

I had always been a drama queen. My grandmother even nicknamed me Sarah Bernhardt, after the queen of Vaudeville melodrama. My high school superlative was "Most Stressed Out". Type A overachiever is the tip of the iceberg.

The problems began during my sophomore year here at Bryn Mawr. My moods swung like a pendulum. I would work productively for days and then suddenly find myself unable to get out of bed in the morning. At the end of fall semester, I decided to apply for the prestigious Hanna Hollborn Gray Fellowship, so I could spend my summer immersed in Irish Women's Literature and take a Gaelic course at Penn before my semester abroad at Trinity College in Dublin. I spent Winter Break up to my elbows in theory and criticism. I had 24-hour reading binges. My sleep cycle was in chaos. I did not even consider seeing a doctor.

My insomnia continued well into second semester. Flash forward to May, week of the Gray announcement: I wrote papers. I went to work. I ate meals with my friends. I did everything but sleep for five consecutive days. I was awarded the Gray. Rapture. I did not sleep that night either. I sobbed uncontrollably on the way to my first class. Someone had to escort me back to my dorm where I still did not sleep. My room was a shambles. I could not ignore the incessant "noise" in my head. I called my mother in a white-knuckled panic and begged her to come from New Jersey and pick me up. By the time she arrived, I was hysterical. I believed that everyone was angry with me and "no one loves me." I insisted that I was a failure and that everything that has ever gone wrong in my life was entirely my fault beginning with the end of my parents' relationship before I was even born. I contended that my life was a lie and demand to be told "the truth" -whatever that meant. At home, even my grandparents could not console me. I started apologizing for God only knows what. My mother called my stepmother and then my father arrived. I begged him to tell me "the truth." No one understood me. At this point, my parents convinced me to go lie down. Both my mother and father stayed with me through the night, and I only slept for two hours. In the morning, my mother called my aunt, her twin, a doctor in Boston. Aunt Katie contacted a mental hospital in Delaware. I committed myself in my pajamas. I remember the questions very clearly, "Who was the President of the United States?" George W. Bush-duh. "Who was the first President?" George Washington-duh. "What was today's date?" May 8-I'm not an idiot. "What were the three things I asked you to remember?" My mind was blank. I began to cry again. I became agitated when they wanted me to sign the forms. I became more agitated and curled into a ball when the nurse came to photograph me. My thoughts were racing. I could not form coherent sentences. The words were slipping away from me, vanishing like snow on a hot pavement, evaporating into the ether. There was only noise. The walls vibrated, colors shifting. I felt as if I was trapped in a Salvador Dalí painting. I began to pace back and forth and wandered the halls. I could not seem to calm down. Eventually, I was sedated.

The next fifteen days were a blur. I ate plain spaghetti and drank only water because I was certain there was something wrong with the food. I wrote compulsively, lists and lists of words, just so I would not forget any. I memorized the faces of the other patients. (I would see them for months afterward: at the movies, at the mall, on the beach.) I had many "visitors" in the hospital: my best friends, their parents, two of my favorite professors, my ex-boyfriend, his parents (whom I had never met), my hairdresser. I talked to even more people on the phone. In reality, my only visitors were my parents, my stepmother, and my grandparents. I have no idea who I spoke to on the phone. Eventually, I told the doctor I would die if I were not sent home.

For some inexplicable reason, he released me. I suppose crazy people are eerily persuasive. I was on ten medications and still hallucinating. I had horrible, violent nightmares. I insisted that someone was trying to kill me in my sleep. The doctor at the hospital was unable to take me on as a regular patient. It took me a month to get an appointment elsewhere. The nightmares continued. I cried for hours on end. I stopped eating. I could not stand to be alone. The TV upset me. There was still "too much noise" in my head.

After four appointments with the Head of Neuropsychiatry at the University of Pennsylvania, who listened patiently as I discuss my insomnia, my paranoid rationalizations, my delusions and hallucinations, I was formally diagnosed with schizoaffective disorder, a mix of schizophrenia and manic-depression. Positive symptoms of schizophrenia, those that should be absent but are present, include: hallucinations, delusions, and disturbed thinking. Negative symptoms, those that should be absent but are present, include: blunted affect, apathy, anhedonia, alogia or aphasia, and inattention (1). Symptoms of mania include: agitation, sleeplessness, paranoia, excessive cheerfulness resulting in extreme irritability, susceptibility to spending sprees and sexual indiscretions, and compulsive talkativeness. Symptoms of depression include: flat affect, constant sadness and fatigue, loss of interest in normal activities, indecisiveness, sleep and appetite deprivation or in excess, and morbid or suicidal ideations (2). The disorder is more common in women, and usually begins between the ages of sixteen and twenty-five. Twins of schizoaffectives have a 50% chance of developing the disease, while first-degree relatives have a 10% chance (1).

Studies of both classic schizophrenia and manic-depression (bipolar disorder) are relevant to studying schizoaffective disorder. In fact, bipolar and schizophrenic patients show susceptibility to both diseases through a distinct linkage pattern along chromosome 18 (3). Previous research on schizophrenia suggests negative symptoms are related to decreased activity in the pre-frontal cortex, which controls executive functioning, while positive symptoms are related to abnormal blood flow in various regions of the brain. There are both over-perfused (too much blood flow) and under-perfused (too little blood flow) regions (4). For example, during delusions, blood flow increases to the Broca's area, which controls language articulation. Furthermore, "schizophrenic brains tend to have larger lateral ventricles and a smaller volume of tissue in the left temporal lobe in comparison to healthy brains" (5).

Another significant factor in the development of the positive symptoms of schizophrenia is overproduction of the neurotransmitter dopamine in the limbic system, which regulates emotion, motivation, and memory. "Dopamine is secreted by cells in the midbrain that send their axons to the basal ganglia and frontal lobe. There are five dopamine receptors in the brain. Each of the receptors contains about 400 amino acids, and they have seven regions spanning the neural membrane. Their function is to bind to dopamine secreted by presynaptic nerve cells. This binding triggers changes in the metabolic activity of the postsynaptic nerve cells" (5). Additionally, there is an increase in the levels of serotonin, the "feel-good" neurotransmitter. Traditional neuroleptic drugs block the dopamine receptors thereby treating schizophrenia. Atypical neuroleptic drugs also block serotonin (5-HT) receptors. Negative symptoms, on the other hand, may be caused by decreased levels of dopamine in the frontal lobes. For both positive and negative symptoms, there is a decrease in the glutamate receptor NDMA, which is involved in the development of learning, memory, and neural processing in general (6).

Like schizophrenia, previous research on bipolar disorder suggests elevated levels of dopamine during manias. There are also elevated levels of the stress hormones norepinephrine and cortisol, and calcium (7). While environmental stressors that cause the brain to produce norepinephrine and cortisol can result in bipolar cycles, after multiple episodes, there is less and less need for a trigger. Eventually, the brain begins to respond automatically and requires no trigger at all. This phenomenon is called "kindling". If untreated, "kindling" worsens over time (9). Depending on whether the patient is manic or depressed, the level of serotonin and norepinephrine varies accordingly (7). Logically, there is an excess in manias and a paucity during depressions. Circadian rhythms, the body's natural cycles that control everything from appetite to sleep and sex drive, are believed to have an effect on bipolar disorder. The center of Circadian rhythms is the suprachiasmatic nucleus in the hypothalamus. The sleep cycle is particularly pivotal in mood shifts and triggers the pineal gland's secretion of melatonin. Patients experience insomnia during mania and hypersomnia during depression. Melatonin responds to light, so patients have been successfully treated with phototherapy to regulate melatonin secretion (8).

Neural structure and functioning also vary in the bipolar brain. There are fewer neurons in the hippocampus, which controls memory and navigation, and fewer glial cells, which provide nutrients to neurons, in the prefrontal cortex. Like schizophrenia, there is also a decrease in the protein myelin, which prevents electrical impulses from leaving the axons and causing a short-circuit in the brain (10).

So what do all these surpluses and deficiencies mean in terms of dealing with schizoaffective disorder in the real world? Remember the three C's. Commitment to taking the neuroleptics and/or mood stabilizers is essential. Coping with side effects can be difficult, but nonetheless, communicate these problems to your psychiatrist and work out an individual regimen of therapy in addition to simply medicating. If the meds are not working, do not be afraid to say so.

As for me, after agonizing tinkering with my medications, where I became depressed and lost the ability to sleep, read, and concentrate in general, I have not had a paranoid or hallucinatory episode in nine months. As the number of my medications was gradually reduced to one, my moods began to stabilize and I was again able to sleep, read, and focus. The journey back from crazy was long and hard, but ultimately worthwhile.

WWW Sources

1)Positive and Negative Symptoms, a rich text resource

2)The Symptoms of Schizoaffective Disorder, a rich text resource

3)Evidence of Genetic Overlap between Schizophrenia and Bipolar Disorder, a news article from

4)Research on Schizophrenia, a news article on schizophrenia

5)The Role of Dopamine Receptors in Schizophrenia, an article on the role of dopamine in schizophrenia

6)Decoding Schizophrenia, a Scientific American article

7)What Causes Bipolar Disorder?, a rich text resource

8)Circadian Rhythms, a rich text resource

9)Kindling, a rich text resource

10)Bipolar Disorder, a rich text resource

Full Name:  Whitney McDonald
Title:  Suggestibility and Hypnosis
Date:  2006-02-20 21:20:20
Message Id:  18235
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Recently an increasing amount of research has been conducted on the cognitive processes of the brain while under hypnosis. This research boom stems from questions regarding perception needing answers. It was found through trials and experiments addressing the mind under hypnosis that the body is able to perform and the mind is able to perceive things otherwise unperceivable or doable in the conscious state. In India a limb amputation was successfully performed while the person was under hypnosis and in this context hypnosis was used as the anesthesia (1). This and many other medical practices involving the use of hypnosis aroused the attention of neurobiologists. Hypnosis is when the brain is not thinking but rather experiencing without analysis. In this state the hypnotist is able to make suggestions to the hypnotized and their body and brain carry out these commands. This willingness to comply with suggestions is an effect of the conscious judgmental mind not being a factor of experience.

An experiment was conducted to compare physical strength in the conscious state to that of the hypnotized state. While conscious, men were asked to hold a brick out for as long as they could, which on average was about 5 minutes. These same men were then hypnotized and were able to hold the brick out for 15-20 minutes (2). This supports the idea that hypnosis crates a unique mindset that enables one to physically breach higher thresholds. Hypnosis is clearly able to influence physical ability but can hypnosis also alter understanding? As a result of many experiments involving color discernment, hypnosis can indeed alter understanding. A professor of clinical neuroscience at Colombia University performed tests investigating conflicts in the brain dealing with the perception of color. This experiment was called the "Stroop Effect"; for example, the word green may be presented in a blue color (1). The subjects would be asked to press the color corresponding to the color of the word (not the color associated with the meaning of the word); this would become a difficult task for all subjects because they would instinctively want to press the color meaning of the word rather than the color displayed, this is the "Stroop Effect". However while people were under hypnosis those that had less difficulty overcoming the Stroop Effect where the ones that performed well under hypnosis and effortlessly chose the color corresponding to the color of the word rather than the color meaning of the word. As evidence of this experiment it is clear that not only can hypnosis alter perception but not everyone is hypnotizable.

To categorize levels of ability to be hypnotized scientist classify people by levels of suggestibility. A person highly suggestible would be one to undergo hypnosis easily while one of lower suggestibility would be more resistant in submitting to hypnosis. Under the Stroop Effect experiment it was found that those who were highly literate had a hard time overcoming the Stroop Effect because of the need to interpret the meaning of the word instead of the color the word is being displayed (1); thus classifying those which did not overcome the Stroop Effect of having low suggestibility. Moreover, this may allude to the reason why there is a large gap between adults and children that are suggestible. It was found that 80-85% of children under age 12 are highly suggestible where as 10-15% of adults are highly suggestible (1) and this difference may be due to literacy levels. This supports the argument that the difference between the low and high suggestible people is not in inherent brain structures but the effect of development over time.

It turns out, from PET scan results; highly suggestible people use different regions of the brain than those of lower suggestibility. While conscious, subjects were asked to perceive color whether they saw color or not, brain activity was recorded and it was found that there was activity on only the right side of the brain. However while under hypnosis both sides of the brain revealed activity. "The left hemisphere...registered what people were told to see only when they were hypnotized the right registered what they were told to see whether or not they were hypnotized."(2) Moreover, because the left side of the brain deals with the logical reasoning mind and the right deals with the emotional illogical mind this supports the idea that while under hypnosis the left side of the brain is disassociated from logical thinking. To sense that there is in fact color where there may be a gray area reveals that hypnosis disassociates the left side of the brain from the senses or changes the senses by altering what exactly is being seen.

Furthermore, it was found that people who were classified to be highly suggestible used their cingulated gyrus region of the brain (2), more than those of low suggestibility. It is this region that connects the right and left sides of the brain and it may be because of the heightened activity in this area that highly suggestible people easily submit to hypnosis because hypnosis requires the use of both sides of their brain. More specifically, it was found that people of higher suggestibility have a larger rostrum, located in the corpus callosum, the rostrum is responsible to the allocation of attention (3). This alludes to further support why highly suggestible people easily submit to hypnosis because of their heightened ability to concentrate when being hypnotized and not be distracted by other thoughts or the surrounding as easily as low suggestible people.

These observations of a change in senses and heightened concentration while under hypnosis support the idea that hypnosis changes perception. Also if the perception of pain can be altered, as observed in the endurance experiment, then many other psychological problems such as addiction, depression, and insomnia can be solved as well. It now becomes clear through the analysis of effects of hypnosis and brain activity associated with hypnosis why 80-85% of children are highly hypnotizable and only 10-15% of adults are. Children would be able to submit to hypnosis with ease because they do not have as much experience as an adult to be analytical of the suggestions. Along these same lines children constantly move between imaginative play and reality, hence this would make the use of their cingulated gyrus of the brain heightened because they naturally use that region to switch between the illogical creative mind and the logical mathematical mind.

Although there are still many un-chartered issues in the area involving hypnosis and perception it is clear that hypnosis does change experience. Also, because experience shapes understanding, those that have the advantage of being highly suggestible can thus perceive life on a different level than those that are not; they can develop a control over involuntary functions of the brain. Accordingly, the possibility arises that through hypnosis the mind will be able to influence the immune system and other functions of the body to prevent ill health. Through the progression of the mind under hypnosis the mind will have more control over the body making many other chemical medications a thing of the past; the brain itself would develop the capacity to influence it's own body's behavior.


1)3,2,1: This is You're Brain Under Hypnosis,New York Science Times

2)Hypnosis found to alter the brain: Subjects see color where none exists.

3)Increased anterior corpus callosus size associated positively with hypnotizability and the ability to control pain.

Full Name:  Astra Bryant
Title:  Emily Dickinson's Morality
Date:  2006-02-20 21:22:47
Message Id:  18236
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Part 1 of 3 in a discussion of the biological implications of moral sense and action. Part 1 discusses the biological mechanisms behind moral action. Part 2 will discuss the evolutionary survival of morality, and Part 3 will look at possibly reasons behind the development of morality.

The concept of morality has long been a keystone of human thought and society. Throughout the history of philosophical thought, morality has retained its status as the principle which differentiates humanity from all other life. But how does morality really work? In this age of bio-imaging, can morality be neatly explained by the intricacies of our brain? Or is morality more than neurochemical signaling; is it instead a collaboration of social cognition and biological structures. This web paper will discuss the biomechanics of morality – how our brain creates our morality.

In order to have a meaningful discussion of the origins and intricacies of morality, it is first necessary to define what morality means. Common dictionaries define morality as the quality of being in accord with standards of right or good conduct; a system of ideas of right and wrong conducts (1). The acting out of this conduct as directed towards others may be divided into three major subsets: Morality for Gain, Morality for Family, and Morality for the World (2).

Morality for Gain encompasses the acts of morality that are undergone with an ulterior motive in mind (even subconsciously). The saying "do unto others are you would have done unto you" is a prime example of morality for gain. Your moral behavior is chiefly governed by the expectation that if you act morally, others around you will reciprocate.

Morality for Family specifically defines your family as the targets of your moral acts. The reasoning behind this distinction is that you are more likely to treat those people close to you - especially blood relations, in a moral fashion that is not dependent on the likelihood of reciprocation. For example, you would be more likely to lend your sister $100, even if you knew she could not pay you back, than you would lend that same $100 to a complete stranger, who you would most likely never see again.

The third subset of moral action is Morality for the World, the treating of everyone and everything in a moral fashion, even if they will neither reciprocate moral actions, nor punish immoral actions. An examples of such action is a yearly anonymous donation to a charity – the benefactors (in, say, a third world country or even in an animal shelter) will neither be able to return your donation (either with money, services, or gratitude), nor will they accuse you (or even know) if you decide not to donate.

In the context of a psychological/anthropomorphic analysis, the existence of these subsets could most likely be explained. But biologically, can the existence of these actions, of theses behaviors, be accounted for?

A biological explanation of morality must take into account two issues. First, if the overarching hypothesis stated so poetically by Emily Dickinson holds, then there must be a physical factor within the nervous system that causes us to behave morally. Second, for any serious discussion of biological functions, the evolutionary purpose and fitness of the function in question must be examined. (To be discussed in parts 2 and 3 of this series)

But before examining the evolution of morality (what does Darwinism have to say on the evolutionary advantages of morality), it is apropos to define the specific physical structures within our nervous systems that are involved in morality.

In terms of biological structures, there is not one section of the brain which propagates feelings of morality. Instead, several different sections combine their individual functions to create the moral sense. Chief amongst these sections is the prefrontal cortex. Located in the very front of the brain proper (right behind the forehead), the prefrontal cortex is responsible for the ability of the brain to integrate learned lessons of moral behavior with current situations (3). The functions that are generated within the prefrontal cortex can be grouped under the title of Executive Function. The Executive Function is a proposed cognitive system that is responsible for the regulation of other cognitive functions. Therefore, the executive function would be the driving force behind our ability to differentiate right from wrong, to choose between conflicting thoughts, to determine future consequences of current actions, and to have a level of social control (i.e. the integration of learned social mores with current behavior) (4). The ability to apply moral codes (as opposed to social) to our actions can logically be another ability regulated by the Executive Function. Damage to the prefrontal cortex would disrupt the Executive Function, destroying (or at least severely disrupting) our ability to differentiate between conflicting signals from the different areas of our brain that are connected to the prefrontal cortex.

One of these areas is the Reticular Activating System, which is believed to be the origin of arousal and motivation. The RAS is located inside the brain stem, between the medulla oblongata and the midbrain. The other major connected area is the limbic system. The limbic system is not a specific area, but instead is a generalized term for all brain structures involved in emotion. Specific structures within the limbic system include the amygdala (generation and control of aggression and fear), the hippocampus (long-term memory formation), the mammilary body (also involved in formation of memory), and the nucleus accumbens (generation of feelings of reward and pleasure; neurobiological center of addiction) (5).

The executive function is important in that it is involved in the processing of situations that lie outside the domain of our automatic processes. The executive function, therefore, is the area of the brain where decision making occurs. It is where the brain must take sensory input and process it to create a novel response, instead of relying on preprogrammed responses. If the executive function is then involved in moral decisions, logically, moral decisions, and morality, are not included in the set parameter of our brains. Instead, the ability to make moral decisions would be a new use of established structures – a use only possible because of our highly developed of the prefrontal cortex. In addition, our moral ability is not yet hardwired into the human brain.

That morality is a learned characteristic which relies of the ability of brain structures, has been shown through a series of experiments which examined subjects who sustained damage to their prefrontal cornets, both during adulthood, and before reaching 16 months of age. The subjects who had sustained the damage during adulthood were unable to apply what they knew about social and moral standards to their own lives. However, they were able to answer hypothetical questions which required a factual knowledge of those social and moral standards. Subjects who sustained prefrontal damage before 16 months of age, as adults, were unable to answer the hypothetical questions that their adult-onset counterparts could (6). This division suggests that moral standards are learned during childhood and that humans are not born with an ability to know what "good" and "bad" is.

If moral codes are indeed learned throughout childhood, and then integrated with our actions via the prefrontal cortex, it must be considered that morality may not be as universal an idea as its use in separating humans from other animals would suggest. For if moral codes are dictated by the environment (i.e. the society) then different environments will have different moral standards. What then truly defines morality? If it is the ability to distinguish against right and wrong, then any healthy human brain has the ability to distinguish between contradictory inputs. But whether these inputs are defined as right and wrong is a judgment left to the society that has generated the moral codes upon which the brain bases its decision. Different societies may therefore look at the moral decisions of another society and see immorality. Morality as a behavior cannot be solely defined as a process of the brain unless we qualify Dickinson's thesis of behavior with the statement that while brain equals behavior, the brain also equals environment plus biomechanics.


1) The American Heritage Dictionary of the English Language. Houghton Mifflin Company. Third Edition,1992.

2) Can Evolution Explain Morality?, A paper written for Macquarie University on morality and Darwinism.

3)Nucleus Accumben, The brain, showing neurological connection between the prefrontal cortex and the various components of the limbic system.

4)Working memory and executive function: evidence from neuroimaging., Paper for a neurobiology journal on the current opinions concerning the executive function.

5) Parts of the Brain and What they do, A Really good diagram of generalized brain centers from a BBC article.

6) Brain: The neurobiology of morals , A short review of an article that appeared in Nature Neuroscience – see next citation.

7) Impairment of social and moral behavior related to early damage in human prefrontal cortex., The article reviewed in the above citation – gives examples of interesting experiments with subjects with prefrontal cortex damage.

8) Social Cognitive Neuroscience: where are we heading?, A general influence, discusses current trends in societal neuroscience.

9) A Basis for Morality , A previous web report on morality – a jumping off point for my thoughts.

10) The Human Brain , Some interesting facts about different parts of the human brain.

Full Name:  Bethany Canver
Title:  Creating Disability
Date:  2006-02-20 22:50:46
Message Id:  18240
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

There exist innumerable ways in which the nervous system can be organized and these permutations are what give rise to the heterogeneity of humanity. Yet the manifestations of certain arrangements of the nervous system have been labeled "abnormal" by medical professionals whose pronouncements have resulted in the devaluation of individuals having these "abnormal" brains. Medicalization, or "the application of medical knowledge to an increasing range of social problems" (Barnes and Mercer 27), affords professionals the authority to ascribe value-laden labels to their patients which often justifies the oppression of those persons whose neuro-anatomy or function deviates from the medical norm. This medical norm provides the ideal to which persons deemed "abnormal" are often pressed to achieve by way of preventative and rehabilitative medicine. The invasive and intrusive presence of medical professionals in the lives of persons with, for example, cerebral palsy, has perpetuated the oppression of this group by the dominant, able-bodied population.

Because of the variability of clinical effects, severity, and causes, cerebral palsy which affects roughly 500,000 individuals in America, is broadly defined as a non-progressive condition resulting from a brain abnormality acquired during the early stages of life which affects motor function. Etiologically, the assumed causes of cerebral palsy can occur during either the prenatal, paranatal, or postnatal stages of development. Cerebral palsy is unique in that an etiological evaluation points not to a single, definite cause, but rather to a plethora of possibilities. During the prenatal stage, a family history of genetic disorders like Wilson's Disease1, Schilder's Disease2, or Lindau's Disease3 may cause cerebral palsy as might the mother's contraction of rubella while the fetus is in utero. In the paranatal stage, a particularly lengthy or abnormal labor during which the baby is breech, forceps are used, a Caesarean is preformed, or excessive hemorrhaging occurs have been pointed to as causes of brain damage that could manifest itself as cerebral palsy. An additional complication that might cause brain damage to occur during the birthing process is an untreated Rh/ABO incompatibility between mother and child. Prematurity and anoxia, or a lack of oxygen, occurring during the birth process can also be a possible cause of cerebral palsy. Anoxia causes cell damage in the cerebral cortex as well as brain lesions and atrophy of the cortex. After birth cerebral palsy can be acquired as the result of brain damage due to head trauma, an infection like meningitis, anoxia, or the ingestion of toxins. Traditionally anoxia has been thought of as the major cause of cerebral palsy, however it is difficult to definitively determine the etiological acquisition of cerebral palsy.
From a clinical perspective cerebral palsy is defined as either spastic or extrapyramidal. Spastic cerebral palsy, which results primarily from damage to either the pyramidal tract or the cerebral cortex, manifests itself as stiffness or tightness of muscles. It is the predominate form of cerebral palsy, affecting 70-80% of all diagnosed individuals. This effect to the muscles can affect one side of the body (hemiplegia), both legs (diplegia), or all four limbs, trunk, mouth, pharynx, and tongue (quadriplegia). Damage to the basal ganglia and/or the cerebellum results in extrapyramidal cerebral palsy which is clinically expressed in a more varied manner than spastic cerebral palsy. For example, these clinical expressions can be athetoic- slow, writhing of the upper extremities- or ataxic-disturbances in balance and depth perception. Brain damage, which may manifest itself as cerebral palsy, can be detected using magnetic resonance imaging (MRI), computed tomography (CT scan), or ultrasound.

The treatment of cerebral palsy is guided by the traditional view that it is first and foremost a "medical issue" (Barnes and Mercer 2). Once diagnosed, the lives of individuals with cerebral palsy become increasingly dominated by "specialists"4, primarily from the medical field, who aggressively pursue rehabilitative techniques and procedures5; these techniques include surgery, occupational and physical therapy, and medication. Ultimately they are attempts to alter the individual with cerebral palsy so that they more closely resemble and function like the prescribed anatomical and physiological norm held by doctors. The treatments that individuals with cerebral palsy receive are exercises in normalization which tend not to be rooted in actual medical necessity but rather cultural value (Barnes and Mercer 37-38). Medical professionals reinforce this idea that cerebral palsied bodies do not conform to the standards that constitute a "normal" human body by actively trying to prevent the births of cerebral palsied infants. A great deal of care is invested in preventative medicine and in the event that this approach fails a women who is carrying a child who is suspected of being cerebral palsy (or brain damaged in any way) is encouraged to consider terminating her pregnancy6. Not only does the "normalizing gaze of modern science" (Barnes and Mercer 30) aid the argument in support of eugenics but it also has spawned an extensive economic empire made up of health services, rehab, devices, therapies, drugs, insurance and technologies7. There are many who stand to lose in the economic realm if society begins to look at cerebral palsied bodies as an acceptable alternative that does not need alteration.

It is not problematic that doctors make distinctions and critical assessments of their patients. It is, however, problematic when there is "established a hierarchical standard for pronouncing some bodies and minds as abnormal and inferior in terms of appearance and performance" (Barnes and Mercer 20). The diagnosis of cerebral palsy is associated with a label which stands in direct opposition to the values that are revered in society. For cerebral palsied individuals their diagnosis often means that they will typically be perceived as, "unfortunate, useless, different, oppressed and sick" (Barnes and Mercer 9). The value attached to being labeled as disabled has a profound affect on the lives of those diagnosed with cerebral palsy. These individuals often undergo invasive surgery and various other medical procedures that can be painful and are followed by a lengthy recovery period, not to mention the discrimination and oppression they experience on a daily basis. People who are labeled as disabled by conditions like cerebral palsy are largely secluded from the rest of society into special education classrooms, group homes, and sheltered workshops8. Their access to education and employment is severely diminished compared with their able-bodied counterparts. Unfortunately, as Freidson asserts, "it is very difficult to remove a medical label" (Barnes and Mercer 4) because of the tremendous authority contemporary American society ascribes to science and medicine. Medical professionals are looked to for "facts" and "certainties" which, though they do not exist, often guide how the society behaves towards cerebral palsied individuals.

The argument being made is not that the medical profession is universally at fault for the oppression of the disabled nor is it aiming to diminish the importance of medicine in the lives of those with legitimate medical conditions that limit their pursuit of a certain standard of living. Rather the question that is being posed is whether or not cultural values are the true driving force behind diagnosis and treatment, specifically with regard to cerebral palsied individuals? Though it is fairly clear that the events that occurred during the early development of individuals with cerebral palsy altered their brains in ways that is manifest in their behavior, the connection between those clinical signs or behaviors that are associated with cerebral palsy and the brain is not as well understood as it might someday be. If Emily Dickenson is right and brain does in fact equal behavior, a more appropriate treatment of cerebral palsy involves the brains of the non-cerebral palsied- the able bodied- who can use their brains in order to change their behavior toward the disabled. Perhaps the most effective treatment of cerebral palsy involves getting the able-bodied to conceive of the disabled, not as pitiable tragedies in need of medical attention, but as examples of the variation that exist within humanity.

1. Hepatolenticular degeneration
2. Cerebral scleroses
3. Hemangioblastoma of Cerebellum and Retina
4. "The end result for disabled children and adults was a widening professional involvement in their lives" (Barnes and Mercer 28-29).
5. "The assumption here is that the individual body which is at fault can be treated largely by medical interventions and technologies" (Butler and Parr 3).
7. "Whatever the stated aims, their latent function has been to create and sustain large numbers of dependent and devalued people in order to secure employment for health and social care staff and profits for private companies (Wolfensberger 1989:37)" (Barnes and Mercer 37).
8. "People with impairments are subjected to wide-ranging processes of social exclusion" (Barnes and Mercer 10).
"Indeed, medical interventions such as surgery or 'mind-changing' medication remain acceptable ways of addressing disability- since the 'cause' is located in those with an impairment, rather than in the society or groups which discriminate against such individuals" (Barnes and Mercer 20).

Barnes, Colin and Geof Mercer. Disability: Key Concepts. Massachusetts: Polity Press, 2003.
Butler, Ruth and Hester Parr. "New geographies of illness, impairment and disability". Mind and Body Spaces. Ed. Ruth Butler and Hester Parr. New York, NY: Routledge, 1999. 1-24.

Crothers, Bronson M.D. and Richard S. Paine, M.D. The Natural History of Cerebral Palsy. Cambridge, MA: Harvard University Press, 1959.

Cruickshank, William M. and George M. Raus. Cerebral Palsy: Its Individual and Community Problems. NY: Syracuse University Press, 1955.

"Culture as Disability."

Dorn, Michael L. "The moral topography of intemperance." Mind and Body Spaces. Ed. Ruth Butler and Hester Parr. New York, NY: Routledge, 1999. 46-69.

Gleeson, Brendan. "Can technology overcome the disabling city?" and Body Spaces. Ed. Ruth Butler and Hester Parr. New York, NY: Routledge, 1999. 98-118.

Imrie, Rob. "The body, disability and Le Corbusier's conception of the radiant environment". Mind and Body Spaces. Ed. Ruth Butler and Hester Parr. New York, NY: Routledge, 1999. 25-45.

Obaray, Jabeen.

Park, Deborah Carter and John Radford. "Rhetoric and Place in the 'mental deficiency' asylum." Mind and Body Spaces. Ed. Ruth Butler and Hester Parr. New York, NY: Routledge, 1999. 70-97.

Full Name:  Marissa Patterson
Username:  mpatters
Title:  Wait, When Did you Become British? Foreign Accent Sydrome
Date:  2006-02-20 23:26:31
Message Id:  18242
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine suffering a terrible, debilitating stroke. You must relearn everything,
how to walk, how to dress yourself, and even more serious, how to speak. Your words
are slow at first, halting, but gradually over time they become stronger, more sure. And
yet there seems to be something different about them. Your friends and neighbors
question whether you've taken a long vacation or perhaps you grew up in some other
country. Your speech has taking the pattern unlike the language you've grown up
speaking and has transitioned to something different, as if your primary language was in
fact your second. This condition you have been struck with is known as "foreign accent
syndrome," and has lead to your sounding as if from some distant, unknown county.

The first recorded case of foreign accent syndrome involved a French patient in
the early 1900's who began speaking with an Alsatian accent (1). In 1941, the first extensively chronicled report of foreign accent syndrome occurred, when a woman in Norway suffered an intense brain injury after being hit by shrapnel. When she recovered, she had developed what appeared to be a strong German accent, leading those who had not known her prior to her accent to shun her (2). While the majority of cases appear to be caused by strokes, traumatic brain injury and even multiple sclerosis have been shown to cause foreign accent syndrome (7). Only about twenty cases of foreign accent syndrome have been recorded in scientific literature, with the majority of them being about English speakers who seem French, Slavic, Spanish, or English (2); however other languages have reported the same phenomena, for example, a native Japanese woman who began speaking in what appeared to be a Korean accent (3). New cases are being recorded as well, with two cases reported at the University of Oxford in 2002 (2) leading to a better understanding of the disease and the mechanism by which it occur.

It is important to emphasize that though these patients appear to have a foreign
accent, linguists and native speakers are not fooled, and observers are often confused. A
study in 1987 found that the same accent on an English speaker was perceived as Eastern
European, French, Dutch, or Scandanavian, and in 1992 an Australian patient was
thought of as having an Asian, Swedish, or German accent (5). For a patient who developed a Scottish accent after a stroke, researchers discovered that only a few vocal traits seemed Scottish, such as slurred diphthongs, while the rest of her speech patterns remained like that of her native British (2). What often happens is that brain injury causes the patient to lengthen syllables, mispronounce sounds, or alter the pitch of their voice, all of which combine to give the perception of a foreign accent (4).

This syndrome, however, is not a sort of compensation for or adaptation to a
stroke, but is rather a "manifestation of damage to underlying brain mechanisms involved
in speech production" (5). The patients are still able to observe the general rules of pronunciation for various world languages, just not those for their prior spoken language (5). This is in a direct contrast to those patients with other speech production problem such as Broca's aphasia (5). It is interesting to note that some scientists wish to specify that the accent acquired is a "generic" foreign accent because the characteristics of the language spoken occur as phonetic characteristics of natural "world" language but do not display the characteristics of any one particular language (5). It appears that many cases of foreign accent syndrome appear to resolve themselves over a period of two to three years (8), though some patients are left with long term affects from their stroke or brain injury.

Scientists are torn on the proposed location of stroke or brain injury that would
cause this condition to occur. Research recently done in Japan suggests that damage in
the left precentral gyrus (3), something that expands on research at Oxford, stating that "injuries deep within the left side of the brain" cause speech to appear to foreign (2). A detailed analysis of the syndrome undertaken at Brown remarks that lesions causing damage have all been less than 3 centimeters and have been located in the prerolandic motor cortex, the frontal motor association cortex, or the striatum, all in the left hemisphere (5). It has also been recently suggested that foreign accent syndrome could be caused by damage to the cerebellum, leading to a difficulty in the motor control of speech (6). Many scientists hesitate to conclude that a single location of damage can cause such a wide constellation of deficits, however (5). This uncertainty comes from the vast differences in speech patterns and changes seen in patients with foreign accent syndrome over time and place. It is certain, however, that the mechanism of foreign accent syndrome is distinct from that of Broca's aphasia, due to the distinctness of the symptoms of both disorders.

Foreign accent syndrome offers a series of interesting issues regarding the basis of language and the origins of speech. Unfortunately, the small number of cases and wide
variety of symptoms it has been extremely difficult thus far to isolate a specific
mechanism that would lead to such specific changes in language. It also raises questions
about the link between brain and behavior, how a small change in the brain can cause
such a seemingly specific change in perceived action. Hopefully more in-depth research
will continue to be done in this field, leading to better answers to these perplexing

WWW Resources
Of Central Florida Clinic Diagnoses Rare Foreign Accent Syndrome
, Science
Daily Article, Nov 19, 2003

2)"Researchers, Long Baffled by
'Foreign-Accent Syndrome,' Are Now Closer to Understanding the Disorder"
, Chronicle of Higher Education article, Nov 15 2002

3) Takayama K et al. "A case of foreign accent syndrome without aphasia caused by a lesion of the left precentral gyrus" Neurology. 1993 Jul;43(7):1361-3

4)"Stroke gives woman British accent", BBC health article, Nov 25 2003

5) Kurowski, K et al. "Foreign accent syndrome: a Reconsideration" Brain and
Languages (54) 1-25 1996

6) Marien P et al. "A role for the cerebellum in motor speech planning: Evidence from foreign accent syndrome" Clinical Neurology and Neurosurgery Jul 28

7) Bakker JI et al. "Foreign accent syndrome in a patient with multiple sclerosis" Canadian Journal of Neurological sciences 2004 May; 31(2):271-2.

8)"Woman has accent after stroke", Kansas City Star article, December 18, 2005

Full Name:  Andrea Goldstein
Title:  Combating Locked-In Syndrome: New Methods of Communication for ALS Patients
Date:  2006-02-20 23:27:27
Message Id:  18243
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine having a fully-functional brain trapped within a non-functioning body. The brain would be conscious and aware of its surroundings; it could think and process stimuli, but it would be unable to translate thought into action. Locked-In Syndrome is a rare disorder that results in just that; all of the body's voluntary muscles, with the exception of those that control eye movement, become completely paralyzed. There are no treatments available, nor is there a cure. (1) While Locked-In Syndrome is most commonly caused by damage to the pons (2), numerous other events or disorders can lead to this tragic locked-in state. Perhaps the most well-known disease that causes Locked-In Syndrome is Amyotrophic Lateral Sclerosis (ALS), known colloquially as Lou Gehrig's disease.

ALS is a progressive neurodegenerative disorder that causes the death of motor neurons. With no motor neurons to receive signals from the brain and cause movement, patients become completely paralyzed. After a period of no input from motor neurons, the muscles themselves atrophy and become weak. Finally, the brain loses the ability to start signals that cause voluntary movement altogether. Many ALS patients die from respiratory failure when their diaphragms and chest wall muscles fail to contract any longer. (3) The majority of ALS patients die within 3-5 years of diagnosis, but about 10% survive for ten years or more past their diagnosis, and 5% survive for twenty years after being diagnosed (4).

People are living longer with ALS due to several therapies. The newest treatment is a drug called riluzole, which reduces motor neuron damage by decreasing the release of glutamate, a neurotransmitter which may cause the degeneration of motor neurons in the first place. Riluzole has been clinically proven to prolong life for at least several months. Other treatments include speech and physical therapy and drugs that reduce symptoms that accompany ALS, such as fatigue, muscle spasms, and excess salivation. (3)

Because ALS destroys motor neurons, its effects are irreversible. Unlike the proportion of people with Locked-In Syndrome that eventually recover some motor function (2), ALS patients can never be freed from the prison of their minds. Despite the promising research being done to find more effective treatments and a cure, the more immediately pertinent research deals with how best to combat the imprisonment of the mind that comes with ALS. Most communication methods use eye movement to convey information, while some more experimental technologies use electrical impulses directly from the brain (5).

The simplest method of communication for ALS patients who are no longer able to move anything but their eyes involves no sophisticated technology at all. With the help of an assistant, patients can use eye blinks to signify which letters or syllables they would like to select from a chart, slowly and methodically putting together words and sentences. Eye response technologies are a more complicated method of communication that allows ALS patients to communicate significantly faster and independent of others. Eye-gaze Response Interface Computer Aid (ERICA), for example, uses a camera and infrared light to detect the position of a person's gaze on a computer screen. In this way, a person can essentially type with his or her eyes, performing computer tasks normally. In addition, the software that ERICA uses can produce a computerized voice, allowing the patient to "talk" to others. (6) This technology can provide a highly effective means of communication for as long as voluntary muscles in the eye remain intact.

In most cases, control of the eye muscles is retained throughout the span of ALS, but researchers are currently looking into devices that will allow ALS patients in advanced stages of the disease to communicate without using the eyes. In one method, an electrode is implanted directly into the brain. The electrode picks up electrical impulses and translates them into instructions for the control of a computer cursor, which in turn allows the patient to communicate via computer. Another method involves electrodes on the scalp that yield much the same result as the electrode in the brain itself. These devices take a relatively long amount of time to process information and create words (about 30 seconds per letter), but for patients whose eye movements are not under voluntary control, it is the only option. (5) Other experimental devices translate EEG activity to translate signals into words through biofeedback (7).

These new technologies give people with ALS hope for more normal lives. With more efficient communication technology, patients with ALS would no longer suffer from the most devastating mental effects of Locked-In Syndrome. Despite the fact that the motor neuron degeneration cannot currently be reversed, patients no longer have to remain imprisoned in their own minds. Eye response technologies and new experimental devices in the future can allow ALS patients to communicate effectively, freeing them from their personal jails. Perhaps this new technology that uses computers translating signals into speech will shed light on what "thoughts" really are and what produces speech. Further research can only lead to new ideas and more information about ALS and the Locked-In Syndrome that it produces.

1)Locked-In Syndrome Information Page, from the National Institute of Neurological Disorders and Stroke website
2)A clinical review of Locked-In Syndrome by Eimear Smith and Mark Delargy
3)Amyotrophic Lateral Sclerosis Fact Sheet, from the National Institute of Neurological Disorders and Stroke website
4) Facts You Should Know About ALS, from the ALS Association website
5) Unlocking Locked-In Syndrome, from the Society for Neuroscience website
6)Eye-gaze technology, from the University of Minnesota Duluth website
7)Biofeedback and Locked-In Syndrome in ALS, from the Futurehealth Inc. website

Full Name:  Julia Patzelt
Title:  Drug Addiction: Which Comes First- Brain or Behavior- and Does it Matter?
Date:  2006-02-20 23:29:13
Message Id:  18244
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

"Drug addiction is most often defined as a chronically relapsing disorder in which the addict experiences uncontrollable compulsion to take drugs, while simultaneously the repertoire of behaviors not related to drug seeking, taking, and recovery, declines dramatically."(1) Recent scientific research has shown significant causal relationships between drug addiction and genetic predisposition as well as between addiction and environmental factors. Both genetics and the environment influence the brain, which in turn effects the behavior of usage. Once an individual begins using psychotropic substances, such as cocaine or heroin, measurable changes in brain chemistry and physiology perpetuate the cycle of addiction. Thus, we have an example of brain affecting behavior, which in turn, affects the brain. This cycle is particularly extreme and insular in the situation of drug addiction where free will and decision making are quickly and severely impaired. In this paper, we will first explore the genetic and environmental theories on drug addiction. We will then investigate how the behavior of drug addiction changes the brain to perpetuate the circle of cause and effect between the brain and behavior.

Genetic Influences on the Behavior of Drug Addiction:
Addiction does not result from a single gene. However, multiple genetic trends have been identified as crucial contributors to the illness of addiction. Alcoholics and cocaine addicts often express the A1 allele of the dopamine receptor gene DRD2 and lack the serotonin receptor gene Htr1b. These genes both fit into the pleasure-response category, but there are numerous ways in which other genes affect an individual's response to drugs, from tolerance of the substance to the severity of withdrawal.(2) One must ask whether these genetic factors exist before the person's first experience with a drug or whether the genes are 'turned on' like a light switch upon first usage.(3) Can these predispositions be observed in other behaviors before the addiction is active? Addiction specialists refer to "addictive behavior" as a category much broader than the limited definition of actual usage, and many of these addictive behaviors can identified in an addict before they ever pick up the drug. Should we assume that those addictive behaviors are purely a direct result of genetic patterns, or can a person learn addictive behavior from their surroundings? Why does not the source of the behavior of drug use affect the prognosis of addiction?

Environmental Influences on the Behavior of Drug Addiction:
While addiction does seem to follow a genetic path in families, even when there is no contact between generations of addicts, a person's environment can contribute to their tendency towards addiction. Community characteristics such as access to education, income level, crime rates, and family dynamic can all affect if and when an individual begins usage. Regardless of these many factors, drug addiction affects all segments of society; the difference between Bel-Air and a Compton ghetto lies merely in the area's drug of choice and the visibility of usage/trafficking. Social risk factors are more difficult to isolate in research studies than specific neurobiological genes, but definitive patterns have emerged within environmental categories.(4) However, even a complete understanding of the relevant risk factors for addiction does not solve the entire equation. Addiction does not only concern the initial usage, but the continued/increased use of a substance and repeated relapse after temporary abstinence. Beyond the roles of genes and the environment in this pattern, a major contributor to continued use, and therefore to addiction, is the change in brain physiology caused by drug use.

Effects of Usage on Brain Physiology:
Pleasure responses in the brain are a type of reward pathway whereby activating dopamine receptors encourages repetition of the responsible behavior.(5) Drug addiction interferes with/over-activates this natural cycle by altering "neural function in such a way as to render the brain circuits mediating various behavioral effects of these drugs more, or less, responsive to those effects."(1) Several neurotransmitter and neuropeptide systems have been shown to disrupt brain circuits mediating mood, affecting the underlying addiction process. Beyond the effects on serotonin and norepinephrine levels, which in turn affect mood and the pleasure-response system, drugs also inhibit an individual's decision-making process, implying an inhibition of free will and a hindrance of the I-function. "The highest levels of human cognition, such as problem solving and complex decision making" are compromised by the addiction through the semi-permanent biochemical changes within the brain that encourage and sustain usage. "Drugs of abuse have a direct influence on the neuronal networks that underlie self-regulation."(6)

These biochemical changes are complicated in adolescent addicts where the physiology of the brain is affected (in addiction to the biochemical signaling pathways) and stunted by early drug use.(7) The frontal cortex, responsible for reasoning, personality, and self-esteem (arguably a component in adolescent drug use), physically matures during the teen years and becomes less oriented toward risk taking behavior during this time.(8) The normal maturation process is replaced by an imbalance between the reward-response pathway, which becomes overactive, and the logic area of the frontal cortex, which is overridden by the drug abuse.

Part of the Normal Development Process?:
Current neurobiological research on drug addiction assumes that addiction interferes with an individual's healthy psychological and mental development and lifestyle. But do the genetic patterns and biochemical changes during addiction necessarily indicate a flaw in the brain's evolutionary development, or do they represent a variation on normal neurochemistry?

Connecting the neuroscience of natural rewards to drug addiction explains the ability of addiction to progressively hijack the brain and prevent decisions that support an individual's survival, such as eating and sleeping. "Indeed, a recurring theme in modern addiction research is the extent to which neuroadaptations responsible for various aspects of the addiction process are similar to those responsible for other forms of neural plasticity studied in cellular models of learning, such as long-term potentiation and long-term depression."(1) Drugs do not replace components in the brain; they only alter them. If a brain's survival mode or natural state of being can be replaced with the pattern of addiction, can not addiction be an inherent part of neurochemical infrastructure?

Current research supports the theory that drug addiction is a result of combined genetic and environmental factors. The findings have led to a better understanding of why people begin and continue using, as well as the most effective forms of treatment.(9) From our current understanding, certain questions remain unanswered: 1.) Why do some people remain drug users/abusers while others fall prey to the illness of drug addiction? and 2.) Is addiction merely a significant standard deviation from 'normal' neurobiological function, or is it an example of evolutionary failure to protect the brain from chemical imbalance? These issues will be addressed in more depth in future web papers.

1)"A Behavioral/Systems Approach to the Neuroscience of Drug Addiction",The Journal of Neuroscience, May 1, 2002
2)"Drugs Alter the Brain's Reward Pathway",Genetics Science Learning Center at The University of Utah
3)"Trigger for Cocaine Addiction Found",Medline Plus
4)NIDA InfoFacts: Nationwide Trends,National Institute on Drug Abuse- The Science of Drug Abuse and Addiction
5)"Marijuana and Its Potential for Addiction",Serendip Web Paper from Neurobiology and Behavior Class, Bryn Mawr College, Spring 2005
6)"Cognitive Neuroscience & Drug Addiction: Primed for Interaction?",A Symposium at the Cognitive Neuroscience Society Meeting, San Fransisco, CA, April 9-11, 2000
7)"More People in Drug Abuse Treatment Began Drug Use Before Age 13",U.S. Dept. of Health and Human Services 2006 Press Release
8)"Genetics is an Important Factor in Addiction",Genetics Science Learning Center at The University of Utah
9)"Wellbutrin plus reward helps cocaine users cut back",Medline Plus

Full Name:  Caroline Troein
Title:  God on the Brain
Date:  2006-02-20 23:36:17
Message Id:  18245
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Rene Descartes imagined the human being as composed of two essential components: the material body and the immaterial soul. The Cartesian dualism of this situation creates many useful devices when thinking about spiritualism and the brain – after all, it is only the spirit of the body communicating with a higher power. When one dies, the soul can live on leaving its material housings. However, it presents a problem referred to as the Cartesian gap. Namely: how does the immaterial soul interact with the body? Where do the spirit and the corporeal interact?
Establishing the spiritual as part of the soul, observing a physical change would seem to correspond to the soul as having a material connection. This would not negate the existence of a soul. However, if the soul can establish a physical change in the body, it would be logical to assume that the soul if affected by the body. Yet if a connection exists, and a person experiences religious phenomena, the body would then be affected. If the reverse would be true, that the soul can be affected to perceive "god" because of stimulation of the body, the nature of religion and the relationship between religion and the mind would be thrown into question.
It is well known that ancient mystics used hallucinogenic drugs or volcanic vents to communicate with the gods or god (1). Indeed, even today, many religions rely on chemical means to communicate with gods or to enhance the experience. Yet this, to some, trivializes faith into a sensation and not a way of life. Yet if religion has a biological component,

This investigation is not trivial. According to New Scientist, "more than half of people report having had some sort of mystical or religious experience" (2) Wars are often fought over religion, and perception of religion has managed to become central to the political debate in the United States. However, in an increasingly secular world, a growing cadre of people is reporting no feeling of a higher power. These atheists and secular humanitists (3) are drastically different from agnostics because of their perception. Agonists still believe in a supernatural power while atheists and secular humanists do not.
If god is a component of the brain (4), such as a "God Module", then these differences may mean that we need to have a more liberal view of religion. Of course, religions can still operate within these confines. For instance, a Calvinist would claim that those not biologically favored to experience God are not members of the elect. Nevertheless, it casts doubt on the universality of any divinity.

A study by Andrew Newberg, a neuroscientist at the University of Pennsylvania, has shown that when experiencing deep religious connections, people seem to lose a sense of their "self". This is a sensation is not limited to ordinary people. "Einstein, with his feelings of humility, awe, and wonder and his sense of oneness with the universe, belongs with the great religious mystics." (5) In addition to this feeling, their brains undergo several physical changes.
It is important to note that the researchers could not replicate the intense religious experience that some people experience because it is difficult to replicate in the lab. Instead they looked at meditation and prayer, conditions which induce similar states, although less intense.
Primarily, part of the parietal lobe shuts down during mediation and prayer, during which the subjects reported that "It feels like a loss of boundary. It's as if the film of your life broke and you were seeing the light that allowed the film to be projected."(6) The left hemisphere of the parietal lobe maintains a sense of the individual's body image, while the right-hemisphere handles its context, or "the space and time inhabited by the self."(7) Newberg hypothesizes that with mediation, people learn to develop this feeling of oneness, and they cut off their perceptions of the outside world. In other words, to experience a religious event, the self-definition of the brain shuts down
The researchers also "found intense activity in the parts of the brain that regulate attention" (8). These parts are components of the brain's reticular activating system. It is comprised of nerves in many parts of the brain, including the thalamus, hypothalamus, brain stem, and cerebral cortex. This is consistent with the results and common sense: people must concentrate in order to meditate or pray. But it also implies that the people in the study have developed control over their experiences.
The implication is that people have a degree of choice, or can develop control, over their definition of self. But it also suggests that since there are biological differences in people, people have a natural different affinity towards religious experiences. This does not mean that some people are more religious than others: training and cultural aspects have a great affect on people.

There is a group of people who have little or no control over their religious experiences: a certain subset of people who are epileptic. These individuals provide evidence that limiting religious experience to the parietal lobes and attention is not simply enough.
Firstly, after experiencing a seizure, some epileptics reportedly felt a "religious experience" or "know why there is a cosmos." (9) In addition, some temporal lobe epileptics display hypergraphia – "writing large, complicated tomes, often of mystical or personally religious significance" – and decide to take part in a number of different religions.
In other cases, as a result of the "kindling", or "strengthening of neurophysical connections, often involving the limbic system," (10) some patients have responded with increased sensitivity to religious ideas and icons. Vilayanur S. Ramachandran (11), the researcher involved in these circumstances, believes that the brain become more sensitive to religious emotion, or that emotions experienced result in increased religious belief. The latter explanation would be in regards to individuals trying to explain their strange experiences through ideas available, namely religion.
Many times, those who suffer limbic system epileptic seizures, or seizures of the temporal lobes, report religious experiences. Jeffery Saver, a neurologist from UCLA, says that "This is similar to people undergoing religious conversion, who have a sense of seeing through their hollow selves or superficial reality to a deeper reality."
Other research supports the role of the limbic system. Jeffery Saver explains why it is so difficult to convey these religious experiences. "That the temporolimbic system is stamping these moments as being intensely important to the individual, as being characterized by great joy and harmony. When the experience is reported to someone else, only the contents and the sense that it's different can be communicated. The visceral sensation can't."

Faith is, by definition, unable to be proved. It is "the substance of things hoped for, the evidence of things unseen."(12) It is could be proved, then there is no need for faith to exist. Finding a material correspondence for spiritual activities does not make them any less real to the perceiver, but it does make the experience more deeply rooted in the material world.
Finding religion as a biological component in the brain does not negate the role of religion in society. More than simply an opiate for the masses, religion helps form and maintain social bonds. However, recognizing its biological roots is important to understanding differences between people's religious experiences. As much as homosexuality is now accepted as a biological difference, hopefully religion can be seen for its biological nature.

Web Sources
1)Delphic Oracle's Lips May Have Been Loosened by Gas Vapors, Example of how mystics used drugs in various forms to stimulate a religious experience
2)In Search of God, New Scientist article on God in the brain
3)Wikipedia of Secular Humanism
4)God in the Brain, collection of articles on God's relationship in the brain
5)Einstein's Religious Views, for more information about the values and morals of Einstein
6)In Search of God
7)God in the Brain
8)In Search of God
9)God in the Brain
10)God in the Brain
11)Vilayanur S. Ramachandran, Page about the researcher
12)Hebrews 11.1, (King James Version)

Full Name:  Rebecca Woodruff
Title:  Glial-Neuron Connections
Date:  2006-02-20 23:40:41
Message Id:  18246
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Advancements in the field of neuroscience within the past decade call the traditional models of brain structure and function into question. With an increased desire to uncover the origin of behavior, many neurobiologists have recently become interested in understanding how brain structure correlates to observable behavior. However, one troublesome observation has repeatedly surfaced. It appears that the brain has the interesting ability to change its structure based on environmental factors. This observation has an array of implications for the previously accepted notion that the structure of the brain directly influences and controls behavior. This observation shakes the foundations of neurobiology, as it calls into question one of its major tenants: that structure unequivocally equals function. What structure within the brain allows for this continual variance? How is this mechanism regulated? What inspires such structural change within one organism?

Brain plasticity is the term given to describing the phenomenon that the nervous system can change structurally, and perhaps functionally, in response to external stimuli. This broad term encompasses many changes that take place among both neurons and glial cells, the two classes of cells present in the nervous system. While much of neurobiology focuses on the interrelationship between sensory neurons, interneurons, and motor neurons, the significance of the glia, the cells that support these communication pathways, often gets neglected. Interestingly, it appears that many of the changes that were once attributed to neurons only are actually taking place in the glia (1). However, due to the enormous increase in research concerning brain plasticity within the past few decades, the role of these vital cells is coming to light.

Perhaps the main reason why glial cells have been written off for such a long time has been their inability to propagate an action potential or transmit any kind of chemical signal. In fact, of the five most common glial cells, only two are involved in any kind of support that isn't physical or housekeeping in nature (2). However, one glial cell, the astrocyte, appears to play a much more active role in the regulation of intercellular communication through the tight regulation of blood flow to each neuron (3). This regulation, also known as the blood-brain barrier (3), is so significant because neuronal communication depends directly on ions and hormones present in the circulatory system. The significance of the role that these astrocytes play can be clearly seen in a Stanford study concerning the ability and efficiency of the functioning of neurons and glia when separate versus when allowed to interact. The findings of the study indicate that while both cells perform their respective functions without each other, they perform then much more efficiently when allowed to interact (4). Because of the wide range of functions that the glial cells must perform in order to keep the nervous system in good shape, it's no wonder that they outnumber neurons by as much ten to one (5).

Due to the dependent nature of neuron and glial cells, much of the research originally aimed at uncovering the mechanisms behind brain plasticity have shed light on the role of glia within the brain. While brain plasticity usually refers to the change of location of the synapses between neurons, glial cells are also largely affected by environmental stimuli. William Greenough led the research in this field in the 1970s when he observed that not only can synapses have the capacity to change well after the developmental period of the brain, but that various glia also have such a capacity (1). Building on Greenough's work, Bryan Kolb and Ian Whishaw's experiments concerning brain plasticity in rats as a result of the level of daily stimulus reveals many more dimensions of the neuron-glia interdependence (1). When the visual field of the rats were stimulated for a period of sixty days, the researchers reported at 20% increase in dendritic fields, which correlates with a substantial increase in glial cells and associated blood supplies (1). The researchers repeated this experiment while manipulating the source of variation from visual stimulus to physical stimulus, to aural stimulus, and each time observed similar findings: that the glial cells of the brain play an important role in maintaining the integrity of the newly formed synapses that result from environmental stimuli (1). Given the close association between the astrocytes and the neurons of the nervous system, it makes perfect sense that as new synapses form, and thus as information gets rerouted within the brain, that the supportive elements of the brain must follow suit to keep up with the ever changing needs of the nervous system.

The research presented thus far indicates that perhaps, even though the importance of the role of glial cells has surfaced much more than in the past, that they are still an essential, yet underrated group of cells within the nervous system. In particular, it seems quite plausible that an important facet of the structure-function argument is lacking without the inclusion of the "higher end" glial cells, such as astrocytes and radial glia. The remarkable functions that these cells provide, be it from the astrocyte's regulation of what essential materials get to the neurons, or the radial glia's guiding function, raise the question, which is higher in function, neuron or glia? In our current classification system of the brain, should glia belong to a box of their own, or should they be included, side by side, with the neurons whose function is so dependent on their presence? Furthermore, considering the importance of the glia's role, and because glia, unlike neurons, are able to divide, what kind of a role could stem cell research someday play in the prevention and treatment of various devastating diseases that result from damaged to the glia, such as Multiple Sclerosis and Alzheimer's Disease? Ultimately, the most important question raised by the observations made concerning the role of glia in the nervous system is a simple one. What is our discussion lacking by not incorporating these vital cells as a focus similar to that of the neuron?

1)"Brain Plasticity and Behavior"

2)"Glia: The Forgotten Brain Cell"

3)Campbell, Neil A. et at. Biology. New York: Pearson, 2005

4)"Lowly Glia Strengthen Brain Connection"


Full Name:  Suzanne Landi
Title:  The Truth About Lying
Date:  2006-02-20 23:56:42
Message Id:  18249
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Shakespeare once said "Oh, what a tangled web we weave / When first we practice to deceive", but it is doubtful that he understood how this relates to neurobiology. A lie can begin a chain of reactions that can wraps up an entire society, but what kind of tangled web exists in the mind of the liar? If we assert that the brain equals behavior, there must be something about lying that changes in the brain because it is not an automatic behavior. Where is there brain activity for lying, and why should the government take notice?

There are different types of lies that we are capable of expressing. One of the more subtle types are lies of omission For example, you meet your best friend and her sister for lunch, and you can't help but notice that her sister has a very strange habit that annoys you. When you talk about the lunch later but don't mention her sister's annoying habit, you're omitting an important piece of the puzzle, and that is considered a lie. A lie of commission is the daily placating statement of "Just what I needed!" when you receive a useless present, or the automatic "Fine" response to "How are you?" These everyday lies generally aren't malicious enough to merit a polygraph test, and leaves the question of whether or not these statements look the same in the brain as lies that threaten a marriage or National Security. (1)

Myths that surround lies mostly concern the definition of a "liar". It is assumed that when a person lies, there is a physiological change in their demeanor. Specifically, a liar may squirm, sweat, or fidget. Strangely there are assumptions of just the opposite – that a liar will hold very still and make direct eye contact. Everyday we lie, and we do it well, whether we lie to a jury of our peers or simply tell a friend that their hair looks nice when we think the contrary. If we started to sweat and fidget every time we faked a compliment, our relationships would quickly be sabotaged. (1)

This is the reason why the polygraph machine method of lie detection is so inaccurate and outdated. The polygraph's purpose is to measure the physiological characteristics that come with lying, as previously mentioned. According to the American Polygraph Association, they test the sweat glands and cardiovascular activity of the subject, but deny that voice stress testing is accurate. (2)
However there have been various neurological tests using a functional-MRI scanner that are simply better. Lying requires a change in behavior, and therefore the brain as well. Assumed signs of a liar can be easily trained away, especially in cases of important secrets regarding National Security. Very few people can identify a liar just based on sight, and the polygraph machine would identify extreme anxiety as lying. (1)

One of these experiments using functional-MRIs is conceived by Daniel Langleben of the University of Pennsylvania. The scan measures how much oxygen is being used in the brain and this information can be plotted, in essence, on an anatomical brain map to demonstrate what part of the brain is activated during a particular task. The experiment requires participants to holds a playing card in their pockets, specifically the five of clubs, while answering yes-no questions about which card they are holding. A screen shows pictures of playing cards and the subject selects "yes" if they have it and "no" if they do not. When the five of clubs is shown, they are required to answer "no", which is a lie. Langleben admits that this doesn't provide a map of where deception takes place, but it does suggest an increase of activity in places like the anterior cingulate cortex and the superior frontal gyrus. Additionally, the prefrontal cortex has an increase in activity, which is the reasoning part of the brain. (3)

With some revisions to his experiment, Langleben notices some activity in the parietal cortex, which is activated during physical stress changes like goosebumps and sweating. This connection to sweating may indicate a link to the polygraph, but it is purely coincidental. The inventors of the polygraph didn't intend that someday this connection would be made, but it gives us some hope for the machine. After all, there's a chance that the first-time criminals and liars that police departments are trying to catch will react to the polygraph. But the functional-MRIs take place in an environment so unnatural that it is only worthy of detecting secrets of national security, or proving the innocence of a death-row inmate. (1)
One other method of lie detection used in the wake of September 11th is called "brain fingerprinting". These tests are EEG-based, and measures the information stored in our brains. It functions by showing a list of words to a person, and then recognized words show a different neural pattern than new ones. This makes the assumption that we store guilty knowledge in our brain. It's not the same as detecting deception, but it may be even more useful to the government in its counterterrorism efforts – that is, if they can get cooperation. As mentioned above, these studies take place in such an unnatural setting that other thoughts could take over the brain. The anxiety associated with interrogation decreases polygraph efficiency, and we can't expect much better results with these tests. But in the spirit of the scientific method, there's no reason to stop trying. (4)

Locating where deception takes place should spark interest in the government's counterterrorism and justice efforts. If you're an innocent citizen waiting for execution or wrongly accused at the airport, it's unlikely that even in strange conditions you will lie. However, it leaves us with even more questions, specifically about truth. Obviously these tests are showing a more complex process for lying, but there are some questions that have no set truth, but rather an individual belief – do these beliefs require activation of less neurons than telling the truth or lying? We may never know answers to our questions that cross philosophy with physiology because the search for lies is so invasive among people who value privacy and free will.

WWW Sources

1) Henig, Robin Marantz. "Looking for the Lie". 05 February 2006. New York Times.
Note: article now only available to New York Times subscribers.
2)"> The American Polygraph Association FAQ, on the American Polygraph Association official website
3) Tran, Trinh. "Truth and deception— the brain tells all". 11 April 2002. The Penn Current.
4) Moenssens, Andre. "'Brain Fingerprinting' – Is It A Reliable Tool?". 02 July 2000.

Full Name:  Ebony Dix
Title:  In Every Element of Genius, Is There an Element of Madness?
Date:  2006-02-21 00:17:49
Message Id:  18250
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The hypothesis that genius and madness are related has been in existence for centuries. Aristotle once claimed that "there is no great genius without a mixture of madness" (1). Many of his contemporaries as well as psychoanalysts, psychiatrists, and psychologists today agree with his statement and have argued that genius and madness are indeed linked to underlying degenerative neurological disorders (2). This paper will discuss some findings that aim to verify the relationship between genius and madness and it will encourage the reader to make his or her own assessments and conclusions about the issue. This paper will also encourage its readers to posit new theories that support or refute the idea that a relationship between genius and madness exists.

While scientific evidence to support this idea is scarce and flawed, recent findings suggest that there may have been some truth behind Aristotle's claim. Historical research has found that the rate and intensity of psychopathological symptoms appear to be higher among creative individuals (2). Compilations of psychiatric research have concluded that there is a higher incidence rate and intensity of mental illness symptoms associated with individuals who possess artistic creativity. It is clear that some of the data collected illustrates a trend and does not imply correlation or causation between genius and madness with any statistical significance.

Psychometric research presented by the American Journal of Psychiatry has obtained empirical evidence that intends to prove the correlation between creative individuals and the occurrence of psychopathological symptoms. In the 1950s and 1960s, tests such as the Minnesota Multiphasic Personality Inventory (MMPI) and the Eysenck Personality Questionnaire (EPQ) were performed on several subjects and the results showed that those with higher levels of creative ability scored higher on these tests. While this suggests that genius and madness may be closely connected, it does not prove that genius and madness are one in the same. Theoretical interpretations imply that because creativity requires the cognitive ability to explore novel and sometimes unconventional ideas, it also requires the creative individual to be capable of defocusing attention, divergent thinking, and nonconformity (3). As a consequence, creative individuals or those who are dubbed geniuses, may exhibit symptoms that are often associated with mental illness. The frequency and intensity of these symptoms will vary according to the magnitude and domain of creative achievements (2).

Another study, presented by researchers at the Stanford University Medical Center in 2002, involved the administration of personality, temperament, and creativity tests to students studying creative or fine arts, design, and mechanical engineering. The test results showed that individuals in the control group and recovered manic depressives were more likely to be moody and neurotic than the healthy control. Moodiness and neuroticism were part of a group of characteristics these researchers used to identify mild, non-clinical forms of depression and bipolar disorder (5).

The Stanford University study paved the way for psychiatric researchers looking to solve the genius/madness paradox that has seemingly been observed in some of the greatest artists and thinkers who thrived over the last three centuries. For instance, John Nash, a renowned economist and mathematical genius, received a noble prize in 1994 for his contributions to the field of game theory, despite a long, arduous bout of schizophrenia. Edgar Allen Poe and Emily Dickenson were both 19th century poets, who were thought to have suffered from bipolar disorder. Edgar Allen Poe once wrote: "Men have called me mad, but the question is not yet settled whether madness is or is not the loftiest intelligence..." (4). Is it a coincidence that these intelligent individuals just happened to suffer from mental illness, or were their talents linked to their illnesses as some doctors and scientists claim?

Further studies published by the American Journal of Psychiatry have suggested that creativity and mental illness run in the same family (2). The genetic basis for most mental illnesses has been found to be only a partial factor, and while the topic is still controversial, most scientific and medical communities agree that one's vulnerability to mental illness is due to the combined effects of genetic and non-genetic factors (3). If creativity and mental illness run in the same family, then it may be reasonable to conclude that creativity, like mental illness, depends on both genetic and non-genetic factors. One's exposure to an intellectual and cultural environment that is neutral with respect to psychopathology can in turn increase the likelihood of one to exhibit the behaviors of a genius.

With that said, it seems to be reasonable to conclude that there is an element of madness present in some cases of genius, but the exact biological basis for this connection is unknown. To what extent is statistically significant data available to link the genetic defects that predispose an individual to exhibiting the traits of a genius and the traits of a madman? This has yet to be determined.


1)Brainy Quote website,a resource with many quotes from famous people
2)Psychiatric Times,an article from June 2005, Vol. XXII, Issue 7 that discusses whether genius and madness are related
3) search under bipolar,a Website that gives some basic information about bipolar disorder
4) site,resource that publishes informational articles on various topics in medicine
5)mednews site at Stanford University,resource describes a study done in 2002 relating to creativity and mental illness

Full Name:  Ebony Dix
Title:  In Every Element of Genius, Is There an Element of Madness?
Date:  2006-02-21 00:22:22
Message Id:  18251
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The hypothesis that genius and madness are related has been in existence for centuries. Aristotle once claimed that "there is no great genius without a mixture of madness" (1). Many of his contemporaries as well as psychoanalysts, psychiatrists, and psychologists today agree with his statement and have argued that genius and madness are indeed linked to underlying degenerative neurological disorders (2). This paper will discuss some findings that aim to verify the relationship between genius and madness and it will encourage the reader to make his or her own assessments and conclusions about the issue. This paper will also encourage its readers to posit new theories that support or refute the idea that a relationship between genius and madness exists.

While scientific evidence to support this idea is scarce and flawed, recent findings suggest that there may have been some truth behind Aristotle's claim. Historical research has found that the rate and intensity of psychopathological symptoms appear to be higher among creative individuals (2). Compilations of psychiatric research have concluded that there is a higher incidence rate and intensity of mental illness symptoms associated with individuals who possess artistic creativity. It is clear that some of the data collected illustrates a trend and does not imply correlation or causation between genius and madness with any statistical significance.

Psychometric research presented by the American Journal of Psychiatry has obtained empirical evidence that intends to prove the correlation between creative individuals and the occurrence of psychopathological symptoms. In the 1950s and 1960s, tests such as the Minnesota Multiphasic Personality Inventory (MMPI) and the Eysenck Personality Questionnaire (EPQ) were performed on several subjects and the results showed that those with higher levels of creative ability scored higher on these tests. While this suggests that genius and madness may be closely connected, it does not prove that genius and madness are one in the same. Theoretical interpretations imply that because creativity requires the cognitive ability to explore novel and sometimes unconventional ideas, it also requires the creative individual to be capable of defocusing attention, divergent thinking, and nonconformity (3). As a consequence, creative individuals or those who are dubbed geniuses, may exhibit symptoms that are often associated with mental illness. The frequency and intensity of these symptoms will vary according to the magnitude and domain of creative achievements (2).

Another study, presented by researchers at the Stanford University Medical Center in 2002, involved the administration of personality, temperament, and creativity tests to students studying creative or fine arts, design, and mechanical engineering. The test results showed that individuals in the control group and recovered manic depressives were more likely to be moody and neurotic than the healthy control. Moodiness and neuroticism were part of a group of characteristics these researchers used to identify mild, non-clinical forms of depression and bipolar disorder (5).

The Stanford University study paved the way for psychiatric researchers looking to solve the genius/madness paradox that has seemingly been observed in some of the greatest artists and thinkers who thrived over the last three centuries. For instance, John Nash, a renowned economist and mathematical genius, received a noble prize in 1994 for his contributions to the field of game theory, despite a long, arduous bout of schizophrenia. Edgar Allen Poe and Emily Dickenson were both 19th century poets, who were thought to have suffered from bipolar disorder. Edgar Allen Poe once wrote: "Men have called me mad, but the question is not yet settled whether madness is or is not the loftiest intelligence..." (4). Is it a coincidence that these intelligent individuals just happened to suffer from mental illness, or were their talents linked to their illnesses as some doctors and scientists claim?

Further studies published by the American Journal of Psychiatry have suggested that creativity and mental illness run in the same family (2). The genetic basis for most mental illnesses has been found to be only a partial factor, and while the topic is still controversial, most scientific and medical communities agree that one's vulnerability to mental illness is due to the combined effects of genetic and non-genetic factors (3). If creativity and mental illness run in the same family, then it may be reasonable to conclude that creativity, like mental illness, depends on both genetic and non-genetic factors. One's exposure to an intellectual and cultural environment that is neutral with respect to psychopathology can in turn increase the likelihood of one to exhibit the behaviors of a genius.

With that said, it seems to be reasonable to conclude that there is an element of madness present in some cases of genius, but the exact biological basis for this connection is unknown. To what extent is statistically significant data available to link the genetic defects that predispose an individual to exhibiting the traits of a genius and the traits of a madman? This has yet to be determined.


1)Brainy Quote website,a resource with many quotes from famous people
2)Psychiatric Times,an article from June 2005, Vol. XXII, Issue 7 that discusses whether genius and madness are related
3) search under bipolar,a Website that gives some basic information about bipolar disorder
4) site,resource that publishes informational articles on various topics in medicine
5)mednews site at Stanford University,resource describes a study done in 2002 relating to creativity and mental illness

Full Name:  Tamara Tomasic
Title:  Personality: Nature vs. Nurture or something in between?
Date:  2006-02-21 00:54:46
Message Id:  18253
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Everyone has a unique personality, a way of experiencing the world and participating in it that is all their own. But is it really? Are our personalities truly unique, or are there others (perhaps thousands of others) with the same personalities as ours? And how is personality determined? Many ways have been proposed in different periods in history and even today. These different propositions can be placed into three categories: personality is caused/influenced by the environment; personality is inherent in our genetic make-up; personality is a mix of both genetic and environmental influences.

In earliest times the most common explanations proposed for personality were dependant on environmental/exogenous factors, such as the day of one's birth or the "demons" that surrounded us in this world. Today still there are those who firmly believe in things such as astrology and that the time and day of your birth will determine your personality. The Greek zodiac is still in use, and (more seriously) Chinese astrology.

In Chinese astrology, entire birth charts are organized in order to determine which signs will hold their influence over an individual in the coming year, and elemental theory is employed to do the same ((1)). In the Greek zodiac birth charts are used as well, but the continued influence of the stars does not change throughout one's life: it is determined by their arrangement at the date and time of one's birth. Numerous websites and books exist where one can look up a "unique" horoscope for the day that one was born; however, these "unique" horoscopes are the same for all those who happen to be born on the same day, sometimes even at the same time. These two astrological theories produce blanket personalities, a one-size-fits-all approach to personality determination.

If personality were determined solely by environmental factors, then it makes sense to think of personalities are only coming in a specified number and applying to more than one person. However, upon closer examination of people it is found that personalities are not the same, even for people born on the same day (example: twins) in the same circumstances, thus disproving the blanket theory that environment is the sole determinant of personality. Another point in favor of a non-environmental approach are siblings and the differences in their personalities. Born to the same parents and raised in the same environment, siblings will still exhibit very unique personalities, different not only from each other but from their parents as well.

Another theory is one of genetics: that personality is passed down from parent to child, or that persons who exhibit similar characteristics will exhibit similar personalities. This theory is the basis behind Japanese thought that personality can be determined by one's blood type ((2)). This process, called "blood-typing" ((3)), is sometimes still used in Japan today for hiring practices and divisions of work in a company. In surveys of Japanese college students, 48% said "blood types make personality 'extremely different' or 'considerably different'" while 96% in another study said "blood types 'have much to do with' or 'have something to do with' personality" ((3)).

Another example of the genetic theory is that of inherited personality disorders, which constitute a type of personality in themselves. If personality disorders are inheritable, why not personality in general, or at least a higher predisposition to a personality? If depression and borderline personalities/predispositions can be inherited, why not a predisposition to a cheerful and outgoing personality? In this argument we would see identical twins with the same personalities, or very similar ones resulting from identical predispositions. This, however, is not generally the case, and there are always some variations that cannot be accounted for by genetics alone, as well as some similarities that cannot be accounted for by random acts of environmental effects.

This is where the third category comes in, a mixture of both genetic and environmental factors. If personality predisposition can be inherited, as is shown in the inheritance pattern of personality disorders ((4)), then ordered personality might be inheritable as well. The inheritance piece itself, however, is not enough. Environmental stressors/influences are what causes the predisposition to develop into a disorder/personality. Here is a study that was done with ASPD (antisocial personality disorder) inheritability in adopted children whose biological and adoptive fathers either did or did not have ASPD ((4)). The study showed:
24% of sons developed ASPD if both biological and adoptive father had ASPD
20% developed ASPD if biological father had it and adoptive father didn't
14% developed ASPD if biological father didn't have it and adoptive father did
13% developed ASPD if neither biological nor adoptive father had it
This study is a great example of how inheritance itself is not enough (the difference between those not predisposed but raised in an ASPD environment and those not predisposed and not raised in an ASPD environment is insignificant), nor is environment the only cause of the disorder (there is not a significant difference in the numbers for the sons who were "predisposed" but raised in a non ASPD environment and those who were predisposed and raised in an ASPD environment). We could then conclude that both the genetic predisposition and the environment play a role in the development of the disorder, and apply this theory to personality. This accounts also for the differences in personality of genetically identical twins, and siblings raised in the same environment born of the same parents.

Personality is difficult to determine, especially because there is not concrete place where it is stored or created; no one can really find the "personality center" of a living being. But the evidence collected from observation and careful study can lead us to believe that there is no one method by which personality acquisition and differences can be explained; only by a mix of internal and external factors, predisposed and random can personality be formed.


1)Year 2000 of Chinese Golden Dragon Year

2)Personality Traits by Blood Type: A Japanese Perspective

3)Special Topic: "Blood Typing" is Still Popular in Japan

4) Butcher, James N., Jill M. Hooley, Susan Mineka. Abnormal Psychology, 12th edition. Pearson: Boston, 1994. 372-376.

Full Name:  Nicolette Belletier
Title:  Theories for Understanding and Treating Autism
Date:  2006-02-21 02:01:14
Message Id:  18255
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

It is clear that no two people have the same behavior. This difference in behavior can be attributed to differences in brain structure. We as humans feel the need to categorize people and in doing so, we must categorize brains. Most of us feel comfortable defining male and female people. After all, students at Bryn Mawr must feel comfortable identifying themselves as women. However, we are perhaps more uncomfortable defining a "male brain" from a "female brain." Similarly, it may seem simple to categorize a person as having a mental illness compared with someone with a "normal" brain. However, upon exploring what qualities make up the definition of a mental disorder, boundaries are no longer clear. A case that is specifically interesting to me is autism. It is considered a mental illness, but symptoms can vary greatly from case to case. As the rate of diagnoses of autism consistently increases, its causes remain unknown and the search for a possible cure has created many, often controversial theories.

Perhaps behaviors linked with autism are simply attributed to the extreme variations in brain structure that is present among all humans. However, there is a level of consistency of symptoms among those diagnosed as autistic and the numbers of children diagnosed is rising. In the 1980's, 1 in every 10,000 births were diagnosed with autism compared with 1 in 166 births in 2003 (1). Although some of this increase may be due to higher awareness of the disorder, this theory does not account for a 500% increase in diagnoses. Such an increase has spurred a great deal of research on the topic. Still, there is little understanding of what causes the condition.

Autism is believed to be caused, at least partially, by genetic factors. One study has explored the possibility that a gene that codes for a peptide hormone which was shown to prolong the life of neurons in rats may have a premature stop codon in people with autism (2). In general, the autistic brain is found to have noticeable differences from a "normal" brain including increased brain volume. However, it is unclear what genes are responsible for these differences, especially since there must be a large number of genes coding for the structures of the brain. The probable multigenic quality of autism accounts for the wide range of severity of symptoms (3).

In light of the fact that autism is manifested in many different forms, patients are diagnosed with an "Autistic Spectrum Disorder". These disorders are grouped together because each fundamentally deals with problems communicating socially. Some people with autism may not be able to communicate verbally while others have no verbal language difficulty but cannot process social cues like body language (4). Though diagnoses of ASD show similarities with classical autism, there remains difficulty in categorizing people under an umbrella term.

Specifically, education of children with Autistic Spectrum Disorders requires understanding of individual children beyond a diagnosis. For example, children diagnosed with autism are not necessarily mentally retarded and when faced with problems in school my simply need a different learning approach than students in the mainstream in order to excel. Autistic people typically exhibit interest in detail, so when other students or a teacher are not interested in that level of detail, the autistic student can be frustrated (4). Likewise, a student with a milder form of autism who has an above average IQ and is "high-functioning" but is having trouble in school may need accommodations in order to carry out his or her potential. However, there is question if children with autistic disorders can receive the education they need in an environment with "normal" children.

Autistic people are considered to be unable to empathize or have trouble empathizing with other people, depending on the severity of the case along the spectrum (5). Instead, they are thought to have strong "systemizing" tendencies. It is these tendencies that contribute to an obsession with details and even rituals. Absorption in a specific interest therefore isolates the person from others and prevents him from understanding social situations. When other children cannot understand why an autistic peer does something insensitive, the autistic child can become even more isolated.

Among information about brain differences between autistic people and non-autistic people is that in those with autism, dendrites are shed around the onset of symptoms therefore losing connections between neurons (6). This supports new information regarding "mirror neurons". These specific types of neurons are responsible for the brain being able to understand what other people are doing. For example, when a person watches someone else wave his hand, mirror neurons fire in the observer's brain as if to make his own hand wave. With this information in mind, it is believed that autism could be caused by "broken" mirror neurons (7). Without the ability to process social languages due to a lack of certain brain structures, autistic people must learn to imitate others and abide by social norms. Because behavioral training and schools particularly tailored for autistic students have had success in teaching social skills, it seems that environment can override deficits in brain structure.

Some theorize that autism is the manifestation of the "extreme male brain" (5). This argument states that women are more likely than men to empathize, or put themselves into another person's shoes and less likely to "systemize" by making schedules and routines, for example. Males are more likely to do the opposite, therefore those with autism exhibit qualities of the male brain to an extreme. This is interesting because autism is far more prevalent among males (9). As we see when autistic children are taught to recognize social cues, it seems that culture can affect the brain therefore altering male and female brains and causing them to reflect the differences society imposes upon them. However, evidence shows that much of these differences are apparent even at very young ages when it would seem that culture has not yet had a chance to effect children. For example, at 12 months of age, girls show more eye contact than boys, reflecting more of an affinity for social connection. Another example is that when a female rat is injected with testosterone it can travel through a maze more easily than a female rat without injected testosterone (5). Females with autism exhibit the same tendencies as males. With this theory in mind there must be something that causes a female person's brain to become more "male." Differences between the male and female brain add some understanding to the roots of autism. Still, it is unknown exactly how brain structures cause these extreme systemizing tendencies.

Although autism is believed to be strongly linked to genes, it is also believed that outside factors may be linked as well (10).One controversial theory is that the presence of the preservative thimerosal in vaccines administered to infants is responsible for the recent and dramatic increase in cases of autism. The preservative contains levels of ethyl mercury, which can cause brain damage. However, health officials deny that the levels present in childhood vaccines can cause autism (1).The World Health Organization performed a study which showed that autism rates in Denmark rose after the preservative was removed from vaccines and a CDC report claimed that there was no difference in cases of autism among children with varied exposure to the preservative (1). However, a recent study has shown that thimerosal affected production of a necessary enzyme (11). Use of gold salts has had some success in removal of mercury, although researchers are hesitant to test on children with autism (12).

Another theory is that childhood infections may be connected with autism in addition to other mental disorders (13). These infections affect the brain causing mental symptoms. If this theory were true, preventative treatment could be administered. Also, antibiotics have been found to be a possible treatment for autism by affecting how transcription of a possibly mutated gene (2). However, these theories remain controversial.

The cause or causes of autism remain mysterious. Although genetic components are certainly partially responsible, it remains unknown exactly what brain structures are responsible for expression of autistic behavioral traits. However, it is clear that there must be a number of genetic components to account for the wide range of possible expressions of Autistic Spectrum Disorders. Environmental factors are understood just as poorly. Even though a cure for autism may never be attained, hopefully research will lead to a better understanding of the many forms the disorder can take and therefore improve education for those with ASD as well as raise public awareness as more and more children are born with autism.

WWW Sources

1) "On Autism's Cause, It's Parents vs. Research" , New York Times

2) "Aminoglycoside antibiotics and autism: a speculative hypothesis"

3), "A question of balance: a proposal for new mouse models of autism"

4) "Autistic Spectrum Disorders: Sorting Out Autism, Asperger's Syndrome and Other Conditions"

5) "They Just Can't Help It" , Information on the male and female brains

6) "Autism"

a name="7">7) "Cells That Read Minds" , New York Times

8) "As Autistic Children Grow So Does Social Gap" , New York Times

9)A question of balance: a proposal for new mouse models of autism., PubMed Citation

10) "A question of balance: a proposal for new mouse models of autism." , PubMed abstract

11)"Mercury and autism: accelerating evidence?" PubMed abstract

12) "The Age of Autism: Gold Standards"

13) "PANDAS PITAND", Information about autism caused by infection

Full Name:  Jennifer Lam
Title:  If my head hurts, do I have a brain tumor? Are you sure?: Hypochondriasis Treatments
Date:  2006-02-21 02:08:39
Message Id:  18256
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Hypochondriacs live in the constant fear that they have a serious disease. Although their suspicions are quite unrealistic, the very fact that they possess such incessant thoughts is reason enough for them to seek professional medical help. Hypochondriacs are keenly sensitive to their body and to their bodily sensations; so to a hypochondriac, a headache is interpreted as a brain tumor and chest pains as a heart attack even though doctors continually assure the patient that it is highly unlikely that he/she would actually have the disease. According to Dr. Arthur Barsky, director of psychiatric research at Brigham and Women's Hospital in Boston, a hypochondriac is so in-tuned to his/her body that what seems to be an "average" sensation to someone who does not have hypochondriasis becomes unbearable to a hypochondriac (1). Unfortunately, medical reassurance does not comfort the ailing patient; instead, he/she insists that more tests be ran or that a second opinion should be sought. Needless to say, disagreeing doctors and patients almost always ends in frustration for both parties involved. About one in ten patients believe that they are inflicted with a terminal disease despite confirmations from their doctors that they are healthy (2). Perhaps, the patients are in denial, but regardless of the issue of whether they have a terminal illness or not, hypochondriacs have a staggering affect on a developed country's healthcare system. It has been estimated that each year hypochondriacs drain $150 billion out of the U.S medical system (3). It has become clear to me that hypochondriacs should not be regarded as illegitimate patients and must not be dismissed from receiving medical care. But, the question remains: how do doctors treat something that really isn't there?

In order to care for a patient, the doctor must have some idea of what is going on to cause the patient to act so obsessively. In the case of hypochondria, so little is known about the condition that there is not yet an effective clinical treatment (3). There can be a bouquet of reasons why a disease that has been recorded since the time of the ancient Greeks is still not well known. No one wants to admit that they are misinterpreting or over exaggerating the messages their bodies are sending them. There is a stigma that surrounds the word "hypochondria;" some medical professionals run the other way when they notice the hypochondriac tendencies of a patient (2). Contrary to the belief that Hypochondriacs fake their symptoms, they, in fact, cannot voluntarily control their physical symptoms. So they are actually experiencing pain, but yet there is no solid medical explanation as to why they feel the way they do. Although being able to categorize hypochondriasis into a broader spectrum of disease whether it be mental or somatic may not seem to be of primary concern to those looking to treat hypochondriasis, it is for being able to relate it to other disorders offers an interesting insight to how the disorder works and possible treatments.

Categorizing hypochondria is still a controversial topic in the medical fields. Some experts believe that it can described as an obsessive compulsive disorder (OCD). Brian Fallon, an assistant of clinical psychiatry at Columbia University, considers hypochondriasis to be a type of OCD since patients are continually obsessing over bodily sensations and consequently seeking medical treatment (4). In his clinical studies, he has shown that Prozac, an antidepressant, can be effective in treating hypochondriasis (4). Prozac, a type of selective serotonin re-uptake inhibitors (SSRIs), is used to treat OCD and other related disorders by inhibiting the reabsorbance of serotonin by the presynaptic cell, thereby increasing the effective amount of serotonin available in the neural synapse (5). This treatment implies that hyponchondriasis is actually a mental disorder—one of chemical imbalances—and that the patient's body is not really "experiencing" the physical symptoms he/she claim to be having, but that it's all a product of the brain. Only the patient has the privilege of accessing what his/her body is experiencing, and I believe that whether a patient is in legitimate pain or not is not to the discretion of anyone but the patient, him/herself. However, I cannot argue against the evidence that Fallon's clinical study produces. Fallon's observations have caused me to re-evaluate my idea of hypochondriasis, but these findings seem to raise more questions than answers. If we envision the nervous system consisting of boxes, then Fallon's research means that hypochondriasis originates inside a box within the larger box, that there does not need to be some external input in order to produce an output. Although this explanation is possible, there are still some inconsistencies that exist within the observations that are available concerning hypochondriasis (6).

Treatment with anti-depressants are not the only option hypochondriacs have in combating their illness. Recently, cognitive-behavioral therapy (CBT) has gained popularity when dealing with hypochondriacs. CBT blends the benefits of both behavioral and cognitive therapy in order to treat the habit of thinking that you're always ill as well as the thinking patterns that may have an effect on your physical symptoms (7). Barsky conducts clinical research on hypochondriacs and CBT. Observations from his research suggests that CBT is an effective treatment plan for hypochondriacs as compared to regular medical care (2). Dr. Ingvard Wilhelmsen, a gastroenterologist in Bergen, Norway, believes in finding the cause of hypochondriacs symptoms and focusing in that rather than managing the physical symptoms (8). Because of his approach, Dr. Wilhelmsen is able to successfully treat many of his patients who have been frustrated by conventional medical treatment.

At first glance, I thought that the two treatments, medication vs. CBT, were pointing to different causes of hypochondria. One suggests a physical chemical imbalance in the central nervous system, while the other indicates a strong psyche control of the body. But perhaps medication and CBT are more similar than I had originally thought. Maybe hypochondriasis is too complicated to neatly categorize it into a type of disorder whether it be mental or physical. If Fallon's Prozac treatment refers to taking care of the neurotransmitter imbalance in the smaller box that is within a larger box, then perhaps Barsky's and Wilhelmsen's ideas could be illustrating the complex organization of boxes, inputs and outputs. The evidence from both Dr. Barsky and Dr. Wilhelmsen experiences does not refute Fallon's observations using Prozac. Neither one completely rules out the other; in fact, they just might be complementing treatments or treatments that focus in on a different "type" of hypochondria. Referring back to the box analogy, there is a possibility that two, unrelated input signals or even a different box in which an input signal begins produces the same or very similar output signals. Although these clinical observations offer new insight to the disease and the management of it, there still lingers that elusive bridge that links the mind with the body, continuing to haunt modern medicine and psychology.


1) Hypochondria? Get Over It, an informative article originating from the New York Times.

2) Sick with Worry. Can Hypochondria be cured?, an article from the New Yorker.

3) Severe Hypochondria helped by Cognitive-Behavioral Therapy , an online article describing Dr. Arthur Barsky's treatment.

4) Study: Hypochondriacs Need Treatment, a link to Columbia University Record, Brian Fallon

5) Prozac, information on Prozac

6)Fallon, BA, et. al. Hypochondriasis and its relationship to obsessive-compulsive disorder. The Psychiatric Clinics of North America. 2000 Sept. 23. Vol 3: 605-16.

7) Cognitive Behavior Therapy, The CBT Website

8) Norwegian Doctor Takes Patients Who Only Need Understanding , Wall Street Journal article on Dr. Ingvard Wilhelmsen

Full Name:  Brom Snyder
Title:  Taste the Rainbow: Synaesthesia
Date:  2006-02-21 03:29:18
Message Id:  18257
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

They walk among us, perhaps you work with one, maybe you listen to the music they create, quite possibly you read the poetry they write, or you have heard them comment that someone's name is "green" when you know for a fact they are talking about Mr. James down the road; who are these mysterious humans, are they talking in code? Are they members of an organization bent on overthrowing the government? Fear not America, they are merely synaesthetes. A synaesthete is someone who experiences synaesthesia, a condition where one stimulus causes two senses to respond to it, its literal translation is "union of senses", and is also sometimes described as the "neurological mixing of the senses." (1)(2) The most common types of synaesthesia involve numbers or letters being a certain color whenever observed by the synaesthete(called grapheme synaesthesia) or an auditory stimulus triggering the perception of a certain color by the synaesthete. (2)(3) These are not the only types of the synaesthesia: tactile sensations or colors triggering tastes, and certain smells eliciting other sensations are other examples of synaesthesia. This phenomena is can be induced by using drugs like LSD or mescaline, but also occurs naturally in the human population with a frequency scientists estimate of around 1 in 2000, or .05 percent. Some estimates place the frequency as high as 1 in 200. (2) (3) In fact many of famous artists of the past 100 years were synaesthetes, including Jimi Hendrix and Vladimir Nabokov. (1)

So what is going on the brain of someone with synaesthesia? For people who experience grapheme synaesthesia is there cross wiring between the parts of the brain that process color and numbers? Many researchers think this a reasonable explanation because both color and numbers are first processed in the fusiform gyrus and then near the angular gyrus; therefore a crossing of neural pathways could induce both parts of the brain to process the signal, causing numbers to be a certain colors. Vilayanur Ramchandran and Edward M. Hubbard, neuroscientists and synaesthesia researchers, advocate another possibility; an imbalance of chemicals between the areas of the brain that process numbers and colors. The various regions of the brain excrete chemicals which inhibit other parts of the brain from processing signals. If not enough of the inhibitor chemical is produced by one region of the brain there is the possibility that another region of the brain will also start processing the signal, resulting in two parts of the brain that normally do not process the same signals both processing the signal. For those experiencing grapheme synaesthesia it could be due to a chemical imbalance between the parts of the fusiform gyrus and the angular gyrus promoting excess communication between the regions of the brain. This interaction would result in response whereby the number would be a certain color. (4)

Numerical sequences appear to play an integral role in grapheme synaesthesia. Hubbard and Ramchandran conjecture " the abstract concept of numerical sequence that drives the color, rather than the visual appearance of the number." (4) This hypothesis accounts for reports the some synaesthetes associate colors with days of the week and months. (4) Although they Hubbard and Ramchandran do not discuss it, this hypothesis also makes sense in the context of the synaesthetes associating color with letters and musical keys. Although they are not based on numbers, both letters and musical keys are well-defined sequences, thus explaining why some synaesthetes associate them with colors. One problem with Hubbard and Ramchandran's sequence hypothesis is none of the synaesthetes studied associated colors with Roman numerals. (4) If numerical sequences were a primary factor behind the expression of synaesthesia it seems strange that Roman numerals would not cause grapheme synaesthesia in at least some synaesthetes. One possible explanation for the lack of grapheme synaesthesia concerning Roman numerals could be that children do not learn to count in Roman numerals or use them in mathematical contexts often when their brains are developing. Arabic numerals, days of the week, the order of the months, and the alphabet are all sequences that children learn at a relatively young age and are constantly exposed to. In contrast, Roman numerals might be learned one day in math class and then promptly not used with the possible exception trying to determine whether it was Super Bowl 33 or 37 that year. It would be interesting to examine whether a child taught to count and do math with Roman numerals would develop grapheme synaesthesia associated with Roman numerals, it seems likely.

Synaesthesia offers possible enlightenment to those who attempting to understand the origin of creativity and the development of language. Synaesthesia proves that the brain is capable of making arbitrary connections between completely unrelated things, like the number 5 and the color red. This process is similar to the creation of metaphors, where two seemingly unrelated things are linked together (i.e. "your eyes are like a foggy morning"). If people experiencing synaesthesia are experiencing an excess of communication between parts of the brain caused by a chemical imbalance, creativity can be explained as excess communication between various parts of the brain leading to the linkage of apparently unrelated things, sounds, colors, textures, leading to the emergence of relationships previously nonexistent. (4) The random connections observed in synaesthesia also could contribute to a greater understanding of the development of language. Language takes concrete things, things observed by the five senses, and then arbitrarily assigns them a sign, the sign is nothing but a placeholder. When viewed like this, it appears as if language could have initially been a form of synaesthesia whose connections could be taught, thus the emergence of language as a form of communication.

Synaesthesia provides a fascinating look into how the brain works. The seemingly random nature of the connections within different areas of the brain as evidenced by synaesthesia offers an explanation for how creativity and language work and developed. On the other hand, synaesthesia may not provide the answers to reasons for the emergence of creativity and language within man, the seemingly random connections made in the brains of synaesthetes may contain an undiscovered pattern.

1)Synaesthesia, an online encyclopedia
2)"Synaesthesia –union of the senses" by Adrianhon Feb 21st 2003,
3) Harrison, John Synaesthesia: The Strangest Thing (Oxford, Oxford University Press, 2001)
4) Vilayanur Ramchandran and Edward M. Hubbard "Hearing Colors and Tasting Shapes" April 15th 2003,

Full Name:  Anna Dejdar
Title:  Obsessive Compulsive Disorder: Is there a biological cause?
Date:  2006-02-21 03:36:14
Message Id:  18258
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Obsessive Compulsive Disorder (OCD) is a disorder where a person is plagued by certain obsessions and as a result is compelled to act out certain compulsions to get relief from those obsessions (4). Approximately 2-3% of the population is affected with OCD (8) and approximately 14% of the population is affected with minor symptoms of OCD (2). The age of onset in childhood is before puberty and in adulthood it is around 20 years old (1).

Obsessions in OCD are constant beliefs or images in people's minds that are illogical and silly, but remain constant because they feel that they have no control over them (4). For example a classic obsession would be that people feel that their hands are not clean enough, but dirty or contaminated by something. They would have this on their mind and become obsessed with it, thinking about it and not being able to get relief from that obsession of germs, dirt, or contamination (3), (4). Compulsions in OCD are behaviors that people feel that they must do many times over again in order to become relieved from something that is bothering them. Therefore, if people have an obsession that they are dirty, then they would have the compulsion of continuously washing their hands even if their hands are raw and bleeding from all of the washing (4). Other examples of compulsions are extreme bathing, checking, counting, organizing, and cleaning (2), (3). These compulsions greatly interfere with people's lives because they are time consuming and do not make them feel good, but people have typical feelings of being fearful, doubtful, or disgusted with themselves and their actions (4).

The people understand that their behavior and thoughts are not normal and they do not want to do or to have them (4), but still they do and as a result they feel frustrated. What makes them have those thoughts and act out those compulsions? It interests me how does OCD start in an individual? Is there a biological cause and is it present from birth or does something happen to the individual? The etiology of OCD is of great interest to researchers, who are trying to figure out answers to many questions. There has been much progress made on figuring out the etiology of the disorder, but the precise etiology has still not been found. One of the tools that is used by researchers is Functional Magnetic Resonance Imaging (fMRI) (3). The way this works is that when a person comes in for testing, he/she is presented with specific physical stimuli such as a sound, a visual stimulus, or a movement by the subject. Then the fMRI can track the increased flow of blood to certain parts of the brain, which occurs when those parts have become activated by the appearance of certain stimuli. This shows up on the scan and can be analyzed (5).

One of the most predominant theories about the etiology of OCD states that there is a problem with the connection between the orbital cortex and the basal ganglia (4). There are many things involved in this relationship and one strong theory believes that there seem to be problems because there is "abnormal metabolic activity" (1) in the orbitofrontal cortex, the anterior cingulate/caudal medial prefrontal cortex, and the caudate nucleus. The interactions between these different parts is called a "cortico-basal ganglia network" (1) and it is believed that these cortico-basal ganglia interactions make up a neural system that is very important in the acquisition of habits and also establishing a fixed routine of performing those habits, which is directly connected to the typical behaviors of OCD where people maintain certain obsessive habits and continue to perform those habits. In this theory, each part of this network has an important contribution to the possible forming of OCD. It is believed that when lesions occur in the orbitofrontal cortex, this affects the ability of planning one's behaviors and also in making decisions. An experiment was done with monkeys where it was observed that the neurons in the orbitofrontal cortex adjust their activity in response to the monkey's motivation towards a certain stimulus. However, when a lesion happens, then the monkey experiences abnormal motivations or preferences towards the stimulus. Therefore, when the monkey is exposed to a specific stimulus, certain autonomic responses become reactivated and in OCD, this reactivation becomes extreme and as a result it continues to compel the repetition of certain behaviors which are present during OCD (1).

The second part of the theory is that there is a very strong connection between the anterior cingulate cortex and the orbitofrontal cortex, where the anterior cingulate cortex sends anatomical connections to the rostral cingulate motor area and then this area sends the connections to the motor cortex. As a result of this strong connection, the orbitofrontal cortex working with the anterior cingulate cortex could possibly influence the emotional value that a person places on a stimulus and also the behavior that the person chooses to respond with (1).

Finally, the third part is the role of the basal ganglia and their possible effect on OCD. In this one part of the network, there are many theories because the basal ganglia are believed to be very important in the possible development of OCD. The basal ganglia are believed to be connected with the neocortex through "parallel loops" (1) of the cortico-basal ganglia network. The loops are thought to run from the neocortex to the basal ganglia and after that to the thalamus, which then goes back to the neocortex. One theory is that these loops are possibly involved in the setting of mental habits and also physical habits that a person performs. If there is something wrong within the loops, then this contributes to a problem with the setting of mental and physical habits which results in the repetition of obsessions and compulsions that a person has with OCD. Another possible theory of the function is that the basal ganglia recode certain inputs into bigger groups called "chunks" (1), which represent actions, and then these "chunks" are organized together, producing a sequence of various behaviors. Before the behaviors are exhibited, priorities are made with regards to the sequence of the various behaviors and the choosing of those behaviors. However, with a problem, these priorities are not made and as a result a person can not move from one prioritized behavior to the next. Therefore, the person becomes stuck with one behavior that can not change, becoming an obsession or compulsion. It is believed that the problems of the cortico-basal ganglia network could arise from brain chemistry that is abnormal, which could then cause OCD. These are all theories about the functioning of this cortico-basal ganglia network; however, there is no actual understanding of the correct and normal working neither of this network with the interaction of the loops and the areas and various functions within nor of the problems that could arise and if they would cause OCD. This is one possible explanation that seems to be one of the main ones where it is believed that the problem lies somewhere within the orbital cortex and the basal ganglia (1).

Another theory is that OCD can occur after a traumatic event, where the serotonin levels in the brain can become imbalanced and cause problems with impulses for functions like thinking. Serotonin is responsible for transporting these impulses to and away from nerves (11). This theory would help to explain why some people may suddenly develop OCD; however, researchers are still trying to figure this theory out precisely (3).

These findings support the statement that we learned in class where "science is about getting things less wrong" (9). The findings are developing past theories further, but do not have the complete answer to many questions. So even though, there seems to definitely be a biological cause of OCD, researchers are not exactly sure of what it is. One question that still persists in my mind is do some people develop OCD in adulthood if they did not have a traumatic incident and no signs of OCD in childhood? If so, then what happened to develop it?

There are treatments available for OCD, where the most common ones are Cognitive Behavioral Therapy (CBT), Medication, or a combination of the two (3). CBT is a form of therapy that is focused on trying to change people's thoughts about their behaviors by changing their behaviors. People work with their therapist and together make up different strategies about how to deal with their obsessions and compulsions, focusing on having people gain back their control (4), (6). Some of the techniques used are: "thought stopping" where something is used to disrupt the thought of the obsession (2), and also "Exposure and Response Prevention" (ERP) (11), where the irrational fears of the people are discussed through exposure and then the compulsive behaviors are also confronted through response prevention (11). Another form of treatment is medication where the medications are selective serotonin reuptake inhibitors (SSRI's) like for example fluoxetine (Prozac) or sertraline (Zoloft) (3). These SSRI's appear to be successful in the treatment of OCD because they seem to reverse the "abnormal metabolic activity" (1) that could be occurring in the cortico-basal ganglia interactions, causing the problems (1) , (7).

WWW Sources:
1)Toward a Neurobiology of Obsessive-Compulsive Disorder ,

2) Disorders- Neurology, Neurobiology, and Psychiatry- University of Newcastle,

3) Stanford Psychiatry Neuroimaging Laboratory: Obsessive-Compulsive Disorder ,
4) Obsessive Compulsive Disorder ,

5) Introduction to FMRI ,

6) A Guide to Understanding Cognitive and Behavioural Psychotherapies,

7) Obsessive-Compulsive Behaviors and Disorders: Symptoms, Treatment, and Support ,
8) Brain Explorer- Focus on Brain Disorders- OCD- Epidemiology ,

9) Biology 202 home page,

10) Anxiety Disorders, Panic Attacks, treated with New Therapy Approach ,

11) Physiological Factors in Obsessive-Compulsive Disorder,

Full Name:  Lori Lee
Title:  Rival
Date:  2006-02-21 04:10:35
Message Id:  18259
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The Brain- is wider than the Sky-
For put them side by side-
The one the other will contain
With ease- and You- beside-
Emily Dickinson wrote of "the brain" [nervous system] being wider than the sky and containing all. But how is it then that such processes and concepts exist which are wider than the sky and our brains? How is it then that the brain is capable of creating and understanding ideas, concepts, abstractions, which are not in its own range? And how can these ideas exist separate from the nervous system? Specifically, how does mathematics fit into the range of the brain? How does the brain create a concept of a number or theory or postulate that is greater than itself? And how can physical structures controlled by the material nervous system exist beyond the nervous system? How can the brain be wider than the sky if the circulatory system of a human can exist without the body and the nervous system?

In considering mathematics, ? is the most controversial number, as it is infinite and irrational. What makes no sense and is left unexplained in Emily Dickenson's poem would then be the rationalization for the "brain's" ability to create something that does not exist, and only exists to some extent of human knowledge and capability. In terms of the material nervous system, a statement is being said about whether or not the brain is really wider than the sky. If the brain were wider than the sky, then how does organ transplantation occur, and how does the circulatory, i.e. the heart, of an individual continue to pump blood through the body, when the body doesn't exist, and the nervous system is not physically connected to the circulatory system anymore?

Like the worm whose nervous system was removed from his body and placed in a Petri culture, the circulatory system outside of the body and detached of the nervous system functions as it normally would, and as if it believed it was still in its body. Unlike the nervous system of the worm who showed action potentials and electrochemical signals that were typical in swimming, oblivious to its actual surroundings, the circulatory system stays constant, and is dependent upon its environment, as it has its own regulation and rhythm as long as it's provided with the proper environmental conditions.

In George Johnson's article in the New York Times, "Useful Invention Or Absolute Truth: What is Math?," he attempts to set a standard for what mathematics really is. The major issue lies in understanding whether we believe that math is a construct of human imagination, or something that is truly grounded in everyday life. "While science is anchored in observations of the physical world, Dr. Hersh insists that mathematics is more of a human creation, like literature, religion or banking." But if Dr. Hersh is right about math, then how is it possible to "imagine" a system that cannot be solved by its creator, one that life happens to obey the laws of, and one that is endless. If ? is so mysterious and infinite, then how can the brain rival it's own infinite creation?

The nervous system, is undoubtedly a material structure, but its creations are emotional, physical, internal, external, everything! If Emily Dickinson is right [that is if "right" exists], then the circulatory system is a creation of the nervous system, as is the sky and all concepts we are familiar with. But does Emily also mean that the material, tangible, and physical structures of these, more-or-less, organ systems are also a part of the nervous system? Because this then raises the issue of organ transplantation, and a physiological system's ability to sustain regular processes when it is isolated in a culture away from the body and the nervous system. If a heart can continue to beat and pump blood throughout the circulatory system independent of the nervous system, then a much larger issue is at hand, which emphasizes that the circulatory system must be different and separate from the nervous system, brain, and thus Emily Dickinson is wrong, and the brain is not wider than the sky.

In seeing that there are systems that exist outside and isolated from the nervous system, through the analysis of organ transplantation, we show that maybe the brain is not everything, and that Emily Dickinson may be wrong. In discussing the meaning and origin of mathematics began with the notion that the brain is able to rival such systems that, assuming Emily Dickinson is right, it creates. ? is infinite, but so is the brain, but how can the brain comprehend what it does not know and cannot compute? But this discussion of the brain's rivalry with its own products led to a discussion of mathematics in terms of the brain: whether the brain creates math and a system of scientific processes like a fairy tale, or whether math is just something that is derived from the nature of our lives.

Ultimately, the brain produces an abundance of outputs, and these outputs can be as simple as involuntarily moving muscles to creating concepts about the origin of mathematics, or the existence of one system which consists of all other systems, or the mathematical system and order by which life obeys. And this further emphasizes the ability and versatility of the brain, but in the end only serves to prove that neurobiology is not just sensory, motor, and inter-neurons, but the patterns of their interactions as well as these interaction's contact with the larger human that contains the brain, and this individual's patterns of interaction with the environmental conditions by which they face.

1) Archived articles

2), Forum Area on Serendip website

3)New York Times Article

4) Campbell N., Reece J. Biology. New York: Pearson, 2005.

Full Name:  Sylvia Ncha
Title:  Anxiety Disorders: Investigation of Phobia's
Date:  2006-02-21 07:34:41
Message Id:  18261
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Panicking, sweating, restlessness, increased heart rate, and, overall, feelings of fear these are a few of many symptoms associated with anxiety disorders. Humans are entitled to their own share of anxiety episodes but for some humans these episodes are at a higher level by which their anxieties have become debilitating to their lives. There are a myriad of anxiety disorders such as compulsive stress disorder, post traumatic stress disorder, and phobias. Furthermore, I will investigate the neurobiology of phobias and find out what factors contribute to the development of a phobia in a person.

Phobias are just one example of anxiety disorders. A phobia is an intense and strong fear of something that poses little or no danger to us at all. Some interesting phobias are: heights, dogs, water, flying, blood, and even pennies. Most adults with phobias such as the ones previously listed realize that their fears are for the most part irrational but they tend to find it difficult to face or even think about facing their phobias(1). The act alone can cause some people to have panic attack or severe anxiety. To understand this specific disorder, we must look at the general picture. Some studies have suggested that there are certain genes that are related to the development of an anxiety disorder such as a phobia. Along with this, there have also been studies suggesting further research in the amygdala, which is the part of the brain that is responsible for fear responses as well as storing memories of fear. Research in this direction is valid because from what we discussed in class and from what I know, the amygdala is like a communication center between the parts of the brain that process incoming sensory signals and the parts of the brain that interpret the signals (2). So if this is the case, then how these signals are interpreted is key to finding out why people with phobias respond the way they do to certain objects, animals, or situations. A question posed by some researchers is whether or not these disorders are actually brain disorders. Perhaps, having a phobia is just the result to being conditioned to react a certain way in response to a given situation, animal or object. In an article by Lea Winterman, psychiatrist Scott Rauch explains that what researchers know about fear and the brain comes from animal research on specifically laboratory rats (3). Rauch explains the fear conditioning model as a model in which rats are conditioned to fear a neutral stimulus, like a specific tone, by pairing it with something aversive, such as an electric shock. Then researchers eliminate this fear by repeatedly playing the tone without the accompanying it with electric shock (3). This model brought back attention to the amygdala.

In Winterman's article, a New York University psychologist Joseph LeDoux, PhD, and researchers found that there is a double pathway leading to and from the amygdala. One path begins directly from a frightening sensory stimulus like seeing a dog or hearing a plane (as phobias of course) to the amygdala in just a few thousandths of a second (3). The second pathway, which is shorter and slower, first travels to the higher cortex before reaching the amygdala. This shorter pathway is apparently fast but it is not precise so the fast pathway therefore, is the early warning system for the brain and this is what leads people with phobias to experience the physical manifestations of fear such as increased heart rate, sweating, and restlessness, according to LeDoux (3).

I agree with the idea of a double pathway but I am not entirely convinced that a phobia is in result to a brain disorder, as stated before. The amygdale sends signals in response to a stimulus that poses a threat to the organism but what exactly determines whether or not a stimulus is dangerous or poses a threat to the organism? If our experiences determine what we perceive to be dangerous and what we perceive to be harmless, then how can researchers say that phobias are part of a brain disorder? I feel like the function or information processing of the amygdala stays the same among regular people and phobics, no matter the stimulus and so being a phobic does not necessarily mean that one has a brain disorder or malfunction of one of the parts of the brain like the amygdala. Instead, I think that the response or actions of the phobic has to do more with his or her personal experiences and the conscious awareness of their fear.

Treatment of some phobias seems to be the next plan of action for those who find themselves in constant fear of seeing or facing their phobias. Presently there are two general forms of treatment for anxiety disorders: anxiety disorder-medication and specific types of psychotherapy (4). For phobias, psychotherapy has been the only form of treatment to be primarily effective on phobics (4). However, Beta-blockers, such as propanolol, are commonly used to treat heart conditions but they have also been found to be effective in certain anxiety disorders, particularly in social phobia. So if one knows that he or she has a presentation coming up and are afraid of a large group of people, then your doctor may prescribe a beta-blocker that can be taken to keep your heart rate from skyrocketing, your hands from skating and sweating, and other physical symptoms from associated. This does not seem to far fetched because if Emily Dickinson is right then, if we change the way the brain responds to a stimulus then we have in turned changed behavior, so if the doctor gives the girl prescription to take, then a few hours later, her behavior will surely change. Furthermore, anxiety disorders are pretty complex situations and phobias specifically, are very tricky but with new ongoing research, we will continue to learn how certain signals are processed as compared to other signals in or near the amgydala.

1 The Neurobiology of Anxiety Disorders: A Preliminary Investigation , an article explaining anxiety disorders

2) National Institute of Mental Health: Anxiety Disorders., talked about the amygdala

3) Figuring out Phobias article by Lea Winerman

4). Consumer: Anxiety Disorders.

Full Name:  Rachel Mabe
Title:  Is ADHD the New Black?
Date:  2006-02-21 07:54:33
Message Id:  18262
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Three to five percent of all school-aged children are diagnosed with Attention-deficit hyperactivity disorder (ADHD) ((1)). ADHD is categorized by inattention, impulsivity, and excessive motor activity. Our school systems are set up for a specific type of learner. However, there are many different ways in which a person can learn. Psychologist Riccio states that, "You may see very different things in terms of what is the expected level of activity for a child if the culture acknowledges that children don't often sit still - compared to a culture that values a more reserved disposition." ((2)). Perhaps our Western school system does not allow for children with less than "perfect" attention spans to learn effectively. American classrooms are designed to focus children's attention on isolated bits of information to use memory strategies. This focus differs in non-western learning styles.

"In no study were the [ADHD] brains considered clinically abnormal, nor is it possible to work out whether any differences seen are caused by (rather than being the causes of) different styles of thinking..." ((3)).. This means that it is perhaps the ways we are forced to learn and think that can cause a lack of attention. Therefore, changing the ways we learn could help reduce the increase in ADHD diagnosis.

Researchers have found that while ADHD has a direct impact on intelligence, it may not be that there is something "wrong" with the child, but perhaps that the types of tests assessing intelligence is what prevents children with the disorder from doing as well as children without it. ((4)). Standerized testing such as state wide tests, the SATs, and IQ tests, are geared to a "general" and yet narrow group (hence the term standerized). Individuals with ADHD may not be as efficient in taking these types of tests because their brains do work differently. Perhaps all this means is that individuals with ADHD need to be taught differently, and therefore tested differently, than "normal" children.

For example, in a recent study, children aged 4-5 were told to either play with, or memorize objects. The children who played with the items later recollected them better than those who did not (involving putting them into a number of practical situations and narrating them) ((5)). This illustrates, at a very young age, the different methods of learning and how each individual reacts differently to them. I remember doing a project in middle school that was supposed to help us figure out which ways of learning were most beneficial to each student. I suppose that this was then supposed to help us in our future studies, but what I was most struck by was that although there was so much variety, thirty (plus) students were stuck into one classroom to be taught in the same way. We were considered "normal" children; yet if we all had such different needs, how is one teacher possibly supposed to cater to all of them?

Another study tested both American and Guatemalan Mayan 9-year-old girls in remembering the placement of 40 common objects. The Guatemalan Mayan girls did slightly better. It was hypothesized that the reason for this was because American children are repeatedly taught to learn through memorization of small parts; in situations where they would be better off applying a different method, such as spatial relation memorization, they fall back on the less efficient method that they were taught. Therefore, the study concludes that it is not necessarily a "matter of a more competent information-processing system. It is also a product of task demands and cultural circumstances" ((5)). If this is known, then why is the focus not being redirected to figuring out differences in the way that people learn rather than "fixing" people through medication?

If ADHD can not be defined explicetly, cannot be found in the brain, ((7)). and if the medicine we are giving children teach ADHD behavior to them, then if they weren't ADHD before they went on the medication then won't they be afterwards? It is reminicent of like anti-depressants in our society. Yes, they may be beneficial but, anti-depressants do not "cure" a depressed person (do not take away all of the symptoms and doesn't teach that person how to deal with things in a more positive way) therefoere it is said that a person should employ combine medication with therapy sessions. However, this doesn't seem to happen on a regular basis, frequently the psychiatric appointment last just long enough for the doctor to write a new prescription every time a refill is needed. In the same way, how often are people actually trying to teach individuals with ADHD different ways of handling the symptoms of their "disorder" in conjunction with medication? It seems that most often the medication is viewed as the cure, however short the duration of its positive effects. Because ADHD medication shows no positive impact in the long-term and possibly damages the brain (shown in animals to have brain disabling effects ((3)), it seems that it would be more beneficial to look at the "disorder" in a different light.

Thom Hartmann explains ADHD in terms of "farmers" (people without ADHD) and "hunters" (people with ADHD). The "hunters" do better at hunting; they can process all the different stimulus coming in at one time, therefore able to stay alert. The "farmers" are better at farming (and therefore factory jobs, etc, after the industrial revolution) because they are able to remain focused on one thing, for an extended period of time, no matter how monotonous. He further explicates that "farmers" in present society have taken over everything and, therefore, the "hunters" have to adapt and learn a few "farmer" skills to get by ((6)). This goes further than a simple metaphor, and if taken very literally, could be the reason why people with ADHD cannot focus the way society demands.

Our society is way ahead of our bodies in terms of evolution. Our bodies were not meant to live the way we do: drive in cars, walk on sidewalks, etc. Hartmann's metaphor elucidates the idea that people with ADHD do not have something "wrong" with them, (and are a defect of society that Darwinism will eventually rid the world of) but that their brains are specialized to be able to take in much more stimulus than an average person at one time. If Hartmann's theory is right, that would mean that more stimuli are getting through to the I-function—couldn't this be positive? Just because there are a smaller percentage of people with ADHD, does not mean that they are disabled. If our society was more open to different types of people, if our school system was reworked, if we dealt with our children's' rambunctiousness rather than sticking them in front of the TV (to receive constant, ever-changing, stimuli) we wouldn't need to prescribe medication to "fix" them. In a society where it is a sin to not be able to sit still, of course we are going to diagnose someone as disabled, if he is not able to adhere to this societal demand ((6)).

The lack of evidence for physical defect and unclear medical testing for ADHD leads to great inconsistency in the diagnosis rates—one study found a variation of .5 to 26 percent ((3)). Therefore, the inability to have a reliable diagnosis, combined with the intolerance of less than perfect students, allow teachers in main-stream classrooms to get "abnormal" students (who are more difficult, cause disturbances, and need more specialized attention) out of the way. For the average student, the school system works; whether or not the teaching method adheres to the way they learn becomes insignificant, since they can adapt. But just because all students cannot adapt as easily does not mean that they have a defect.

The idea that an inability to concentrate is a psychological disorder, allows us to disconnect the problem from the person and blame it on a deficiency in their brain. This highlights the problem of believing that the brain equals behavior. It simplifies the problem, allowing us to clump groups of people together, even when it is obvious that there is no clear definition or boundary of ADHD. If this disorder can be fixed by chemicals, can't everything be chalked up to a malfunction in our brain, until our brains just become machines that are fueled by drugs to make us all the same super-human people? ADHD was voted into existence in the 1980's, what's next?

1) American Psychiatric Association, (1994). Diagnostic and statistaical manual of mental disorders (4th ed.). Washington, DC.
2) Cultural And Gender Biases May Influence Diagnosing Of ADHD In Kids , an interesting article on ADHD.
3)British Journal of Psychiatry, a journal article on culture and ADHD
4)Intelligence and ADHD, question on how intelligence effects ADHD.
5) Berk, Laura. Child Development. Boston: Allyn and Bacon, 2003.
6)The Gift of ADHD, Positive aspects about ADHD.
7)Psych Minded, an article about the increase in ADHD diagnosis.

Full Name:  Erin Schifeling
Title:  Memory Loss and Recovery
Date:  2006-02-21 08:19:44
Message Id:  18263
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Memory loss occurs for a variety of reasons: Alzheimer's disease, strokes, head injuries, and prolonged alcohol abuse are only a few (1). In some instances memory loss may be slowed, prevented, or regained. These cases provide insight into how memory and certain aspects of the brain in general work.

Beginning with the more physical aspects of memory loss, each of the examples of memory loss cause listed above can be traced to physical problems. A stroke occurs when too much or too little blood is in a part of the brain, damaging cells (2). Excessive alcohol consumption changes the balance of molecules in many parts of the body, including the brain. Head injuries that produce memory loss such as concussions are maybe the most tangible example of a physical source for memory loss problems.

Even diseases like Alzheimer's can be traced to specific molecules within the brain-either too many of the wrong molecules or too few of the right ones. The use of medications with cholinesterase inhibitors and research on new Alzheimer's drugs highlight this connection. Cholinesterase inhibitors are the only drugs approved for middle stages of Alzheimer's disease. They are part of a chain of enzymes that determines how many of certain molecules are present in the brain. Cholinesterase inhibitors slow the molecules that break down acetylcholine, allowing more acetylcholine to accumulate. The related studies suggest that a decrease in acetylcholine is part of many memory problems. (3)

In addition to the effects of molecules, the destruction and re-growth of nervous system cells, called neurogenesis, accounts for changes in memory. Former alcoholics were found to have adult neurogenesis in areas of the hippocampus (4). However, although short term memory improves as the length of abstinence increases, long term memory remaines impaired. This suggests that the parts of the brain responsible for short term memory can resume their activities after re-growing, but that either long-term memory cells are harder to re-grow or that the damage to the long-term memory requires more than the right kind of cells. (5)

The physical, tangible aspects of the nervous system -parts of the brain, cells and molecules- are one part of the explanation for memory and memory loss. Culture, behavior and other less tangible factors add to that explanation. Memory impaired individuals can take mental notes more carefully, write notes, practice memorization with clues, and compensate with less damaged areas of the brain. These behavior changes can increase independence for dementia patients early on through learning to use the memory capacity they have in all situations. (6)

Similar to making a conscious effort to remember small details, in "The Culture of Memory" the researchers explored the impact of culture in what individuals remember (7). They found that in cultures that emphasize the individual, people remember farther back in than those from more community based cultures. Also the types of memories vary from personal, single event memories to memories of routine and group activities. Finally this effect was paralleled in familial influences within the same culture. Children whose mothers encourage them to tell personal stores are more likely to remember events and details of those events than children whose mothers place less emphasis on personal story telling.

Besides restructuring and paying more attention to what is remembered, practice can also help. A smaller working memory –the number of ideas that can be held simultaneously in one's thoughts- may be part of the problem in ADHD. While the human brain seems to reach a limit of thinking about four different items at once, individuals with smaller working memory capacities can increase their working memories up to four items through practice. (8)

These studies together highlight some aspects of how memory works. First, there is a difference between short term and long term memory, and probably a difference between immediate or working memory, short term memory, and long term memory (5), (8). Somewhere in the process, the nervous system decides to move certain bits of information, or memories, from shorter term storage to longer term storage or to forget them. These are partially distinct operations because shorter term and longer term operations are not uniformly affected by memory losses and memory recoveries. This means that individuals, like those in the Cognitive Loss and Recovery study may recover short term memory without equivalent long term memory improvements (5). At the same time, children in different cultures with identical short term memory abilities may have farther or shorter-reaching long term memories (7). Related to short-term/long-term distinction, memory works in different parts of the brain, and some processes and places can be trained to do the job of other parts (6). Also, taking in information, storing information, and then recalling the information are distinct though connected processes.

Secondly, memory works within a biological system and, just like the muscles that allow a person to walk, depend on biological, physical, and chemical processes. When cells die or the wrong molecules are present memory suffers. Furthermore, these problems are sometimes treatable or curable and sometimes permanent. (1), (3), (4)

However there are just as important social and cultural elements that affect the nervous system. Although they may at some level affect physical processes, the solutions that these elements provide for memory loss are not applied with pills or surgeries. Individuals make conscious and unconscious decisions about if, where, and how to store memories (6), (7). These influences are manifested in individuals without memory loss and can be usefully applied to help those with less severe memory loss problems cope with, work around, or fight their memory loss.

Finally, these pieces to the puzzle of memory, memory loss, and memory recovery parallel many aspects of nervous system problems that are more traditionally called mental illnesses. Depression, for example, also has physical, biological causes as well as cultural and behavioral influences. It changes the ways people are able to interact with others and to think. This similarity raises questions about why and if there is a distinction between memory problems and other problems that appear in parallel ways, but are more commonly labeled illnesses.

WWW Sources

1) Poor memory's multiple causes, R. Adleson

2) NINDS Stroke Information Page

3) Brain study sheds light on anti-Alzheimer's drugs, R. Adelson

4) Temporally Specific Burst in Cell Proliferation Increases Hippocampal Neurogenesis in Protracted Abstinence from Alcohol, Kimberly Nixon and Fulton T. Crews

5) Cognitive loss and recovery in long-term alcohol abusers, J. Brandt, et. al.

6) Mending memory, Rachel Adelson

7) he culture of memory, Lea Winerman

8) A workout for working memory, Sadie F. Dingfelder

Full Name:  Em Madsen
Title:  Sexing the Brain: A Risky Proposition
Date:  2006-02-21 08:43:00
Message Id:  18264
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine: one particular sperm with a certain je ne sais quois is chosen by an egg, and at that very moment of conception, the chromosomal sex of an individual is determined. This sex depends on whether the sperm contributes either an X or a Y chromosome to the egg's preexisting material. "If a Y chromosome is present, testes develop [from the bipotential embryonic gonad] and their hormonal secretions result in the development of a phenotypic male. If only X chromosomes are present, ovaries develop and the female phenotype results." (1) What does this mean? It means that even though chromosomal sex differs as early as conception, up until the seventh week of gestation, male and female fetuses are the same. "[These] "indifferent genitals" have a phallus, labioscrotal swellings, urogenital folds, and a urogenital membrane." (2) All humans begin with the same bodies, at least until that tricky seventh week. That's where all the trouble starts.

Part of the trouble stems from the fact that XX does not always a girl make, nor does the presence of a Y ensure a penis. Not only are there many chromosomal variations (such as XO or XXY), there are men and women who have the opposite sex's chromosomal arrangement (about one male and woman in 20,000). (1) Embarking on questions of sex and gender means that biologists and feminist theorists are building on already shaky ground. I mean, what to do about the chromosomal variations alone, never mind those individuals who are born male and undergo a sex-change operation after puberty to become the woman they always felt they were inside?

I began this paper with a discussion of the basic biological components of sex because both in class and in the larger world, debates about sex and gender depend on two major components, nature and culture. I wanted to briefly complicate the nature aspect: what humans see as immutable and inherent (biological sex) is often a very tangled and multi-layered affair. Understandably, culture is not exempt from scrutiny in this affair either. Biologists may study the male and female brain to better comprehend male's and female's strengths in various areas of reasoning. This process puts a lot at stake: what discoveries might there be, and how could this affect the war between the sexes. Would it be ammunition, or a subtle undermining? For these reasons, feminist theorists remain suspicious of biology, and tend to focus more on culture, which can be just as reductionist as giving primacy to the body.

Feminist/Quaker/Biologist Anne Fausto-Sterling describes the split between biology/nature and feminist theory/culture as follows: "Molecular biologists rarely think about interacting organs within an individual body, and even less often about how a body bounded by skin interacts with the world on the other side of the skin." (3) In addition, "Unlike molecular biologists, ...feminist theorists view the body not as essence, but as a bare scaffolding on which discourse and performance build a completely acculturated thing." (3) So how can these two groups effectively talk to one another and do good theory and good science? Fausto-Sterling presents a third approach to the study of sex and gender which seems to me to be a good option. This new way of thinking both acknowledges the shakiness of nature's and culture's standpoints, and allows for the richness and complexity of the subjects to thrive. She writes: "Developmental systems theorists deny that there are fundamentally two kinds of processes: one guided by genes, hormones, and brain cells (that is, nature), the other by the environment, experience, learning, or inchoate social forces (that is, nurture)." (3) Her main example of this new way of thinking is as follows: a goat loses its front legs after it has been born. As a result, it learns to hop around on its back legs. When the goat dies, scientists realize that this repeated action has resulted in a huma-like S-shaped spine in the goat. This S-shaped spine was shaped neither by nature or culture, but through a subtle combination of the two, as well as atmospheric conditions and factors which do not fall in either camp. As a feminist myself, I find this school of theory to be a refreshing change. It does not limit discourse to the body, nor does it make the body into a performance site. What it allows for is space. This is valuable and needs to be preserved at all costs in the study of sex and gender. When we press our faces too close to the subject, we often cannot see anything at all.

For this reason, I find the study of the brain in regards to sex is a territory that is fraught with danger. Unless scientists and feminists alike can utilize the developmental systems theorists' models, or similar manners of thought, the issue will remain a dichotomy, and little or no progress will be made. And while biologists can study the brain and let the public know that an androgenized brain shows little behavioral response to estrogen, while in male brains this suppresses the lordotic response while eliciting it in female brains, (1) this is only part of the picture.

As Fausto-Sterling points out, study of the brain even when not gender/sex-specific is difficult. "To prepare the brains [for examination], one must pickle them... Different laboratories use different... methods, and all methods result in some shape distortion and shrinkage." (3) Also, by concentrating exclusively on certain areas as a source for sex differentiation, such as the corpus callosum, biologists actively ignore the interconnected functioning of the brain itself. "The winter of 1992 was a hard one... Newsweek and Time magazines started the trend by running feature stories about gender differences and the brain. Women, a Time illustration informed its readers, often had wider corpus callosums than men." (3) Again, this is a dangerous proposition. I'm not saying that it is a mistake to study the brain, I am just saying that it needs to be done in a more integrated manner. Developmental systems theories would argue for a wider camera-angle to be placed before the brain, with a thorough examination of many aspects of the individual's life and functioning, not only the nanometers involved in the corpus callosum. The danger of using a telephoto lens is explicitly shown in Werner Herzog's film The Enigma of Kaspar Hauser (1974). Hauser, an unusual man who is raised without learning how to speak or write, dies and is subjected to an autopsy. At the conclusion, the doctors observe that there are abnormalities in his brain. They determine that Hauser's strange behavior in life must stem from these abnormalities. In the process, they completely ignore the fact that the first 25 years of his life were spent in isolation, language-less and lonely.

Theory does not exist in a vacuum, however, neither does science. Not only should developmental systems theories be at the forefront of any future work in sex and gender in both biology and feminist theory, there must be a fundamental examination of the perpetuants of the biological and theoretical work. Aren't they just as much a part of the system as the subject? I've revealed myself to be a feminist, so take this as you will--perhaps with a grain of salt. However, I do believe that biology and feminism have a lot to learn from each other, and neither is blameless in what has been a historical fear and loathing. It's time to lay those past dichotomies aside and engage in a more active and comprehensive look at what these systems humans both partake in and build mean in terms of future discoveries.

1) Kandel, Schwartz, & Jessell. Principles of Neuroscience. Appleton & Lange, East Norwalk, CT. 1991.

2)Child Physiology: Genital Development web site, There's a really cool interactive diagram here, too.

3) Fausto-Sterling, Anne. Sexing the Body. Basic Books, New York, NY. 2000.

Full Name:  Gray Vargas
Title:  Mind Over...Mind? How Attention Modulates Pain
Date:  2006-02-21 09:17:52
Message Id:  18265
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Several years ago, at the Biofeedback Research Institute in California, researchers and friends watched as Joo Bang Lee drove a bicycle spoke through the fleshy part of his forearm (1). While this scene is already strange enough, the most remarkable part about it is that this man did not feel any pain. If you were only looking at the recordings of his brain waves researchers were making, you would not be able to tell that anything significant had happened to him (the expected spike of activity was not present). How was this man able to ignore his screaming sensory neurons? Or were his neurons even screaming in the first place? He explained that he was concentrating on his "ki," a small area at the bottom of his stomach, and once he applied his mind in that way he no longer existed in this world and felt no pain (1). He was focusing his attention on something besides the painful stimulus, and this redirection of focus let him turn off his conscious sensation of pain. In this paper I will discuss how this might be possible, and the implications that follow.

When subjected to the same painful stimulus, different individuals may experience differing levels of intensity and unpleasantness. In addition, one individual may feel different levels of pain depending on the situation. Thus, the nervous system and the brain are not a purely reactive stimulus/response machine when it comes to pain. There are steps in between the sensation and perception (a cognitive interpretation of the sensations) that determine how the pain is experienced (2). Some researchers claim that in order to feel pain, one needs to attend to and process the stimulus in an emotional way. If pain is not attended to or processed in a certain way then it might not reach the level of conscious awareness. Thus, how much attention one gives to pain determines how intense and unpleasant the sensation will be.

There are many situations in which an individual might not attend to their pain as much as they normally would—such as a stressful situation like war or in competitive situations like a sports event. There are countless stories of athletes and soldiers being terribly injured and only realizing after the event that something was wrong (3). Normally, pain serves to notify us of a problem and point our attention towards it. This way we can alter our behavior in such a way that we can treat the injury and somehow reduce the pain. But there were times when we have bigger problems than pain—such as survival, when attending to an injury could be costly or even fatal. (For instance, in our evolutionary past, if we were injured and being chased by a tiger.) Hence, in the classic evolutionary crisis, we could fight or flee without being bothered by an injury. Thus, it is adaptive to prioritize what we attend to and in some cases, to be able to ignore pain. Therefore, if one could fool their brain into thinking that there was something more important than the upcoming pain, they could theoretically feel the pain less—or none at all.

There is scientific evidence that individuals in much less stressful settings can be distracted in various ways so that they do not feel as much pain (4)(5)(6). And likewise, paying attention to a painful stimulus increases its intensity ratings (5). Studies have shown that being hypnotized, either by a hypnotist/experimenter or through self-hypnosis, diminishes pain sensation (6)(7). Since 1998, in a Seattle Hospital, burn patients experience a virtual reality environment called "Snowworld" while they are being subjected to a painful procedure to care for their wounds (4). Patients report feeling less pain during these virtual reality sessions, and the effect is not diminished with multiple treatments (4)(8). It has been found that during the more difficult trials of a cognitive task, subjects report lower pain intensity from a painful stimulus (9). Even during childbirth, part of the popular Lamaze strategy is finding a focal point to focus on to distract the mother from the pains of childbirth (2). Listening to music has been found to reduce postoperative pain (11). However, one study found that using mental imagery and music during suturing procedures did not reduce pain or distress ratings relative to other patients who did not experience the imagery and music. Regardless, almost all of the patients reported that the treatment was beneficial, that they would use it again, and that they would recommend it to others (9). This is consistent with many other studies that find no positive effect of distraction while the subjects are still confident in the treatment. The reason for these inconsistencies is unclear, besides differing intensities of pain and individual differences in response to distraction. Interestingly enough, though, it has been found that individuals that were high or low self-controllers, and with different cognitive styles, did not differ consistently on how well distraction helped their pain (2). In general, though, when this distraction method is found to be useful, it is in alleviating low intensity pain.

All of these findings support the idea that we all have a finite pool of attention that we must divide between different tasks or stimuli. Thus, if a good amount of attention is devoted to an activity, there is less attention available to devote to the processing of the pain (2). The catch, according to some researchers, and the reason we cannot all completely will away our pain, is that focused attention is not perfect. It has been shown in many studies that when people are told to attend to specific stimuli they can still detect certain "outside" stimuli (2). There are individual differences in this variable, too. Therefore, perhaps Joo Bang Lee is so talented at focused attention that he really does not have any attention left to devote to his pain. It would be interesting to run Lee on selective attention tests to see how his results are different from others, if at all. If this theory is true, then we should all practice our focused attention. But how can we perfect this ability, and is everyone capable of doing so with enough practice?

How are these modulating effects of attention on pain manifested in the brain? One candidate region is the prefrontal cortex, a region in the frontal lobe responsible for many higher order brain functions. Studies have shown that activity in a region of this cortex (the dorsolateral prefrontal cortex) is related to attending to pain (10). Another region of the prefrontal cortex (the orbitofrontal cortex) was shown to be more active when individuals are being distracted from pain, and in this study, also experiencing less pain (5). Interestingly, activation of the prefrontal cortex has also been shown to lower the midbrain response to painful stimulus in rats and cats (10). Researchers have postulated that there is a pain modulation pathway, at least in rats, that includes the midbrain, medial thalamus, and prefrontal cortex (10). It is known that the prefrontal cortex is active during selective attention, and these findings point towards an inhibitory role of this region on activity in the "lower," midbrain areas that are responsible for the sensation of pain. Therefore, it appears that "willing away pain" is a function of the prefrontal cortex.

All of this research has left me with several questions. For one, the two scenarios discussed here where attention is directed away from pain—when someone is in either a very stressed, excited state or a very relaxed, calm one—are very different in their levels of arousal and in general mental state. And in the former, adrenaline plays a large role in causing analgesia. It would be interesting to research how adrenaline interacts with the prefrontal cortex, and whether levels of adrenaline are consciously controllable. I also wonder what it means in terms of the brain to have a finite pool of attention. Can only so many neurons fire at once? Or is it that only certain numbers of signals can be simultaneously and consciously processed by the frontal lobe and prefrontal cortex? (A function of our limited short term memory capacity.) I also wonder if alpha waves are associated with analgesic effects—since these are the types of brain waves that tend to be present during meditation, hypnosis, and relaxed states.

When Professor Grobstein asked in class whether anyone was able to "will away pain" a large portion of the class raised their hands. This along with our discussion of pain made me very interested in the topic. One of the most interesting issues this topic raised for me was the idea of a hierarchy in the brain—the ability of some regions to inhibit or diminish activity in other areas of the brain/nervous system. We are not always ruled by our more basic, instinctive brain regions and functions. And this, I think, is a key part of what makes us human. Before starting this research, I assumed that pain responses/perceptions were much more automatic than I found them to be. The idea of individual differences in pain also fascinates me—that in some individuals the ruling regions in the brain's hierarchy have more or less power. I wonder how neurons in the peripheral nervous system fit into the hierarchy, and how levels of activity in these neurons change with different attention and different levels of prefrontal cortex activity.

This area of research could lead to pain relief for millions of patients—and a simple, cheap one at that. However, all of these treatment strategies have a high level of variability between individuals—e.g. some people are more or less susceptible to being hypnotized or able to focus selectively. This means that even if these strategies are found to have analgesic effects, not every patient will be able to benefit to the same extent. But regardless, if we can find a way of emulating Joo Bang Lee and his attentional state, it is possible that we too can have conscious control over our pain.

1)Turn Off Your Mind to Turn Off Pain, an interesting article about Joo Bang Lee

2) McCaul, K.D. & Malott, J.M. (1984). Distaction and Coping With Pain. Pschological Bulletin, 95(3): 516-533.

3)Iverson Puts Heart Online, Ignores Injuries, a fun article about Allen Iverson

4)VR Devices Trick the Brain into Ignoring Pain , an interesting article about virtual reality pain treatment

5) Bantick, S.J., Wisel, R.G., Ploghaus, A., Clare, S., Smith, S.M., and Tracey, I. (2002). Imaging how attention modulates pain in humans using functional MRI. Brain, 125(2): 310-319.

6) Syrjala, K.L., Cummings, C., Donaldson, G.W. (1992). Hypnosis or cognitive behavioral training for the reduction of pain and nausea during cancer treatment: a controlled clinical trial. Pain. 48(2):137-46.

7) Spiegel, D., & Bloom, J.R. (1983). Group therapy and hypnosis reduce metastatic breast carcinoma pain. Psychosomatic Medicine, 45(4): 333-339.

8) Hoffman, H.G., Patterson,D.R., Carrougher, G.J., Sharar, S.R. (2001). Effectiveness of virtual reality-based pain control with multiple treatments. Clinical Journal of Pain, 17(3): 229-235.

9) Albert, R.E. (2002). The effect of guided imagery and music on pain and anxiety during laceration repair. Dissertation Abstracts International: Section B: The Sciences and Engineering, 62(11-B):5030.

10) Lorenz, J., Minoshima, S., and Casey, K.L. (2003). Keeping pain out of mind: the role of the dorsolateral prefrontal cortex in pain modulation. Brain, 126:1079-1091.

11) Good et al, 1999, cited in (9)

Full Name:  Carolyn Theresa Dahlgren
Title:  Brain Impressions
Date:  2006-02-21 09:41:26
Message Id:  18266
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

In our neurobiology and behavior class, we began our exploration of the brain by discussing an Emily Dickinson poem. In the poem, Dickinson describes the brain as "wider than the Sky -/For - put them side by side -/The one the other will contain/With ease - and You - beside-... The one the other will absorb -/As sponges - Buckets - do." (1) From this description of the brain, information and knowledge are 'contained' within the brain. The brain, however, is not just a 'Bucket' that can be filled up with knowledge. In class, we have looked at several different models of the brain. We have been working to get these models progressively 'less wrong'. For this task, we have focused mainly on describing the brain in its functions of immediate input and output. We have not, however, discussed how the brain 'contains' information. What is memory? How does the brain learn? We have had some discussion about spontaneous output which seems to be generated from inside the brain, but this still does not address the issue of how an input can be retained inside the brain. We have talked about how we experience but we have not talked about how we remember experiences or learn from them.

What are learning and memory? Tortora and Grabowski define learning as "the ability to acquire new knowledge or skills through instruction or experience. Memory is the process by which that knowledge is retained over time." Our class model of the brain involves boxes within boxes, inputs from sensory neurons, outputs via motor neurons, and an 'I Function' which can create spontaneous output and gives us a sense of self. This model does not, however, offer an explanation for how we learn. How do some inputs become contained within the brain? How can we explain how we are able to retrieve information and produce an output long after an input has been experienced? It seems like learning requires some kind of long lasting change in the brain. Something in the brain must change; something inside the boxes or in the connections between the boxes. How do we account for these brain alterations in our current model of the brain? Our current model is too static to explain learning; it does not account for the dynamic, constant physical fluctuation and alteration of the brain which occur as a result of encoding experience.

One theory about memory altering the brain involves a memory trace called an engram. Engrams are defined as a "physical or biochemical change in the brain (and other neural tissue) in response to external stimuli." (6) As we experience life, our brains are constantly changing to physically record our memories. "The existence of neurologically defined engrams is not significantly disputed, though its exact mechanism and location has been a persistent focus of research for many decades." (6) Brain plasticity is a property of the nervous system that is related to engrams. Plasticity describes the brain's ability to change the organization of the brain in order to adapt to certain circumstances. Unlike the continuous, gradual effect of engrams, brain plasticity deals more with reorganization of the brain during periods of development or after trauma.

According the Vanderbilt Kennedy Center, "understanding the mechanisms of brain plasticity is essential to developing interventions to overcome brain damage." Research on plasticity has been hailed as the pathway towards curing paralysis which is caused by the severing of the spinal cord. Why isn't the brain able to naturally knit the spinal cord back together after it has been severed? If the spinal cord is cut, the nerves do not reconnect, but rather become independent and function separately. Why doesn't the brain reconnect? Is there a reason why the brain doesn't reconnect? If we could harness the brain's property of plasticity, we might be able to cure paralysis, but we do not know the drawbacks. Is there a reason why there is a limit to brain plasticity? The brain naturally mediates the grow of its neural pathways. "Experience determines which connections will be strengthened and which will be pruned; connections that have been activated most frequently are preserved. Neurons must have a purpose to survive." (2) Why do we have this pruning? Can there be too many neural paths? Is it necessary to prune to avoid conflict within the brain?

I propose a new model for thinking about the brain. I understand that models are supposed to be simplified versions of what they represent, but, in order to incorporate engram theory and the property of plasticity, we need to address some problems with our current model of the brain. The first issue concerns the "I function", the identity or consciousness box in the brain. When the "I function" is a closed box inside the brain, it is hard to place it within our model. Some information is an essential part of our identity while other knowledge is less so yet it can all be brought to conscious awareness. I suppose that the fact that we can store knowledge, that our brains have engrams and plasticity, is how the "I function" theory accounts for the multitude of knowledge that our brain contains. Still, I feel that the "I function" should be a more encompassing box.

Another problem with our model of the brain is the fact that our present model is based on square shaped boxes. Why should we have boxes and not any other shape? The boxes have been compared to different nuclei of the brain, but how can we know if these nuclei are truly responsible for our outputs? The box shape is too uniform; the brain is too complex to be made solely of boxes. Also, I do not think that the boxes should have closed edges. Like the membrane of a neuron, I think the brain's boxes have different permeability under certain conditions. These may be bold statements, during one class discussion; we managed to boil down all brain activity to action potentials. Action potentials, and boxes too, are just one piece of the story. Nothing is so simple that it is based out of one thing. There are always more players in each story. Look at action potentials, they can be broken down into ions and membrane permeability and many other complicated features and processes. There is always more information, a further break down of the smallest known pieces. Part of the journey to 'get it less wrong' involves breaking things down more and connecting information together in new ways.


1)Course Home Page1) Grobstein, Paul. "Neurobiology and Behavior 2006". (Our class notes)

2)Brain Plasticity: What Is It? Learning and Memory2) Hoiland, Erin. "Brain Plasticity: What Is It? Learning and Memory." (A general overview of how Learning and Brain Plasticity are connected)

3)Brain Plasticity3) McCormick, Kat. "Brain Plasticity". (A previous student's webpaper-lots of applications for brain plasticity)

4) Tortora, G. and Grabowski, S. (1996). Principles of Anatomy and Physiology. (8th ed.), New York: HarperCollins College Publishers.

5)Brain Plasticity5) Vanderbilt Kennedy Center for Research on Human Development. "Brain Plasticity". (Research site connected to Vanderbilt University)

6)ngram (neuropsychology)6) Wikipedia. "Engram (neuropsychology)." (Online encyclopedia source)

7)Plasticity (brain)7) Wikipedia. "Plasticity (brain)." (Online encyclopedia source)

Full Name:  Jessica Engelman
Title:  Cytokines - A Missing Link in Internal Diseases?
Date:  2006-02-21 10:29:37
Message Id:  18267
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Initially, this project was supposed to focus on allergies and depression and the studies finding a positive correlation between the two, but as my research progressed, I discovered similar correlations between depression and chronic fatigue, then depression and central hypothyroidism, then allergies and inflammation, then inflammation and cancer, and then of many other diseases all caused by internal factors, and all of these linked by a single shared trait—an overabundance of certain cytokines. Cytokines are a type of protein that is secreted by a variety of cells (primarily helper-T cells and macrophages) that serve a variety of purposes, such as inducing or inhibiting inflammation, regulating blood cell formation, and prompting the immune system. Not all cytokines cause the same reaction—different kinds of cytokines can even counter each other, so although confusing, use of cytokines' specific names is imperative. (1)

To best understand how all the above-mentioned diseases are connected, let us go through them one-by-one, starting with inflammation, and focusing on the role cytokines play. Scientists are continually discovering the impact inflammation has on the body; it plays a role in arthritis, PMS, heart disease, gingivitis, stroke, Alzheimer's disease, and cancer for starters. Not that inflammation is all bad, it's a necessary part of the immune system that helps heal injuries and prevent infection. A major factor in inflammation is cyclooxygenase-2 (Cox-2)—an enzyme that produces cytokines. Cox-2 converts arachidonic acid (an omega-6 fatty acid) into inflammation-inducing tumor necrosis factor alpha (TNF alpha) and cytokines interleukin-1 (IL-1) and interleukin-6 (IL-6). IL-1 and TNF alpha then prompt the release of free radicals, which can destroy foreign objects, but also wreck havoc on the body, destroying cells and their DNA. (2)

Meanwhile, a study conducted by Marshall, O'Hara, and Steinberg on allergies and fatigue and mood indicated patients with ragweed allergies reported during ragweed season higher general fatigue, mental fatigue, and feelings of depression, and reduced motivation, alertness, attentiveness, and pleasure than during winter (this is contrary to the general population which tends to feel more depressed during winter). However, they did not indicate higher levels of physical fatigue, which the researchers took to indicate an affect on the central nervous system by the allergic reaction. If this is true, it also explains why allergies can negatively impact scores on tests of mental activities. Rather than relying on the traditional explanation that the physical symptoms of allergies lead to feeling depressed because feeling unwell physically makes one feel unwell emotionally, they propose a different explanation. Ragweed can prompt the release of IL-1 and TNF alpha in the lungs, causing inflammation and allergic and asthmatic reactions. Additionally, this inflammation may increase sensitivity of the central nervous system (specifically the vagus nerves); this increased sensitivity may in turn incite symptoms of depression. Marshall et. all cite several studies connecting depression with increased levels of TNF alpha, IL-1, and IL-6 in cerebrospinal fluid of test subjects injected with an endotoxin, similar to levels in severely depressed patients. Rats bred to have an extra-sensitive CNS (like that of allergy sufferers) exhibit symptoms of depression as well. Additionally, IL-1 increases sensitivity to psychological stresses, which leads to a higher susceptibility to depression. (3) Although this may seem slightly far-fetched, the statistics from several other studies on allergies, asthma, and depression support this theory. For instance, in a study conducted in Hungary by Kovács, Stauder, and Szedmák, 32.2% of subjects with allergies scored above the normal level of depression, 12.5% had clinically significant depressive symptomatology (the national averages were 22.4% and 8.3%, respectively), and those with perennial allergies and asthma scored higher on the depression scale than those with other types of allergies. Additionally, the worse the allergic symptoms, the higher the level of depression indicated. (4) A study by Rimington, Davies, Lowe, and Pearson shows a positive correlation between asthma and depression and anxiety, although they suggest that the asthma might be caused by the depression, rather than the other way around. They found that symptom scores beyond the effects of lung function could be explained by scores on the Hospital Anxiety and Depression scale that was administered to subjects. (5) Mancuso, Margaret, Peterson, and Charison conducted a study that also showed a positive correlation between depression and health-status of asthma, although they did not indicate whether the correlation was causational. (6) So whether causational or not, there is a clear correlation among allergies, asthma, inflammation, and depression, with the possible link of cytokines.

Now it starts getting interesting. IL-1, IL-6, and TNF also play a role in hypothyroidism, AKA low thyroid. In hypothyroidism, there are insufficient levels of thyroid hormones, leading to the upset of metabolism and homeostasis. (7) The thyroid gland secretes the hormones T4 and T3, which maintain metabolism in cells. T4 can be converted to the more active T3 with the help of cortisone, but our aforementioned cytokines can prevent this conversion. Thus, high levels of cytokines result in lower levels of T3, leading to hypothyroidism. (8) Things get stranger upon realization that Candida (a digestive disease caused by bacteria or yeast) can lead to an increase in IL-1, IL-6, and TNF. (7) So to wrap up, increased levels of inflammatory cytokines caused by Candida, allergies, or asthma can lead to depression, inflammation, and hypothyroidism. Inflammation can lead to arthritis, PMS, heart disease, and cancer while hypothyroidism can lead to a range of problems, including fatigue, susceptibility to cold and flu viruses, high sensitivity to cold, and disruption of the reproductive system.

At first this research was fairly uninspiring; the connection between allergies and depression was interesting but nothing revolutionary. However, I started noticing a strange trend. The more I discovered about cytokines, the more health problems I came across that my mother has had at one point or another. I ended up calling her after seeing the connections between allergies, depression, and chronic fatigue (all problems she has had at some point or another) and asked her to list out the other major diseases she's had to see if I could get lucky and find a connection among these and cytokines as well. She listed Candida, hypothyroidism, and PMS—a few google searches later, I found sources connecting these to the abnormal levels of cytokines. Imagine the excitement of accidentally finding a link between every major medical problem in an individual—even more so when you find the link on your own! Of course this all sounded too easy, but further research into the subject showed these were even the same types of cytokines involved in these medical conditions: IL-1 and IL-6, along with TNF. Although I can't do any more research in time for this paper, I want to continue reading up on cytokines to see if I can find any other connections. The strangest part is, I found very few sources that had also connected the dots—-one of which is a website listing the many diseases that can be brought about by Candida (although it does not cite cytokines as being the primary cause for most of the conditions, since fungus, bacteria, and yeast growth is a more prominent result of Candida). (7) Additionally, the sources that found correlations between the other diseases (such as allergies and depression) were fairly recent and indicated that many correlations made ten or more years ago were merely speculative or based on case studies, and the cytokine link is an idea from only the last decade or so.

This indicates a problem with the approach of many scientists and doctors when it comes to understanding and healing the body. Many conventional doctors ignore medical problems other than the one at hand. When my mother was first trying to cure the above-mentioned medical problems ten years ago, she said only the doctors specializing in alternative medication would try to find the underlying causes of a disease and cure that one, instead of just prescribing medication to relieve the visible symptoms. All four cited studies on allergies/asthma and depression concluded that further research in the area is recommended to better understand how the three are related, and that doctors should start taking into consideration depression and other psychological factors that could influence (or be influenced by) the allergic reactions. After all, if it is depression leading to an asthma attack, asthma medication may not be sufficient, and if depression is caused by allergic reactions, patients would be much better-off if they could eliminate their allergies than if they merely took anti-depressants. Perhaps medical science needs to be more open to the possibility of other contributing factors and give more credit and attention to the many alternative methods that do consider connections within the body. As an article on inflammation remedies suggests, instead of turning to conventional drugs that target only the immediate problem, we should be looking into remedies that correct whatever condition is causing the immediate problem. This article recommends a dietary change to relieve excessive inflammation--reducing intake of the omega-6 fatty acids that can be converted into IL-1, IL-6 and TNF and increasing intake of the omega-3 fatty acids that can be converted into anti-inflammatory compounds. More specifically, this means eating more cold-water fish, leafy green vegetables, extra-virgin olive oil, and flaxseed, and less vegetable oil and processed foods. Additionally, eating more foods high in antioxidants (such as pomegranates and blueberries) will help to neutralize the damage caused by free radicals. Anti-inflammatory drugs such as Celebrex and Vioxx only target the Cox-2 and never address any underlying dietary problems. (2)

All the while, we must remember to consider the effect any disease has on the brain. New discoveries are being made every year connecting functions in the nervous system and the rest of the body. An article from the Psychiatric Times recognizes the importance of omega-3 fatty acids in curbing inflammatory cytokines, and cites evidence that a lack of omega-3 may lead to not only symptoms of depression, but also schizophrenia, alcoholism, and bipolar disorder. Yet even this article states that much of this is "suggestive" and needs further research before becoming accepted fact. (9) We are still not certain how cytokines affect the brain, but this question clearly deserves our attention. Even more importantly, though, we should not lose sight of the other end as well--but rather to always consider the cause in addition to the result.



2)Natural Remedies for Inflammation

3)Allergies, Fatigue Level, and Mood

4)Severity of Allergic Complains, The Importance of Depressed Mood DOI code - doi:10.1016/S0022-3999(02)00477-4

5) Relationship between anxiety, depression, and morbidity in adult asthma patients

6) Effects of Depressive Symptoms on Health-Related Quality of Life in Asthma Patients



9) Dietary Fatty Acids Essential for Mental Health

Full Name:  Amber Hopkins
Title:  Emotionally Attached: the Role of Feelings in Decision Making
Date:  2006-02-21 11:40:52
Message Id:  18268
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Our society today is very structured on the concepts of reason and logic, with little to no credibility given to things based on feelings or emotions. According to David Borenstein, "Feelings are not supposed to be logical. Dangerous is the man who has rationalized his emotions." However, everyone, at some point, makes a decision that they know is emotionally based, whether they are willing to admit it to the world or not. Recently, the validity of the old saying that "emotion is the antithesis of reason" has come in to question. As our understanding of the brain increases and its various functions are being mapped out, more importance is being given to the role of emotions in mental activities.

Perhaps one of the best explanations as to why reason is given such a higher emphasis is because of the control we seem to believe it gives us over our situations. Conceptions of emotion include images of extreme volatility and lack of control, leaving us apprehensive and overwhelmed. The reality of the fact, however, is that most often, decisions are made by combining reason and emotion.

Science has termed the section of the brain most involved with emotions as the Limbic System. This system includes the amygdala, (where fear and aggression are found), the hippocampus, (for memory), the hypothalamus, (for homeostasis, which we will come back to), the pre-frontal cortex (for thinking about the future, and organizing behavior towards specific goals, contributes to pleasure and addiction), as well as a few small surrounding structures (1). This system works to create an emotional association of physical sensations with memories of an emotional state(2). Through the functioning of the pre-frontal cortex, the potential possible actions have for pleasure or pain is evaluated, and the Limbic system guides our reason towards actions that will result in our happiness and self-preservation(3). It is interesting to note, that when cases where a "pre-frontal lobotomy" have taken place, the patients seem to lose their abilities to express any traces of joy, fear, hope, sadness, or any other emotions(4).

Following this understanding of the Limbic system, and the nature of the hypothalamus, it seems to follow that emotions are a part of homeostasis. In order for living creatures to maximize experiences that promote their survival, certain basic actions, such as eating and reproduction, are linked with agreeable emotions, while actions that would threaten the stability of their existence are linked with negative emotions. Hence we have the natural distinction between the two basic classifications of emotion, pleasure and pain(3).

Because of the nature of the Limbic system, and the way it correlates memory with emotions, it provides us with a necessary source of information about our relationship with the world around us. Every emotion that we possess is the result of a non-consensual experience, where involuntary input entered the nervous system, and had to be sorted through by the Limbic system. Evolution has expanded on the ability of humans to associate different experiences with different emotions, so that we can experience varying degrees of agreeable and disagreeable emotions. By combining the emotions that our Limbic systems have established towards the subject with our reasoning of it when making a decision about something, we increase our chances at maintaining our homeostasis. This is not to say that everyone's emotions will be the same, or that the decision they make in the same circumstance would be the same. No, quite contrary to that, each person's conclusion would be distinct and individualized, because individual reactions vary as a result of different experiences

Recently this ability to acquire and apply knowledge from emotions and the emotions of others in order to be more successful and lead a more fulfilling life has been defined as Emotional Intelligence(5). This concept stresses the ideas that humans are born with certain emotional potentials, and that by recognizing these potentials, they can be used to enhance thinking, while thinking can be used to understand emotions(6). Thus, steps are being made to change the conception that emotional decision making is unacceptable in society. It is when emotionally based decisions are not combined with our ability to reason that our judgments tend to become volatile and unpredictable.

1)General Psychology: the Emotional Nervous System,
2)Limbic System-Wikipedia,
3)Anthony Reading. Hope and Despair. Johns Hopkins University Press, 2004.
4)Limbic System: Center of Emotions,
5)Definition of Emotional Intelligence,
6)What is Emotional Intelligence?,

Full Name:  Anne-Marie Schmid
Title:  In the Absence of Pain
Date:  2006-02-21 12:37:06
Message Id:  18271
Paper Text:
<mytitle> Biology 202
2006 First Web Paper
On Serendip

Pain is an integral part of the defense system of the body. It signals that something is wrong, and helps to minimize the physical harm that is done to the body. In the majority of cases, when a person finds something to be painful, they react in such a way to alleviate the pain, resulting in the harm to their body being minimized; however, in certain individuals, the pain is either not felt, or no reaction is observed, resulting in more harm being done to the body (1).

Congenital analgesia, also known as congenital indifference to pain, is a rare condition in which there is an absence of pain sensation from birth without the loss of other sensations or demonstrable nerve pathology (2). This can result in the individual unintentionally harming him or herself, or in an injury being made worse by the individual not realizing its severity. The first report of the condition was made in 1932, concerning a man who acted as a human pin cushion. Since then, there have been fewer than 100 reported cases in the United States (3). The exact cause of the condition is unknown; the nerves appear to be normal and functioning properly in the majority of cases. The condition is believed to be hereditary (2,, 3). The higher frequency of occurrence among the children of consanguineous parents suggests that the responsible allele is recessive, although there have been reports of what appears to be an autosomal dominant version of the condition. The reports of the autosomal dominant variation of congenital analgesia are too infrequent to come to any real conclusion at this time, but it is possible that the condition may be caused by more than one allele (5). Congenital analgesia is sometimes associated with auditory imperception, along with a trisomy of one or more chromosomes in the 13-15 group; however, this association is by no means proved (3).

Another condition with similar effects is congenital insensitivity to pain with anhidrosis (CIPA) (4). Unlike congenital analgesia, CIPA appears to be caused by a mutation in the NRTK1 gene, which codes for a nerve growth factor-specific tyrosine kinase receptor, which, as the name suggests, affects the growth of nerves. Individuals with CIPA have a highly decreased number of small myelinated and unmediated nerve fibers, to the point that they may be entirely missing in the epidermis (4). These missing fibers may explain why pain is not felt, but do not explain why most other sensations are felt, with the possible exception of temperature. In a large portion of the reported cases of CIPA, the individual lacks sensitivity to temperature changes. This may or may not be related to the anhidrosis portion of the condition, which is the inability to regulate one's body temperature by producing sweat. In individuals with CIPA, the sweat glands appear to be normal, but no sweat is produced when elicited by a variety of stimuli. This may be due at least in part to the individual's inability to sense temperature changes, as sweating is also not seen when the person with CIPA develops a fever, even when it is in excess of 109 degrees Fahrenheit (4).

A third condition involving the inability to feel pain is hereditary sensory and autonomic neuropathy type 5 (HSAN5) (6). Individuals with HSAN5 have a loss of pain sensation as well as the ability to sense temperature changes, as with individuals with CIPA. Unlike those with CIPA, individuals that have HSAN5 do not have anhidrosis; they responded normally to stimuli that were meant to induce sweating. In individuals with HSAN5, there is a virtual absence of small myelinated afferent fibers, but only a small reduction in the number of small unmyelinated fibers. The nerve conduction velocities of the tested patients were normal, but no response was seen when attempting to record an evoked response over the spine via tibial nerve stimulation. Unlike both CIPA and congenital analgesia, some individuals with HSAN5 only had a loss of pain sensation in their limbs (3, 6). There was also evidence in some cases of HSAN5 of degeneration of the unmyelinated axons, suggesting that the condition, unlike CIPA and congenital analgesia, may progress over time. Like congenital analgesia, HSAN5 appears to be caused by an autosomal allele or set of alleles, with the majority of cases appearing in children of parents who are first cousins, or a closer relation (6).

With all of the conditions, there is a high incidence of self-mutilation from infancy, as the individuals with the conditions cannot feel the pain that they are causing themselves, and thus do not know when to stop. Injuries to the lips and tongue are relatively common during teething, as the child does not realize that they are harming themselves. As the individuals age, problems from injuries such as broken bones become more common, as they do not realize that the bones are broken, and may attempt, for instance, to walk on a broken leg, feeling nothing more than slight uncomfort. In individuals with CIPA and HSAN5, there is a high incidence of complications from infection, as they cannot detect the pain or that they have a fever, and may not realize that they are ill until the infection has become serious. In the past, there was a high chance of death during childhood for those with any of these conditions, due to the inability of doctors to diagnose and treat the conditions, and the inability of the individual to detect illness at an early stage, along with their inability to realize when they were harming themselves. Today, survival rates have increased, although raising a child with one of the conditions mentioned above is very difficult. While they are young, they require near constant supervision to make sure that they are not harming themselves, and must visit a doctor more frequently than children without one of the conditions. Once they are older, the majority of the supervision may end, but extra care must be taken to prevent them from accidentally injuring themselves (3, 4, 5, 6).

At this time, the exact causes of congenital analgesia, CIPA, and HSAN5 are not known, although mutations that tend to occur in individuals with these conditions have been noted. I am surprised that there hasn't been more research done on the subject, as it could lead to advances in other areas, especially if the nerve degeneration in HSAN5 occurs on a similar manner to nerve degeneration in other diseases. Further research into the causes of CIPA and congenital analgesia may also prove fruitful, as it could lead to new methods of blocking pain.


1. Mogil, Jeffery S. "The Genetics of Pain and Pain Inhibition." Proceedings of the National Academy of Sciences of the United States of America. Vol. 93, No. 7. (Apr., 1996), pp. 3048-3055.

2. Mogil, Jeffery S. "The Genetic Mediation of Individual Differences in Sensitivity to Pain and Its Inhibition." Proceedings of the National Academy of Sciences of the United States of America. Vol. 96, No.14. (Jul., 1999), pp. 7744-7751.

3. OMIM - Indifference to Pain, Congenital, Autosomal Recessive.

4. OMIM - Insensitivity to Pain, Congenital, with Anhidrosis.

5. OMIM - Indifference to Pain, Congenital, Autosomal Dominant.

6. OMIM - Neuropathy, Hereditary Sensory and Autonomic, Type 5.

Full Name:  Liz Paterek
Title:  Autism: A Disconnected Mind
Date:  2006-02-21 12:39:37
Message Id:  18272
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Many people still believe that autistic children are the equivalent of a normal child trapped within a glass shell (3). The information that is open to the masses is vague and minimal. It is described as a flaw in the ability to communicate and interact socially. Causes of autism often point simply to structural abnormalities in the brain (1). There is a general focus that each child is an individual, with a variety and symptoms and expressions of symptoms (1) (4). The reasons and theories about the causes of autism and relationship between symptoms are missing.

The mind of an autistic child is very different from that of a normal child. It is defined by four common behaviors: a desire for sameness, a preference for aloneness, a desire to follow complex routines, and abilities that seem exceptional compared with deficits (3). Autism does not always include mental retardation, although this is common (3) (6). The behaviors expressed often have to do with problems in communication, socialization and imagination (3).

Autistics may have trouble with second order representation, which involves imagination and integration of ideas leading to problems in communication, socialization and imagination (3). . They know the visible events of the world but cannot understand metaphoric or incongruous information (3). They see many details but cannot form full picture or concept (4) (6) (8). While they may be able to perform complex tasks their understanding of what is happening is minimal; for example they may memorize 7000 novels, but cannot understand them (4) (7). They take everything in the literal sense (3) (4) (7). Conversation is often full of facts and rarely interactive (4). They may also lack theory of mind, which is the ability to understand the mental state or intention of another (3) (6). High functioning autistics can learn social routines, camouflaging their disorder, because social skills that do not involve an exchange between minds can be learned (3). .

The biology of autism is not well understood. It may be controlled by up to 20 genes, where autistics can carry only some of the genes, and the genes can remain silent in others (5) (6). Even in identical twins, if one has the autism there is only a 60% chance of the twin also expressing it (5). Different autistics express different genes (6). This results in possible structural variations between individuals.

Chemical agents can cause damage to the brain resulting in autism. Thalidomide babies showed higher than normal rates of autism. Further studies and comparison with other related developmental problems showed evidence that the brain damage that causes autism occurs early in pregnancy, when the brain is first forming (5). It has been suggested testosterone early in development damages the left brain of male babies and accounts for the higher rates of autism in males than females (5). Oxytocin, a hormone which regulates social behavior in mammals through receptors in the brain, is present in lower levels in autistics. When levels are increased, repetitive behaviors decreased (6).
Autistics receive information from the outside world as well as normal children, as demonstrated by the abilities of some to create flawless renderings of their surroundings (7). What they cannot do is integrate and understand the input (3). Therefore, it can be concluded that it is a problem in the brain's interpretation of the input and not the input that is altered.

Evidence points to both disconnections in the brain and deformities in different regions as causing the symptoms. MRI's during questioning sessions make it appear as though some areas of the brain are disconnected href="#8">(8) (7). It is speculated that the long fiber tracts that connect mirror neurons are less organized in autistics altering the way that information is integrated href="#8">(8). They also have a greater amount of white matter, especially in the frontal regions where information integration occurs href="#5">(5) href="#8">(8). It is suggested by the pattern of white matter that brain regions like the prefrontal cortex may have hyper-efficient internal processing but may have poor connections to those of other areas href="#8">(8). This may be the reason autistics show incredible talents in only a few areas. Frontal regions active in understanding other's intent tend to be less active in autistics. The visual region as well was out of synch with the mental-strategy network, which may be the reason autistics have trouble with motor function href="#8">(8).

The prevalence of savant-like abilities in autistics suggests that there are problems in communication with the left hemisphere of the brain for which the right compensates. Autistics comprise half of all savants (7). These individuals can perform activities that are functions of the right brain, such as math, art, and memorization but the understanding and creativity of the left brain are lost. This has been shown in brain scans that there is often damage to the left hemisphere. It has also been shown that the right hemisphere can be hyperactive (7).

Both the amygdala, which controls emotion, and the hippocampus, which is responsible for learning and memory, are decreased in size. They both have fewer connections to other regions of the brain, possibly leading to the inability to interpret emotions and understand concepts (6). When viewing faces, the amygdala becomes over stimulated leading to the aversion of eye to eye gaze (2). Cerebellums often show deficiencies in Purkinje cells, which are important in brain circuitry leading to further disconnection (6). The brain stem just above the spinal chord is shorter with the pons and medulla closer to the lower medulla, as though a piece is missing (3). The pons is important in the relay of sensory information between the cerebrum and cerebellum. The medulla relays information between the brain and spinal chord (3). These deficiencies further point to a disconnected brain at the root of the disorder.

There is an abundance of evidence suggesting that autism is linked to malfunctions in areas of the brains but mostly in the communication of one brain region to another. These malfunctions change the way input is integrated and trap the autistic in a world they cannot interpret. Functions of understanding and communication become very difficult. While autism has a genetic link, it seems that environment plays a huge role in the expression of the genes. While there is still a lot that is unknown, the best available information is published in online journals and not on the web.

1) Autism Society of America1) Autism Society of America. Accessed 20 Feb 2006.
2) Beard J. New View on Autism. Scientific American Mind. 2005
3) Frith U. Autism. Scientific American ©1997 reprinted from June 1993 issue
1) National Institute on deafness and other communication disorders 4) National Institute on Deafness and other Communication Disorders. Autism and Communication. NIH Pub No 99-4315. Oct 1998. Updated Jan 2003. Accessed 20 Feb 2006
5) Rodier P. The Early Origins of Autism. Scientific American. Feb 2000
6) Stokstad E. New Hints into the Biological Basis of Autism. Science Magazine. 5 Oct 2001. Vol 294 no.5540. pp 33-37
7) Treffert D, Wallace G. Islands of Genius. Scientific American Mind. 2003
8) Wickelgren I. Autistic Brains Out of Synch? Science Magazine. Vol 308 no 5730

Full Name:  Faiza Mahmood
Title:  What Causes Depression?
Date:  2006-02-21 14:13:48
Message Id:  18274
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

We all have felt depressed at one time or another in our lives. However, there are individuals that experience this very same feeling over much longer periods of time. Clinical and major depression is characterized by an array of symptoms that primarily deal with a change in one's behavior. If Emily Dickinson's theory of brain being analogous to behavior is in fact true, this would mean that a change in the brain would trigger individuals to behave in the manner they do. However, this notion is not necessarily supported by what some believe to be causes of depression. In that, the behavior of a depressed individual may solely have to do with environmental factors that don't necessarily change the brains composition or circuits. Most studies and evidence I have come across show this is not the case and that the brain does indeed equal behavior in the case of depression.

Major depression is growing in all different age groups, crossing all borders of different backgrounds and ethnicities. Even the president of the United States is on anti-depressants. (2)
At the rate of increase, it will be the 2nd most disabling condition in the world by 2020, behind heart disease. (1).

Being clinically depressed is quite different from just feeling down. It is considered an actual disease. Many different depressive episodes exist and can last for months, and even years. This state of mind can interfere with your social and work and overall functioning. It is usually characterized by at least five of the following symptoms that represent a change in lifestyle, and thus behavior: having a depressed mood most of the day, almost everyday, a decreased interest or pleasure out of all, or almost all, activities, a significant weight loss or weight gain –or just an increase or decrease in appetite nearly everyday, insomnia or sleeping too much, fatigue or loss of energy nearly everyday, feelings of worthlessness or excessive or inappropriate guilt, diminished ability to think or concentrate, or indecisiveness, and recurrent thoughts of death, suicidal idealation or an actual suicide attempt. (1)

The actual basis of depression is unknown but it may be attributed to and influenced by genetic, environmental and neurobiological factors. Perhaps, the biggest debate on what causes depression is based on a debate on whether neurochemical imbalances or environmental influences such as unfortunate events, certain life experiences or negative thinking cause depression.

Many brain chemicals, neurochemicals (such as nonrepinephrine) and hormones have been linked to the development of depression. Monoamine depletion is most often the disturbance that is commonly detected in depressed individuals. Serotonin, norepinephrine, and dopamine have been identified as the main trigger causing components in depression with serotonin and norepinephrine being evidenced as the more prevalent of the bunch. "Among the findings linking impoverished synaptic norepinephrine levels to depression is the discovery in may studies that indirect markers of norepinephrine levels in the brain-levels of its metabolites, or by-products, in more accessible material are often low in depressed individuals. In addition, postmortem studies have revealed increased densities of certain norepinephrine receptors in the cortex of depressed suicide victims" (3)

Deficiencies in the serotonin 5-HT system are observed in depressed individuals as well. These depletions may interact with and may be responsible for falls in norepinephrine levels mentioned above. Serotonin secretion may also account for the emotional, appetite, libido, and sleep disturbances associated with depression. (3)

Hormonal abnormalities may also characterize the depressed brain especially those caused by the release of an excessive amount of stress hormones. The most significant irregularity lies in the hypothalamic-pituitary-adrenal (HPA) axis, the system that manages the body's response to stress. When a threat to physical or psychological well-being is detected, the hypothalamus increases production of corticotropin-releasing factor (CRF), which, in turn, induces the pituitary to secrete adrenocorticotropic hormone (ACTH). ACTH then instructs the adrenal glands to release cortisol. Thus, chronic activation of the HPA axis may result in illness and depression. (3)

Some attribute these neurochemical abnormalities to be caused by genetic factors providing support for the theory that brain does indeed equal behavior. As your genes may carry information to cause your brain to alter your behavior. It has been found that depression and manic-depression frequently run in families. Thus, close blood relatives (children, siblings and parents) of patients with severe depressive or bipolar disorder are much more likely to suffer from those or related conditions than are members of the general population. This observation was largely made by studies of identical twins and fraternal twins support an inherited component. For example, if one identical twin suffers from depression or manic-depressive disorder, the other twin has a 70 percent chance of also having the illness. (4).

Then there is the notion that ego-damaging experiences and self-deprecating thoughts cause depression. The mind, however, does not exist without the brain. A considerable amount of evidence though, indicates that regardless of the initial triggers, the final common pathways to depression involve biochemical changes in the brain. It is these changes that are giving rise to the characteristics of depression. (5).

In conclusion, it seems as though depression is caused by a variety of different factors, all of which ultimately induce the same biochemical pathways to produce the effects and onset of depression. There doesn't seem to be one main absolute cause. However, it does seem that all the causes seem to be in accordance with the fact that brain does equal behavior, in that they all seem to induce certain brain activity and the onset of similar biochemical pathways that cause changes in the brain, causing depression. Depression is most likely onset by a combination of the causes mentioned previously and may vary from individual from individual. It is almost analogous with something like heart disease, although one may be predisposed to it, it doesn't mean you will necessarily get it and others may not predisposed to it, but experience it solely because of environmental factors. Similar observations can be observed with depressive episodes, by the fact that there are individuals that exist , that encounter depressive episodes with no history of stress or trauma, thus making the imbalance of neurochemicals or abnormalities in hormone production questionable, yet still display similar brain circuit patterns as depressed individuals. (5). Genetic factors may play a role in this case. However, it can also be argued that genetics isn't the sole cause, perhaps certain people may be predisposed to experiencing depressive episodes but one can't assume by the sole fact that depression runs in families that there is a strong genetic basis, as depressed parents may induce the onset of depression in their kids. Then there are examples that because the emotional needs of an individual are not being met based on ones environmental influences, depression occurs. An example supporting this is observed by the contrast of traditional communities. They tend to naturally meet many basic needs for emotional support. In the traditional Amish society in the US major depression is almost unknown, as it is in the equally traditional Kaluli tribe of New Guinea. In these societies individual concerns are group concerns and vise-versa. (1). Thus, depression can be caused by a combination of factors, such as a combination of individual being pre-disposed to depression and experiencing unfortunate life events simultaneously, or it may be primarily be caused by one or two factors. Lastly, one of the most significant things that most people may miss in the argument of what causes depression is the fact that there is substantial evidence that environmental factors are indeed affecting the chemical pathways of our brain, thus altering one's behavior. (5). So, essentially it may be possible to say that there are two generalized major causes of depression, genetic influences and environmental factors, which cause neurochemical or biological changes producing the symptoms of depression.

1) Depression Learning Path
2) Bush Taking Anti Depressants to control mood swings, amusing article although not sure how legit all of it is.
3) The Neurobiology of Depression
4) Depression
5) Depression Center

Full Name:  Brooks Ambrose
Title:  Neurobiology ? Sociology
Date:  2006-02-21 15:04:20
Message Id:  18275
Paper Text:
<mytitle> Biology 202
2006 First Web Paper
On Serendip

"The basis of the parallel between organic evolution and human progress is what is known as the postulate of reductionism: that is, that biology should eventually be reduced to physics and chemistry and, correspondingly, the behavioral sciences to biology...A living organism, it is assumed, is an intricate physiochemical system; hence, human behavior is a particularly involved complex of the ways and factors of behavior present in subhuman species. Human values are viewed as being derived from and ultimately reducible to biological values which essentially entail maintenance of the individual, survival of the group, and evolution of the species (1) (2)."

"Man, as the old saying goes, is a denizen of two worlds. He is a biological organism with the physical equipment, drives, instincts, and limitations of his species. At the same time, he creates, uses, dominates, and is dominated by a higher world which, without theological and philosophical implications and in behavioral terms, can be best defined as the universe (or universes) of symbols. This is what we call human culture; and values-esthetic, scientific, ethical, religious-are all part of this symbolic universe. This is what man tries to achieve beyond satisfaction of his biological needs and drives; in turn, it governs and controls his behavior (3)."

- Ludwig von Bertalanffy (1959)

This paper problematizes the often explicit hope among neurobiologists that all aspects of behavior can be explained in terms of highly complex material structures, most often inter-assemblages of neurons. Through the language of general systems theory, I characterize the theoretical and empirical condition at which neurobiological theory necessarily reaches its limit as an explanatory paradigm. I posit patterns of human social action as one example of an anomaly beyond the reach of neurobiology. I end by asking speculatory questions about the nature of the theoretical revolution that could potentially resolve the anomaly I construct.

As it is central to the paper, I will begin with a discussion of general systems theory (GST). Sometimes accused of being an empty theory of everything empirical, GST is in reality any of a variety of highly abstract schema designed to organize theory itself; it is a theory of theories, and it relates to the empirical world only as mediated by the scientific paradigms that are its objects of inquiry (4) (5).

GST is a theoretical resource which researchers may use to more clearly articulate whether the formal logics of two scientific disciplines are sufficiently isomorphic to allow a productive exchange of formal theoretical relationships (6). GST establishes a common set of terms that have the capacity to abstract the formal logic of a theory to a plane where it can be compared to theories that seem relatively distant in normal academic parlance. As its practitioners clearly state, such a process of abstraction strips particular empirical theories of almost all of their content and leaves the theorist with only the most general relationships available within the theory (7). These general relationships are not without their usefulness. Indeed they can clarify relationships not apparent at concrete levels of analysis.

The category of cybernetic theory is an example of a generalized logic applicable across a wide range of phenomena and it is one we will make use of in our discussion. Cybernetic theory elucidates a particular type of relationship within a system, for our purposes, a living system (8). A cybernetic relationship exists between two structures, one high in energy and the other high in information. The energy structure represents a finite range of variability. The information structure establishes the particular value to which the energy structure responds. If the information structure sets a value within the range specified by the energy structure, the value is achieved by the system. In this case the information is said to control the energy. If the information sets a value outside of the range of energy, the value will not be achieved. In this instance the energy is said to condition the information.

How does the human organism fit into the logic of a cybernetic relationship? It is plausible to treat the body and behavior as a package constituting energy for the human organism. The question then becomes, what is the information that is in systematic relationship with that energy? Neurobiologists base their science on the premise that it is the material structure of the nervous system that is the structure of information in control of the body's energy (9).

Does the neurobiologist's response qualify as the type of biological reductionism that Bertalanffy denounces in the passage at the head of this paper? I think Bertalanffy's criticism stands only if there is a disjuncture between his preferred information structure, the symbolic universe, and the preferred information structure of the neurobiologist, the nervous system. In other words, does the neurobiologist take into account both of man's worlds, or just the non-symbolic world of "subhuman" behavior?

I am not in a position to evaluate this question, but I can lay down the rules of the game, which amount to the location of information in relation to the boundary of the nervous system. (For the sake of argument ignore DNA as a source of information in this construction.) Simply, if an information structure anything like a "symbolic universe" exists outside of the boundary of the nervous system but within the boundary of the human organism, the neurobiologist loses. If no structure of information exists within the human organism between the nervous system and the environment, then the neurobiologist wins.

If the first question is, "Where is the information that controls behavior located?" We must also ask the following question: for any given information structure within the nervous system, where was the pattern of that information originally constructed? If patterning within the nervous system has a birth in something other than a neural structure, the nervous system can claim credit only for acquiring the information, not for constructing it out of whole cloth. Also, what is the potential scale of this criticism? If five percent of the nervous system owes its organization to phenomena that are fundamentally outside of itself, then perhaps neurobiology has little to gain by submitting to the trauma of a scientific revolution. However, what if fifty percent of the organization of the nervous system is exogenous? What if eighty percent is exogenous?

Under these circumstances it seems clear that a researcher would not be able to understand a particular neurological pattern unless she already understood the exogenous information structures at play, be they symbolic patterns or something else. Any effort to achieve an understanding of these exogenous structures would require the researcher to extend beyond the bounds of an explanatory system in which the basic unit is the neuron.

To close, this discussion must be elaborated from the standpoint of a superior conceptualization of the difficult concept of information. Also, if it is true that the disciplines of sociology and biology intersected in the intellectuals of the General Systems Theory movement, it may be instructive to understand why they seem to have separated entirely by the present day.

Web References

1) Bertalanffy, Ludwig von. 1981. (1959). "Human values in a changing world." Ch. 2 in A Systems View of Man. Boulder: Westview Press. pp 9-22. Originally in New Knowledge in Human Values. Ed. A. H. Maslow. New York: Harper. pp 65-74.

2) Ibid, pp 14-15.

3) Ibid, pp 17.

4) At the core of GST is a dichotomy between theories that are descriptive and theories that are explanatory.

Descriptive concepts serve only to provide handles to approach empirical phenomena. Though often tied together by the logic of a nomenclature, within a given descriptive schema, concepts are in a strict sense analytically isolated from each other. Each is defined not by other concepts but by its empirical reference. Descriptive schemas can often be characterized as maps or catalogs. Generally weak on their own, descriptive schemas form a basic theoretical resource used in the creation of explanatory theory. As a result, the implicit "accuracy" of a description can directly affect the usefulness of an explanation derived from it. The neuroanatomy that underlies contemporary neurobiology is an example of a descriptive theory which was used heavily as a resource in the development of a more explanatory theory.

Explanatory concepts are relational, that is, they derive their meaning from other concepts to which they are systematically related. Unlike descriptive concepts which derive meaning from an empirical reference, explanatory concepts lose all meaning when isolated from the constellation of concepts defining the schema. For example, whereas within an anatomical schema the concept "foot" makes sense without the concept "ear," the concept of the lever does not make sense unless one grasps its relationships to the concepts of fulcrum, effort, and load. Understood together, the four concepts constitute an explanatory schema, an indivisible network in which a change in any component can be understood in terms of its effect on other components in the system.

5) Boulding, Kenneth. 1956. "General systems theory - The skeleton of science." Management Science. 2: 197-208. Reprinted in Emergence: Complexity and Organization; The descriptive/explanatory dichotomy corresponds roughly to the difference between "frameworks" and "clockworks," which are Boulding's first and second "levels of theoretical discourse" (pp 202). Because Boulding conflates categories of logic with particular models of logic, he makes the mistake of relegating "static" and "catalogical" models to the descriptive category and "dynamic" models to the explanatory category. In fact "static" models are often a viable basis for explanatory theory, comparative-static explanations within economics being a good example.

6) The GST's many models grow along two trajectories, one weak and one strong. Theory within the weak trajectory was developed with the intention of opening up lines of communication between increasingly specialized sciences operating within idiosyncratic theories. Respectful of the autonomy of scientific disciplines, the weak form of GST seeks to develop a common formal language that can serve as a set of "generalized ears... to enable one specialist to catch relevant communications from others". The strong form of GST also seeks to open up lines of communication, but it does so with the specific intention of prosecuting a critical reconstruction of one paradigm by another. The strong form of GST is like an intellectual Trojan horse coaxing one paradigm into a critical debate so that it can be colonized by the logic of an "invading" paradigm.

The weak form of GST tends to treat scientific disciplines as sovereign within relatively clear empirical boundaries. The strong form of GST is likely to emerge when these boundaries are contested, when two fundamentally different paradigmatic logics claim sovereignty over the same set of empirical phenomena.

7) Ibid, pp 197-198.

8) Grobstein, Paul. 1994. "Variability in brain function and behavior." In Vol. 4 The Encyclopedia of Human Behavior. Ed. V.S. Ramachandran. Academic Press. pp 447-58. The relevant passage is the first three paragraphs of section two, entitled, "Behavior and the nervous system."

9) (Boulding, pp 198-199).

Full Name:  Scott Sheppard
Title:  Creativity Machine's: Giving Them Elbow Room
Date:  2006-02-21 17:05:09
Message Id:  18278
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Before Stephen Thaler perhaps it was the words of Poe, Dickenson, or Delillo that kept men and women shivering in their insomnia as they pondered the questions of identity, questions of freedom, human creativity, and death; but now a new set of words has the potential to strike such fear in the hearts of humans—the dying words of a hallucinating computer program. In 1989 Thaler took a giant step towards the possibility of artificial intelligence as he witnessed a machine begin to take on aspects of human creativity. On Christmas Eve Thaler was wondering if he could learn anything about near death experiences by observing the 'death' of a computer program, so he designed a simple program to spit out the words of familiar Christmas Carols. This program was not extraordinary in any way—it utilized a switch-based, Boolian-logic configuration where every action follows deterministically from other actions. Its structure prohibited it from deviating from the information or rules it had been given, but Thaler made things interesting when he introduced a "Grim Reaper" program into the Christmas Carol program. This second program was designed to gradually and systematically destroy the connective switches by disassembling the interlocking patterns that defined the Caroling program's integral organization. As the program 'died' it began to run through all the combinations of songs that it knew—it's life "flashed before its eyes." This phenomenon was not the end of the discoveries however as the program's destruction became a catalyst for unexpected creative processes:
" began to hallucinate. The network wove its remaining strands of memory together, producing what someone else might interpret as damaged memories, but what Thaler recognized as new ideas. In its death spiral, the program dreamed up new carols, each created from shards of its shattered memories. "'Its last dying gasp was, 'All men go to good earth in one eternal silent night,'" Thaler said" (7).

Although the meaning of this sentence is eerily self-reflective, the significance of the program's last statement is not in the words' natural meaning. It is rather the phenomenon of an un-programmed Christmas Carol line that was created in the liminal space between established memory and random deviation. Human consciousness and creativity have remained sacred ideas even into the twenty-first century, but this unexpected output exemplifies how a controlled amount of chaos in a parameterized system can create results that are neither irrelevant nor expected. Thaler saw the potential for computer systems to literally think outside of boxes that had originally been closed, and it was this basic principle that inspired the invention of a creativity machine (4). A creativity machine is one whose architecture is changing and adapting in very specific ways to produce more imaginative outputs than closed computer programs are capable. This does not imply that a computer system can now have an imagination, but that by disrupting the established weights and thresholds of certain internal switches with fractal algorithms, a program will create new information that is born from probabilistic rules rather than deterministic ones. Before a set group of interactions might always output five ones and five zeros, but by imposing the very specific fractal equation that Thaler began to use, the output was not restricted to the same gate openings and closings all the time (6). Probabilistic programs force the system to create irrational results so that they can be figured into the map of conceptual space that that a program explores. These conceptual spaces can be anything from songwriting, durability of plastics, mixed drink combinations, or chess.

When an 'un-creative' computer chess program, for example, sets out to make the best move possible in a certain situation, it begins to sort through its memory. This memory contains the objectives and rules of the game and also contains a rich and diverse history of millions of grandmaster games. Obviously, if a computer program were given enough time it could run through every combination of possible moves, but this type of processing is inefficient and lacks the type of insight that is at work in human thinking. In order to emulate the human's ability to remember and learn, the un-creative chess program will refer to large sets of games and chess knowledge in its memory, but the effectiveness of the chess program still depends on set patterns that it has seen work before based on games that have already been played. Despite a combination of thousands of chess styles and situation-based information, its decisions are still limited to its past and its improvement depends upon new memory input from the outside. As the game progresses the computer becomes more likely to miss a move because it is less probable that it will perfectly 'recognize' a situation from its memory bank.

A chess program driven by the model of a creative machine acts differently because it does not require input in order to learn. Similarly to the un-creative program, the creative program has a wealth of knowledge that guides and influences its decisions, but it also incorporates low-level random perturbances that will cause the program to break away from its historical patterns and 'test out' decisions that go against its history. The results of this experiment will then be re-introduced to the program's history so that it knows why something does not work that it usually ignores (2). By controlling the perturbance level, the program will be more likely to deviate when it has little background evidence supporting a decision. It turns out that by trying out moves that have no basis in memory a program will create its own discovery drive where more unfamiliar situations are given more flexibility which abets learning rather than deterministic ignorance (6).

Chess is a unique conceptual space because chess' objectives exist independently from human revaluation, and therefore a creativity machine can verify which creative ideas are useful according to a set of rules. According to sources Thaler's creativity machine has figured out 11, 000 new potential hooks for pop songs and 15, 000 mixed drink combinations, but whether or not these ideas are good is a function of human validation (2). Creativity is the combining together of old ideas together to form new ones, but these ideas must be useful or interesting in some way. Combination-theory is the idea that the most improbable combination of old ideas are also the most creative idea, but this theory fails to recognize the complexity behind human evaluation (1).

Thaler's creativity machine will continue to prove most valuable when its purposes can be objectified and quantified, but when it seeks to make drawings, music, and literature a program's ability to learn and adapt at very fast rates is put into check by human variability. Even as a creative machine begins to learn how to create songs or food that people like, these opinions may change as tastes and fads tend to do. The machine's creativity can never get too far ahead of itself because humans will adapt to the machine's creations and factor this into their likes and dislikes. They will begin to reject certain creative ideas that they would have liked five years ago to pursue a niche that is inherently more mystifying and unsuspected. Where the objectives are clear, the creative machine can continue a process of hyper-evolution. Already the human imagination can see how scary the machine's imagination could be because it will improve upon its own methods the more it works on a task. The implications of a creativity machine whose objectives are dangerous do not need to be unpacked. When the words "All good men go to good earth in one eternal silent night" echo, the poignant fear is not about threatened identity or a de-mystification of the human spirit, but what resonates profoundly is the fear that machines with creative technology could be set to many horrible, destructive tasks, and they could learn to complete them with more mastery than was ever imaginable.


1)Creativity and Unpredictability

2)The Creativity Machine Paradigm

3)The Biology of a Creative Mind

4)Artificial Neural Networks

5)Fractal Chaos

6)Fractal Geometry

7)Thaler's NDE Experiment

Full Name:  Stefanie Fedak
Title:  Does Brain Always Equal Behavior? Behavioral Therapy and OCD
Date:  2006-02-21 17:52:10
Message Id:  18280
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Imagine leaving for your morning commute an hour earlier than necessary, in order to accommodate a series of ritualistic behaviors, which to an uninformed observer appear non-sensical, excessive, or bizarre. What if you had to wash your hands multiple times before leaving your home? What if you needed to check and re-check to make sure the front door was locked, and once you had checked the door sufficiently, you had to count out exactly 20 steps from your front door to car door? Imagine that if any portion of your morning ritual is done improperly, you must begin again, performing the rituals as many times as necessary in order to satisfy an unwavering and unsettling impulse or obsession. Roughly 2.2 million Americans over the age of 18 suffer these, or similar symptoms associated with Obsessive Compulsive Disorder (1).

Obsessive Compulsive Disorder (OCD) is a common anxiety disorder, characterized by "intense, recurrent, unwanted thoughts and rituals that are beyond the person's control" (2). Records of OCD and similar disorders are well documented for at least the last 300 years. As with many mental health conditions prior to advances in modern science, OCD was attributed to bad religious experiences, demonic possessions, or general loss of will on behalf of the afflicted (3). Modern science has continued the process of "getting it less wrong" by using new technology to uncover potential causes of OCD rooted in the brain, with the hope of working toward more effective treatment options; however, if OCD is a problem relating to brain function and/or neurochemistry as some hypothesize, how can options such as behavioral therapy be effective in OCD treatment? Can behavioral treatments change inherent differences in brain function?

Throughout the 20th century, a psychoanalytic approach to OCD was adopted; the medical community believed that OCD could be attributed to feelings of unresolved conflict from early stages of psychological development (3). Psychoanalysis, while effective in uncovering symbolic meanings for obsessions and compulsions, has no root in scientific evidence, specifically studies relating to the human brain and has become a less used theory to explain the onset of OCD.

The use of positron-emission tomography (PET) has allowed for researchers to view images of the brain in order to see where differences between individuals with OCD and individuals in the control group differ, with the hope of uncovering a structural disparity between the groups (6). Differences have been noted in metabolic activity within the frontal cortex and basal ganglia regions. Regulation of brain abnormality is more difficult to tackle, whereas if differences exist in the neurochemistry of a patient with OCD, the most sensible option would be to adminster a drug to adjust the brain chemistry of the affected patient in order to produce a normal pattern of function. Through clinical experiments, the chemical serotonin was found to be lacking in patients who exhibit OCD. Serotonin reuptake inhibitors (SRIs) such as Zoloft, Paxil, and Prozac were administered to patients. Administering SRIs to patients has had a markedly high success rate, near 75%, in the reduction of behaviors associated with OCD (3). The introduction of SRIs has shown in PET scans visible changes in the brain activity of OCD patients, bringing it more in line with the scans of persons in the control group. Though medication is effective, is it the only possible recourse available to afflicted persons?

Growing evidence shows that behavior therapy may have a similar effect on brain chemistry as medication (4). Behavioral or cognitive therapy is meant to help individuals conquer mental health problems including, but not limited to OCD and associated anxiety disorders, by exposing the person to their source of anxiety and forcing them to overcome the feelings and compulsions associated with it (5). Therefore alterations in behavior rather than brain/neurochemistry can bring about not only a visible change in the actions of OCD individuals, but an actual change in neurological scans such as PET and MRI (6).

While the causes of OCD largely remain unknown and the best course of treatment – drugs, therapy, or combination of the two – differ on a case by case basis, scientists continue to uncover new ways of approaching OCD and similar disorders. When I initially thought about brain equating to behavior, I thought the brain could only be altered internally – by way of chemicals and other treatments directly impacting the brain – and that behavior is in turn altered by changes in neurochemistry. My eyes are now opened to the possibility that behavior can equal the brain, and a change in behavior can lead to an actual change in neurological composition and function.

1)National Institute of Mental Health, This aspect of the site is devoted to statistical information regarding mental health in the United States.

2)Web MD, A basic defintion of Obsessive Compulsive Disorder.

3)Psych Central , A resource for psychological information produced by Dr. John Grohol.

4)OCD Online , A website devoted completely to OCD facts, developments in research, and frequently asked questions.

5)Bio-Behavioral Institute , Website of a private, New York based treatment and research facility offering medical, psychological, and nutritional services.

6)National Institute of Mental Health , Site provided by the National Institute of Mental Health devoted solely to OCD and related information.

Full Name:  Trinh Truong
Title:  The Source of All Fears
Date:  2006-02-22 00:46:37
Message Id:  18282
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

What are fears but voices airy?
Whispering harm where harm is not.
And deluding the unwary
Till the fatal bolt is shot! — Williams Wordsworth

Contrary to what Wordworth believes biologists might argue that fears are more than empty threats deluding us until our deaths. Fear serves as a purpose to caution us about the consequences of our actions as well as events in our surroundings. When we feel the presence of fear we know to be more alert, to look out and think more carefully about participating in dangerous activities. From spiders and snakes to heights and flying on planes, there is something that makes our breath a little shorter, our hearts beat faster, our palms sweaty and limbs go weak; something that makes us fearful. But sometimes these fears grow out of control and hinder us from conducting daily functions. For some people this happens more often than others, which presents the question: Why are fears better managed or conquered in some people than in others? To examine this question we must first look for the source of fear in the brain.

The part of the brain that manfactures and processes the feeling of fear is believed to be in the connections between nerves in the amygdala, a small almond structure positioned at the tip of the hippocampus. (3) Along with its important role in producing fear, it is also associated with memory learning and aggression. Research has shown that this region of the brain does not necessarily produce the response to fear but rather mediate in learning the association between a memory of harm or pain with another stimulus and sends signals to other region that will then produce the effects of fear. (1) For example, even when the amygdala is injured in rats, they will still show a fear response such as increased heart rate and breath, and release of stress hormones when they experience a shock that is associated with light. However, this fear response is not produced when the rat is only exposed to the stimulus of light associated with the shock. In a rat with a functioning amygdala, the fear response is evident simply from the light stimulus alone because the rat has learned fear from making an association between the pain of the shock and light. Still, a person could make an association between pain or harm and a stimulus but this is not necessarily fear learning itself. When people with damaged amygdala were used as subjects in the same experiment of shock and light, they were aware and able to make the connection between the appearance of light and the pain of the shock, but they did not exhibit any expressions or symptoms of fear at the exposure to the shock. The loss of their amygdala disabled them from learning fear. (1)

Just as there is a place in our brains to learn fear there is another that calms or learns to no longer be afraid of a stimulus that has once evoked fear. Research has been able to identify the prefrontal cortex as the region where fear is calmed in the brain once it is stimulated. (2) In the experiments that led to this discovery rats, conditioned to identify a tone with a shock, were presented with the tone without the shock, causing them to freeze. However, after many repeated tones without shock, the rats no longer freeze. As the rats learn to not be afraid of the stimulus the measured activity of neurons at their prefrontal cortex increased and activity at their amygdala decreased. (2) In rats with damaged prefrontal cortex the new "safety memory" is learned on the day of the experiment but never stored causing it to continually be freeze at the sound of the tone the next day. This indicated that the activity in the prefrontal cortex is able to inhibit activity in amygdala, enabling the rat to learn new memories that will inhibit their fears. The fear memory continues to be stored in the amygdala but it is prevented from inducing symptoms of fears. (4) Although there are no similar tests conducted in humans, it is believed that those with anxiety disorders have less activity in this region of their brains, in which case the amygdala's "fear memories" will overpower their prefrontal cortex "safety memories." (2) Brain-imaging has shown that in humans with posttraumatic stress disorder the prefrontal cortex is unusually smaller and less active than in normal people. (4)

Based on researches of the amygdala and the prefrontal cortex, it is safe to say that the differences in fearfulness between people lie the organization of these regions of their brain. Still we can go a little further and tracing causes of fear beyond both of these regions of the brain, and it comes down to our genes and their differences. Scientists believe that they have stumbled upon the fear gene "stathmin." which is found in high levels in the amygdala and believed to control our ability to remember and identify stimulus of fear. Mice that have been genetically engineered to be stripped of the stathmin gene have a reduced anxiety to fear stimulating situations that normal mice would respond to with fear. Although the mice lacking the gene were not less sensitive to pain than normal mice they were less sensitive to a fear stimulus linked to pain, because there was no fear memory of the stimulus and pain in their brain. (5)

Examining the sources of fear more thoroughly will perhaps enable us to develop techniques that might control our fears and help those with fear related disorders. I think there are several general approaches we can take. First of all, we can manipulate the amygdala and subdue its effects and ability to connect fear to stimulus by interferring with the neurochemical signaling among its neurons. Another option could be the prefrontal cortex, in which we will enhance its ability to inhibit the amygdala and create and store "safety memory." A third, but more controversial option would be the manipulation of our genes. However, there is a possibility that gene could produces multiple effects on the brain that we still unknown to us, and affecting it could produce unanticipated detrimental effects in other regions other than the amgydala. Although significant in understanding our fears, genetic engineering is probably not the best approach to controlling them at the moment.

These fact that a fear gene exists then suggests that we all come into this world with a predisposition for a certain level of fear. The notion that some people over-respond and some under-respond to certain situations seems to lie greatly on their genes differences. For me this new understanding of fear certainly shakes my perception about personality, character and society's conception of virtues. For example, if courage is the resistance of fear as Mark Twain says, then perhaps courage is simply a product of our genetic make up. Should society then praise someone for being courageous when it was simply pure luck that this person was born with genes that controls certain regions of his/her brain better than another? Also, should cowardice be considered shameful when it is a possibility that the person who is attributed with this trait has little control over his fear? This causes me to then question what other personality traits might simply be manifestations of genetics and to what extend people can change who they are and their personalities. Furthermore perhaps all personal traits can be traced to some genetic sequence encoded in our genes, which then organizes the neurons in a certain manner that produce a certain degree of that trait. Just as we can manipulate the chemical interactions in our body and brain to better our health and prolong our lives, we might be able to manipulate our genes to produce desirable personality traits. Whether we want to or not has yet to be disputed.

WWW Sources

1)Fear Conditioning: How the Brain Learns about Danger
2)Doctors: Front of brain control fears
3)Amygdala:Body's Alarm System
4)Fear Not:Scientists are how people can unlearn fear
5) >Scientists Face Fear Gene

Full Name:  Brittany Peterson
Title:  What Makes Us Different? The Peculiarity of the Human Brain
Date:  2006-02-22 11:44:36
Message Id:  18284
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Human beings are exceptionally good at wondering. Many of the most famous pieces of writing in history have been on the subject of human nature. These writings are so popular because they address a subject of interest to all of us: what lies at the root of our humanity? The forces that most commonly motivate human beings reflect this desire: in each religion can be found a particular definition of what it is to be human; in possessions, wealth and career lie a way to define oneself based on goods and accomplishments; and in the bonds we choose to form with other human beings, we seek to find a reflection of ourselves and a way to define ourselves based on how we fit in with others.

A major part of being human lies in the differences between us and other animals. Long before humans could map out the brains of various animals using computers, these essential differences were instinctively sensed. The writers of Genesis, for example, depict Adam as separate from other creatures; created last, in the image of God, and wielding power over other creatures- specifically the power to name them.(4)

These differences are a result of the gradual process of evolution. The most important thing separating humans from other creatures is the structure and sheer power of our brain. Time after time, it has proven to be selectively advantageous to have a large amount of brainpower, and the composition of the brain has been the most potent force in the evolution of human beings.

How did this process begin? The first organisms were single-celled, it is not until around 600 million years ago that we have evidence of multicellular life on Earth.(3) Cells began living in colonies because it was evolutionarily advantageous to do so- possibly because they were less likely to be consumed by predators as a larger group, or perhaps to share energy resources. At some point, these cells began to take on different functions within their colonies.

The most primitive organisms with nervous systems- that is, a system of interconnected nerve cells- are the cnidarians, which have a nerve net consisting of nerve cells scattered throughout the epidermis. Another type of primitive nervous systems include those of echinoderms, such as starfish, which consist of a central nerve ring and five radiating nerves. The most primitive nervous system that includes a brain is that of the annelid. Leeches, for example, have only a brain, two nerve cords, and segmental ganglia running throughout their bodies. Insects have a similar system.(2)

Mammalian brains are fundamentally different from these types of organisms in one particular way: the three main functions of the non-mammalian brain work in three separate sections of the brain, but in mammals they are centralized and are all located in the forebrain.(6)

Humans possess the most complex brains of any mammal, with a number and density of neurons that allows for highly complex thought. This density allows for infinite numbers of thought and for infinite numbers of individual brains. This type of variability is part of what gives humans their unique consciousness. It is difficult to define the sense of "me" that humans have, the sense that we are capable of change, of moral decisions. The complexity that allows for this has evolved over millions of years. It is thought that the first ape-like humans split off from apes at around 5 to 7 million years ago.(5) The reasons that larger brains were continually selected for over the next several million years is unclear. Considering the great amounts of energy needed to support such a brain during fetal development and during life itself, the benefits must have been enormous. These benefits probably included the ability to continually make more complex tools that allowed humans to take more efficient advantage of the resources around them, the ability to understand and control fire, and the ability to think creatively to escape predators and threats involving the elements. Whatever the reason, brain size continued to increase, from the first apelike humans to the slightly more human-like Australopithecines to the early homo sapiens, later humans, and their cousins the Neandartals.(1)

Our consciousness of being is what makes us human. We value it before we even know what it is; small children respond to faces more than to any other stimuli and newborn infants know their mother's voices. The connections we have to others, and the sense of individuals as entities to be learned about and explored in order to learn about and explore ourselves is ingrained. I believe that this tendency to consider individual identity important has itself been selected for over time, since it is with this sense that people strike out on their own to invent and create. Creativity and the ability to think of new ways of doing things- from new, more ingenious stone tools to the wheel to the Internet to quantum physics- has allowed the human race to continually improve its lifestyle and to remain the preeminent species in the world. Our consciousness of being human is what allows us to continue being human.

1) 1) Palomar College Anthropology , Very informative regarding human evolution over time- e.g. Australopithecines, early homo- good reference for basic facts on this subject.

2) 2) Gilbert, Scott F. Developmental Biology, seventh ed. Sinauer Associates, Inc.: Sunderland, 2003.
I used this textbook to find information on the form of the nervous system in various types of organisms.

3) 3) The Evolution of Life On Earth- Scientific American, Even though I only used this site to reference the time of the evolution of the first multicellular organisms, I enjoyed reading Gould's piece, and have in fact enjoyed all of his writings that I have read; he had a gift for making science interesting and thus accessible.

4) 4) Holy Bible: New Revised Standard Edition. Cokesbury: Nashville, Burlingame, 1990.
This is where the reference to Adam's ability to name the other animals in Genesis comes from.

5) 5) IT "Scientists narrow time limit for human, chimp split." , An interesting article discussing the debate on when humans diverged from apes; I used it to find the currently agreed-upon date.

6) 6) The origin and detailed structure of the human brain , This site provided an interesting bit of information that I had not previously realized, about the way in which various structures, each performing a different function in the premammalian brain, are more condensed in the mammalian brain; a structural distinction I found intriguing and meaningful.

Full Name:  Andrew Garza
Title:  How does Branding Affect the Brain?
Date:  2006-02-23 08:10:19
Message Id:  18307
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

In an age largely dominated by huge multinational corporations, people around the world are bombarded with an incredible array of advertisements on a daily basis. These advertisements are designed to change consumers' behavior, whether that means getting them to buy a certain product, vote for a political candidate or take action on a social justice issue. Advertising ties in closely with branding, the spreading of symbols that represent organizations, products and services. One of the key pillars behind branding, Robert Zajonc's Exposure Effect (1) says that, up to a certain extent, people tend to like things more the more familiar they are with those them. The emergence of a new field called neurobiology (2) that applies neurobiological technology to gaining deeper insights into consumer behavior and better exploring concepts like branding and Exposure Effect.

Several researchers at Baylor Colleges of Medicine in Texas recently conducted an experiment that examined how people's preferences for Coca-Cola (Coke) or Pepsi were influenced by their prior perceptions of the two brands (3). The Baylor researchers administered several different kinds of taste tests, in which subjects indicated their preferences between a variety of different combinations of two cups of soda: labeled and unlabeled Coke and Pepsi and visually primed and unprimed conditions. During the course of the experiment, researchers also measured participants' neural responses with functional magnetic resonance imaging (fMRI) (4), technology that monitors blood flow, and thus energy allocation, in the various areas of the brain.

The Baylor team found that there was an interesting discrepancy between the areas of the brain that lit up on the fMRI just before participants chose between unlabeled Coke and Pepsi vs. the areas that activated before participants chose between a branded beverage and an unbranded one. fMRI scans show that, when presented with one unlabeled cup of Coke and one unlabeled cup of Pepsi, about half the people stated that they prefered Coke and the other half said they prefer Pepsi; their verbal responses to the unlabeled tests corresponded with increased activity in the ventromedial prefrontal cortex (VMPFC), an area of the brain associated with pleasure due to sensory stimulus. On the other hand, when participants had to choose between two cups of identical Coke, one labeled as Coke and the other left ambiguously unlabeled (people were told it could be either Coke or Pepsi, even though it was actually Coke), people overwhelmingly said they preferred the cup labeled as Coke. Interestingly, the VMPFC lit up equally when people drank the labeled and unlabeled cups, but there was far more activity in other parts of the brain for people who expressed preference for the labeled Coke over the unlabeled. These other areas of the brain are ones that some scientists believe are connected with applying emotional information on behavior and remembering cultural information that biases decisions: the dorsolateral prefrontal cortex (DLPFC) and the hippocampus.

The surprising results of this study indicate that there are non-economic factors (i.e. not price, accessibility, etc.) in addition to taste that determine consumers' beverage preferences. The researchers suggest that the mystery factors that cause people's illogical preference for labeled Coke over unlabeled Coke are advertising and branding. It is worth noting that the same experiment with the labeled and unlabeled cups was administered with Pepsi, and there was no overall participant preference for one cup over another. A piece of evidence that suggests that branding is the reason why the Coke name invoked stronger feelings in people than the Pepsi name is that Coke was named the World's Most Valuable Brand in a 2001 study by Interbrand (5), while Pepsi ranked # 44 on the same list. From the fact that the participants' preference for the labeled Coke corresponds with more activity in the DLPFC and hippocampus than in the VMPFC, one might extrapolate that preferences for highly branded goods are based more on advertising-induced "cultural knowledge" (3) than on pleasurable sensations located in the VMPFC. It appears that the neural pathways for perceptions about sensory pleasures operate independently and distinctly from the pathways that control "cultural knowledge". (3) This distinction challenges the notion that our perceptions are formed in a clear, logical way. On the contrary, action potentials that form perceptions fire from starting points in different areas of the brain and travel along different paths, until they potentially meet in another conceptual "box" (6), where they come together to actually form whole perceptions.

The question of whether perceptions of well-branded goods are more based on subconscious biases caused by the advertising or by conscious reflection on the quality of the product begs further analysis. For the purpose of this conversation, I will define "conscious" as being anything that involves neurons firing from or passing through the box in the brain that defines our sense of self; some would call this space the Identity-function. Although the DLPFC is an important part of the prefrontal cortex, a region of the brain commonly associated with people's personalities, I would argue that this connection does not mean that everything that goes on in the DLPFC counts as conscious activity. I think repetitive, catchy advertising lodges concepts in the brain in ways that make the information immediately fire through neural patterns when it is triggered by conscious thoughts about or sensory interaction with the product. The hippocampus and the DLPFC are the vehicles through which the action potential patterns travel and eventually reach the conscious mind, which forms, or at least realizes, the final cognition.

A theoretical example of how branded information ends travels through subconscious pathways to eventually reach the conscious mind in its near final stage has to do with Aspirin. Aspirin is branded drug that can be found in many households in the U.S. But most supermarkets that sell Aspirin also sell a much cheaper generic version of it called by its full name, acetylsalicylic acid; Aspirin and the generic drug are essentially the same. However, people often don't even think to look at the drug placed next to Aspirin on the aisle because the concept of Aspirin has already been so deeply entrenched in their minds. It is illogical to buy Aspirin. To be sure, I don't mean to say the area of the brain that makes buying decisions is the same as the part that forms perceptions. But my point is that perceptions definitely inform decisions, and the perceptions are based on information that largely travels through that brain via subconscious neural pathways. If it was mainly logical, conscious activity that led to perceptions of brands, every person who regularly goes to supermarkets in the U.S. and buys Aspirin would change their perception of Aspirin to a ridiculously high priced drug that is of no higher quality than its alternative. In reality, many of our perceptions of branded items seem to be based on complicated subconscious patterns of action potentials that result in our conscious mind assuming we have a good reason for liking something, making up a reason for liking it, or saying we like it "just because."

The concept that many of our perceptions of heavily branded items are based on subconscious neural patterns has several implications: like almost anything else, it can be good or bad, and sometimes it is hard to judge the effect. An example of a positive application is that psychologists are working with governments worldwide, especially in Sub-Saharan Africa, to design and implement social campaigns (7) that de-stigmatize AIDs. These campaigns largely aim to attack perceptions that AIDs is dirty and wrong, and encourage people to take preventative actions and get tested for it on a regular basis. An example of the negative effects of branding is that oftentimes as teenagers in the U.S. seek to fit in with peer groups, they partially define their social groups' identities by the kinds of brands they associate themselves with. This association with particular brands can lead groups to ostracize those who wear different brands (8).

Researchers and scientists should continue to explore the effects of advertising on the brain so that we can learn more about how it can be used to spread positive messages and how messages promoting harmful causes or goods can be negated.

1)Wikipedia entry on Exposure Effect, A helpful definition of a widely recognized advertising principle
2)Neuroco Website , A great overview about the emergence of neuromarketing, written by the operators of one of Europe's first neuromarketing companies
3) Experiment PDF, Details how the Baylor research team looked into the issue of branding and perceptions of soft drinks
4) Wikipedia entre on fMRI, Talks about what exactly fMRIs measure
5) Broadchannel Web site, Interbrand's list of the World's Most Valuable Brands
6) Serendip Forum Page, A place to look for more information about box theory
7) APA Article, Interesting and informative article about the role psychologists have played and do play in selling products and implementing social campaigns
8) JSTOR Article, Article about the role of the media and branding upon teenagers

Full Name:  Beatrice Johnson
Title:  The Soul and The Brain
Date:  2006-02-26 15:35:42
Message Id:  18351
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

The Soul and The Brain

Beatrice Johnson

What is the soul and what is its connection to the brain if there is any? This question has puzzled me most of my life. There is something in us that is separate from the brain, something we have no knowledge of, but we know it's there. The brain in contrast, we can see, we can touch and we can feel it. I have read about the soul. I have talked about the soul. Is it some unopenable box with all the answers inside?
Plato and Socrates say the soul is the essence of the person and that it is separate. It controls the way we act. (1) I say no to that, but I do agree that it is separate. Aristotle agreed with Plato that the soul is the essence of the person, but is not separate. (1) I place actions in the domain of the brain.
The Bible gives many instances where the soul is separate from the body. (1) The religious aspect leaves me a little baffled. It is clear that the soul leaves the body with death, but what is it doing while in the body, from a religious point of view. Does it play an active part in our living which we are not aware of?
The Islamic view is that soul gives life to the body, which is also true of the Christian faith. (1) But I'm still left with same question, what does the soul do while it is in the body?
I have talked to many people about the soul, some say the soul is the mind. What is the Mind? I yet have an answer to that question. Others don't believe we have a soul. It's all in the brain and when we die it is over. I refuse to believe that the brain is all, that is, when I know there is something more, something greater than the brain. The brain does well at what it does, but is physical and it controls what is physical. The brain has its limitations and the most obvious one is that it can't answer my question concerning the soul. Sure it can give me definitions of what the soul is through reasoning, but is that what the soul really is a definition, or does it have a meaning? I have tried to think it out but have grown tired.
I have come to the conclusion that the soul is beyond my realm, but yet it dwells within me. It is something I know of but know nothing about. I am allowed to think about it, ponder about it. The soul is there and is aware of me knows more of me, than I know of myself. But it will not let itself be known. Science says that in time through research and investigations it will provide some of the answers or even more questions that will help enlighten the mystery of the soul. (1)
Science has done much in unraveling the mysteries of the brain.
Is there an accepted answer of what the soul is? Plato, Socrates and Aristotle all agreed on certain aspects of "their" soul, but failed to come to full agreement. Religious faiths have similar beliefs about what the soul is but don't come into full agreement. Is there an answer that will satisfy and identify what the soul really is? .
For myself, I know it's there and I know it will continue to plague me. If there is not an answer why does it plague so? Is it that the brain is working overtime? Is it trying to make sense of something that has no sense? Is it going through its normal procedure of functioning? I don't know because it has not come up with an answer. I don't feel that bad after all. I am sure that I am not the only in this predicament. Afer all Plato, Socrates and Aristotle were plagued by this very same predicament.

WWW Sources

Full Name:  Mariya Simakova
Title:  Neurobiology and Theology: Friends or Foes?
Date:  2006-03-03 23:16:55
Message Id:  18447
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Science and theology have been traditionally regarded as intellectual opposites, sometimes even as foes. Scientific research and findings are viewed as rational truths, providing real pictures of the real world, while theology, especially its mystical component, is regarded as an irrational discipline, dealing with the murky and inaccessible "beyond". Moreover, many expect science to provide insurmountable proofs against the existence of God. First Soviet cosmonaut, Yuri Gagarin, derisively dismissed religious belief upon returning from his voyage around the planet. "I've been to heaven," he said, "but I have not seen Grandfather God there." An Orthodox priest Dmitrii Dudko countered: "If you have not seen God while here on Earth, it is pointless to look for Him in the heavens." What Fr. Dudko had in mind, it seems, were spiritual encounters, experienced by believers and unbelievers alike. Indeed, many claim to have seen God face-to-face, and even to have merged with Him, without leaving the Earth and without leaving one's corporeal body. What is more, many theologians resist the notion of the Cartesian split between the immaterial soul/mind and the material brain/body. Following Apostle Paul, they speak of the soul incarnate: not merely inhabiting, but intimately interconnected with its "temple," the body. If this is indeed the case, could science, especially modern neurobiology, investigate the nature of religious experience from its "material" side? And would such an inquiry necessarily undermine the validity of systematic theology, mystical states, or religious beliefs?

With the development of new brain imaging technology, scientists began to be interested in the neurobiological underpinnings of mystical experiences. Dr. V. S. Ramachandran, a neuropsychologist at the University of California San Diego, focuses on temporal lobe epilepsy (TLE) patients, who are prone to excessive activity in their temporal lobes. TLE patients experience micro-seizures, which result in powerful and deeply emotional religious experiences. What is more, the effect of these seizures is not fleeting: most TLE patients are religious during the periods between the seizures, sometimes to the point of fanaticism. Dr. Ramachandran and his colleagues proposed that heightened electrical activity during these seizures strengthens connections between the subject's temporal lobe sensory areas and the amygdala (a brain region usually associated with emotion), resulting in the patients' intensely personal and emotional reaction to their experiences. With the help of skin conductance response (measuring small rapid changes in perspiration), Ramachandran investigated whether TLE patients would have a stronger emotional response to sexual/violent stimuli or to the stimuli with religious nature. His subjects, indeed, showed heightened arousal when presented with religious words and symbols. In contrast, control subjects displayed the strongest responses to sexual stimuli. Dr. Ramachandran's findings, however, were inconclusive, due to the limited number of test subjects and to the fact that TLE patients often have changes in sexuality. Nevertheless, his studies suggest that the temporal lobe is involved in religious experiences and, according to Ramachandran's 1997 presentation at the conference of the Society for Neuroscience, that individual neural differences in that area may influence the degree of personal religiosity in healthy people. (1)

Some neuroscientists search for a particular neural module, responsible for processing, and perhaps producing, religious experiences. They are also interested in the degree to which this "God-module" is genetically determined and in its significance in the evolution of the human brain. Dr. Michael Persinger of Laurentian University in Canada, like Ramachandran, suggests that activity in the temporal lobe is the neurological basis of spiritual experiences. Unlike his colleague, he works with healthy adults – religious, agnostic, and atheistic. Over the years, he developed what has been dubbed "Persinger's helmet," literally a yellow motorcycle helmet equipped with solenoids, emitting weak electro-magnetic fields (4) and capable of producing "micro-seizures" in the temporal lobes, akin to the seizures in TLE patients (1). These micro-seizures, or "temporal lobe transients" (TLT), are "short-lived rate increases and instability in the firing patterns of neurons in the temporal lobe" (1). During the experiments, the subjects are placed on a recliner in a sound-proof dark chamber, which is designed to minimize sensory input (4). Impulses directed at the subcortical (limbic) areas in the temporal lobe produce distortion of body image, forced motion, and strong emotion. When temporal cortical areas are targeted, subjects report dreamlike visions, a "sense of presence," and strong emotions. According to Persinger, the visions are easily influenced by particular religious suggestions – a view of a crucifix prior to the study or playing Eastern music during the experiment (3). Some subjects report a pleasant experience, while others exhibit a sharply negative emotional response: their heart rate goes up; they cut the experiment short because of intense fear and even "struggle to take off the electrodes" (4).

Persinger's explanation of the "sensed presence" denies any external influence. According to him, the process leading to this experience can be described as follows. The activity of the neural systems in our left hemisphere temporal cortex mediates our sense of self. This activity is normally matched by the neural activity in the corresponding parts of the right hemisphere temporal cortex. During TLT events, these patterns of activity are mismatched, and the left hemisphere (also associated with language) interprets the discord as "another self" or a "sensed presence," whether divine or demonic. Excessive stimulation of the subcortical areas in the temporal lobe, particularly of the amygdala (the seat of emotion) and of the hippocampus (associated with autobiographical memory) lends personal and deeply emotional character to the experience (3). Persinger, who has tested more than 900 subjects, says that the intensity of one's response depends on individual lability, or sensitivity to TLT events (4). On the one hand, this sensitivity is natural (across healthy subjects, some show a tendency for TLT events even in the absence of Persinger's helmet) (3). On the other, it is itself a fluctuating condition: TLT events may be triggered without the helmet by anxiety, personal crisis, lack of oxygen, low blood sugar, and even fatigue (3).

It is interesting that the subjects give different names to the "presence of another" that they felt during the study. These names are usually appropriate to their religious beliefs, upbringing, or knowledge, but some identify that "other" as a parent or relative, or report childhood memories, with or without spiritual content. Moreover, still others insist that the presence was demonic, or describe the experience in terms of the UFO abduction stories (4).

When discussing the implications of his findings, Persinger denies the "God module" theory. Instead, he proposes that the brain areas that mediate our sense of self, general emotion, and autobiographical memory also participate in religious experiences. Although his studies do not specifically address the question of genetic innateness, Persinger believes that "the god experience" has survival value, since it allows humans to overcome their anxiety and the fear of death by connecting to something that is perceived as both eternal and outside oneself (2).

Unlike Persinger, Dr. Andrew Newberg of the University of Pennsylvania does not strive to produce "the god experience." Instead, his research focuses on mapping the brain activity of religious subjects at the highest points of prayer and meditation, particularly in Tibetan Buddhists and Franciscan nuns. First, a baseline scan of the subject's brain is taken – in order to obtain a picture of his or her normal neurological activity (5). The subjects are then placed in a room, where they are allowed to create an environment appropriate for the reaching of high mystical states. They then go through their usual routines, such as quieting their conscious mind and allowing their "true self" to emerge (for Buddhists) or repeating prayers and allowing oneself to open to God (for the nuns). When the subject reaches the highest point of his or her experience, he or she pulls on a string, signaling readiness to Dr. Newberg. The scientist then injects a radioactive tracer into an IV line in the subject's arm and places him or her into the SPECT (single photon emission computed tomography) machine. The tracer allows Newberg to locate and take a picture of the areas of the brain with the highest blood flow, which correlate with neuronal activity. (3)

As expected, the images show heightened activity in the prefrontal cortex, associated with attention, which correlates with the subjects' concentration. A bundle of neurons in the superior parietal lobe, which is often called "orientation association area" (OAA) and which mediates our orientation in space and time and creates the boundary between our self and the outside world, however, shows an unusually low activity. Normally, the activity in the OAA area is consistent, allowing us to reliably navigate through space and to tell time. Dr. Newberg suggests that the OAA continues to work, but that the subjects somehow block the sensory input to this area during meditation or prayer. This process, known as deafferentation (a neural structure is cut off from sensory inputs or afferents), results in perceiving oneself as endless and connected with the rest of the world (5). This is in agreement with the subjects' reports on their feelings of oneness – with the universe (for the Buddhists) and with God (for the nuns). The usual dualistic split between "I" and "the world" and the reality of time disappear. (3)

It is noteworthy that, although both the Buddhist meditators and the Catholic nuns report experiencing unitary states (and exhibit similar patterns of neural activity), there are differences between their SPECT scans. The nuns' vehicle to reaching peak spiritual states was the Centering Prayer, involving repetitions of words. Appropriately, their right inferior parietal lobe, associated with evaluating the emotional weight and inflection of words and phrases, showed increased activity. This pattern was not observed in the Buddhists, whose normal practices include emptying of the mind of any conscious thought. These correlations confirm the reliability of Dr. Newberg's findings. (5)

Like Persinger, Newberg believes that spiritual experiences, which include emotions, thoughts, sensations, and behaviors, are too complex to be mediated by a particular "God module" within the brain. Instead, the activity is distributed throughout, involving the arousal and quiescent systems, the limbic system, the hypothalamus, the amygdala, and the hippocampus. He suggests that "the human brain has been genetically wired to encourage religious belief," and that this "machinery of transcendence may have arisen from the neural circuitry that evolved for mating and sexual experience" (5). He also proposes that the ability of the brain to mediate spiritual experience has a survival value, increasing human physical and psychological health and well-being. Moreover, he believes that mystical practices may be able to positively alter human behavior. (5)

While he insists that the mystical experiences are events mediated by the brain, Newberg does not wish to undermine their religious validity or even outside reality. For centuries, rational human beings (at least in the Western tradition) accepted the reality of the everyday world, of the objective universe existing independently of us. However, the human condition is such that we cannot have an absolute, direct experience of this reality. Everything we do or see, from the taste of an apple pie to a beautiful sunset, is mediated and processed by our brain. We cannot know (and science cannot tell us) whether there is, in fact, a world out there or whether our brains – immense and complicated systems that can not only process, but also generate signals – simply make it up. Of course, Newberg agrees that our shared realism is a good working hypothesis and that, in fact, we all rely on the deep conviction (one might even call it a belief) that the chairs we sit on or the people we talk to are real. But he points out that mystics par excellence, as well as ordinary believers and even unbelievers who have had a mystical experience, also have this conviction of the reality of their visions. What is more, they often insist that these experiences were "more real than reality itself." Therefore, just as we cannot dismiss the objective reality of the apple pie solely on the basis of the fact that we can make a scan of the brain's "apple pie experience," we cannot treat the neurobiological data of mystical states as the conclusive proof of God's non-existence. (6)

Such a view certainly shows that modern "neurotheology" does not necessarily debunk theology proper. On the contrary, current studies may be even consistent with some theological dogmas that for centuries were taken on faith alone. For instance, if one believes in the soul intimately connected to the body, one can now see the physical changes their coexistence produces in the brain. Similarly, now we can understand how it is possible for the dualistic time and space distinctions to disappear during meditation or prayer – something that could not be explained before. Moreover, science itself reaffirmed the central postulate of any faith: God's existence or non-existence cannot be proved, it must be experienced and believed in.

Current research also calls for new, more rigorous, inquiry into the neurobiology of spiritual experiences. For instance, most researchers operate under an assumption that all mystical experiences are similar and that the names and symbols attached to them are merely cultural creations. Even some religious writers, for instance, Rich Heffern of the National Catholic Reporter, claim that throughout the history of religion we can find "the same generic description, couched in the language of [a] particular culture and tradition – a description of unitary states" (5). But this assumption fails to take into account the fine distinction between the unitary states experienced by Buddhists as opposed to, for example, Christians. While Buddhist meditators strive towards and sometimes achieve a feeling of oneness with the universe, of the disappearance of self, and of non-existence par excellence, Christian mystics insist that God is personal, that an encounter with Him will have the features of both unity and separateness. The biological correlate of this distinction remains to be found.

Moreover, scientists should take into consideration the fact that mystical teachers and practitioners throughout the world warned their students of "false" and "true" experiences. When Persinger describes how the brain can create a presence of another self, he does not realize that he restates a warning given by theologians – do not make up a god in your head, strive to encounter a real one – in neurobiological terms. Spiritual discipline and asceticism that allowed mystics to differentiate between genuine and false experiences are difficult to acquire, but it would be interesting (if, perhaps, impossible) to trace the neurobiological differences that distinguish the two. Also, neurobiologists need to realize that it is manifestly not the same thing for believers to feel a demonic presence, a divine presence, or to have a "visit" from one's father or an alien. Persinger, who seems to place these distinct experiences into one model, may need to refine both his methods and his style of data analysis. Other interesting questions not addressed in the current studies are the long-term effect of spiritual experiences on the brain and the fact that many people are believers without ever having an encounter on the scale of Newberg's subjects.

While neurobiologists may want to brush up on theology, theologians should familiarize themselves with the progress of science. Neurotheology has a direct bearing on mysticism, dogmatic theology, ecumenism, and religious evolutionism. The religious community should cease regarding science as an enemy, now that the scientists themselves acknowledge their inability to prove or disprove the existence of God. Collaboration of theology and neurobiology may lead not only to important theoretical findings, but also help improve human psychological and physical health. There are only two things that neither systematic theology nor neurobiology will ever be able to prove or to explain: first, the existence of God and, second, the experience of God's call directed to the individual person, a call that can happen in the midst of the everyday bustle or of the most rational and skeptical human activity. A sudden and unwaited-for call that we cannot ourselves reach through meditation or prayer and that, therefore, may never be registered and captured by the most advanced technology.

Web Resources

1)"Searching for God in the Machine", an article on neurotheology from the Summer 1998 issue of Free Inquiry; also available through Tripod.

2)"Religion and the Brain", transcript of a PBS broadcast on November 9, 2001.

3)"Religion and the Brain", article on neurotheology in the May 7, 2001 issue of Newsweek; also available through Tripod.

4)"This Is Your Brain on God", an article on Persinger's experiments by one of his subjects.

5)"Exploring the Biology of Religious Experience", an article on neurotheology and faith by a believer.

6)"Brain Science and The Biology of Belief, Part 3", one of the series of articles by Dr. Andrew Newberg on the Metanexus Institute site.

Full Name:  Oh Alice
Title:  False Memories
Date:  2006-04-04 10:06:52
Message Id:  18829
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

One of my earliest unusual childhood memories is of falling into a pond at a park. My father was swinging me in his arms jokingly pretending to throw me into the pond and the next thing I knew, I was in the water! Luckily, a nearby stranger quickly fished me out of the water and I was safe again. Though one would wonder why my father wasn't the one to pull me out since he would have been the closest. Years later when I asked my older brother about this humorous event, to my surprise I learned that what I had remembered of that even was not accurate. My father had not accidentally thrown me in but I had fallen in myself! What a clumsy child I was. What happened that made me remember bits and pieces of this event? How can the brain be misled to acquire false memories, including little changes in details in an otherwise accurate recollection?

One popular theory about the formation of memories begins with the notion that the brain does not record memories like a videotape. (1) Instead, different parts of the brain are responsible for storing different aspects of a memory. The memory is more like a collage stored in the brain. For example, injuries to the limbic system has show that injury to the right side of the brain results in a loss of visual memories, while an injury to the left side of the brain results in a loss of verbal information. (2) Memories involve sound, sights, words, tastes, fears, expectations, desires and other emotions. Thus all these aspects of a memory are stored as bits and pieces in different parts of the brain.

In my memory, perhaps the action of falling into the water was so instantaneous that my brain had not encoded the information well. Therefore in trying to make sense of the recollection, my brain may have filled in the gap with an earlier event of my father pretending to throw me in.

Other methods by which false memories can occur are due to the misinformation effect and imagination inflation. Misinformation occurs when "people who witness an event are later exposed to new and misleading information, and their recollections often become distorted. For example, in one study, research participants were shown an automobile accident that occurred at an intersection with a stop sign. Half of the participants were given the information that the intersection had a yield sigh. When questioned later, these participants recalled seeing a yield sign at the intersection while the group that did not receive the suggestion more accurately recalled a stop sign. (3)

Imagination can be as powerful as true memory, resulting in what is called imagination inflation. Psychologists can instruct their patients to let their imagination run wild. Specific questions such as, "What time of day is it? Where are you, indoors or outdoors? What is going on around you?" When these scenarios are imagined over and over, it becomes familiar enough to light up areas of the brain associated with real sounds and sights. The hippocampus of the brain then indicates to the frontal lobe that something strikes is as familiar. (4) The frontal lobe then searches for the source of the familiarity.

How can imagination inflation be prevented? By remembering that something was imagined and was not an actual memory. This is called source confusion, in which the context of a memory and the source become confused. Therefore it is very helpful to remember the context in which the imagination exercise took place. Damage to the frontal lobe may allow the memory to be remembered, but may incorrectly place the source. (5) To prevent misinformation from occurring, it is important to be aware of how one's emotions, fears, expectations and desires will influence what is remembered. By the power of suggestion, the memory can be easily manipulated.

By exploring the irregularities of memory, light has been shed on a possible method in which memories are stored in the brain. This theory of memory as a collage stored in all parts of the brain as bits and pieces is also consistent with other irregularities of memory, such as the déjà vu phenomenon. Déjà vu can be explained as a sense of familiarity occurring, but no recollection taking place. This exploration of how false memories are created has shown that memories are very fragile. Though many may believe that what they remember is the truth, it is good to be aware that memory is very susceptible to suggestion. With this knowledge, it could even be entertaining to watch criminal, court or even eyewitness accounts on the news to see how people might alter their memory due to suggestion.

WWW Sources

1)False Memories

2)Forget What You Heard About Amnesia
3)Creating False Memories

4)The Fragile Power of Human Memory

5)The Fragile Power of Human Memory

Full Name:  Rachel Mabe
Title:  Academic Achievement is Biased: Owls vs. Larks
Date:  2006-04-06 08:11:55
Message Id:  18870
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Many people say that they are more of a "night person" than a "morning person." Surprisingly, however, these traits are scientifically proven to be true. In fact, it may even be traced back to an innate genetic factor (which can be influenced by enivironmental cues) (1). Researchers refer to those who are morning types as Larks. People who fare better at night are referred to as Owls. Larks often describe themselves as getting up early and being more alert earlier in the day. Owls, as the name indicates, prefer to wake up later and stay up late, feeling more awake later in the day than Larks.

Researchers have found that owls and larks have different hours for alertness, mood, activity, and sleep. Owls tend to have peak alertness around six in the evening, whereas larks tend to peak around noon. Furthermore, Owls are most active around 5:30 in the evening, with larks falling behind around 2:30 in the afternoon. Even mood is influenced by this trait; Larks reach their best mood between 9:00 in the morning and 4:00 in the afternoon, while Owls mood rises steadily from 8:00 in the morning to 10:00 at night (1) .

The contrasting characteristics of these two types can be attributed to differences in circadian rhythms, which depends upon whether a person falls under the category of a Lark, an Owl, or somewhere in between (a Hummingbird) (2). The circadian rhythm is our internal body clock. It is important because it controls our everyday activities via body temperature and hormone regulation. Melatonin and cortisol are two essential hormones that the circadian rhythm regulates. These hormones play an essential role in our sleep/wake cycle. "People who are owls, who have to function on a 'normal' schedule, can end up sleep deprived due to insomnia. Larks tend to have fewer problems due to their sleep habits, though their social lives may suffer" (3).

What interests me most about this research is how adolesents change sleeping patterns once they reach puberty, needing more sleep than prepubertal children. It is often noted that young children wake up at the crack of dawn to watch Saturday morning cartoons, and teenagers are seen as lazy for sleeping in. However, it should be acknowledged that this change in sleep behavior happens as a result of a shift in circadian rhythm. This causes a perference to later bedtimes and rise times, essentially making all teenagers Owls (4).

Although the switch from Lark to Owl is natural for teens, high schools seem to ignore this fact. The average starting time for high schools is 7:30, earlier than elementary and middle school. As a result, high school students wake up around 6:00 to get ready for school, if not earlier to finish homework or catch the bus. Unfortunately, research has found that the temperture for Owls is lowest around 6:00 a.m. When a person's temperature is at its lowest, waking up is most difficult. (5). Not only is it difficult for teens to wake up early in the morning, but it is almost impossible for them to go to sleep early enough to get the full 9 hours of sleep needed per night (4). This can be attributed to their circadian rhythm not winding down until around 11 at night (6).

In addition to it simply being more difficult for students to wake up at such early times, the school's inability to accommodate to an Owl's needs also affects academics. Generally, high school students attend school from approximately 7:30am until 2:50pm. Hence, for the period of time that they are actually in classes, their attention span is not at its peak. It is only around the time that students are let out of school that they are becoming more alert and receptive to learning (1). This causes many negative affects, such as lower levels of attention during the school day, sleeping in class, and poor grades on exams. A study done by the British Medical Research Council found that students have a much better long-term retention rate of material presented to them at 3 p.m. rather than 9 a.m. (7).

Furthermore, not allowing students to carry out their natural sleep cycle forces them to function in school on less sleep than they should be getting. This not only effects them academically, but socially and behaviorally as well. Sleep deprivation causes mood swings, irritability, issues with confidence and, in extreme cases, depression. Although teenagers have difficulties with these issues regardless, sleep deprivation only enhances these negative characteristics (5). Therefore, it seems accurate to conclude that a lack of sleep contributes to students having more difficultly in social situations and controlling behavior in class. Perhaps there would be less "problem students" if teenagers simply had more sleep on the weekdays.

As a result of this research, schools need to take into account these biological facts and change the start times of schools. A 1997 study, done in the Minneapolis school district, confirms that students function better when the start time for high school is later. The school district switched the start time for high schools from 7:15 to 8:40. Researchers found that not only did students attend classes more regularly, but they were also more interested and retained the material better. Additionally some teachers saw fewer disciplinary problems (6). Another study tested students' reaction times on mood and cognitive performance over a period of four days, at three different time intervals, (6:30-8:00; 11:30-1:00; 3:00-4:30). Students performed better on the tests in the afternoon, compared to the morning tests. Additionally, they completed the tests in the afternoon 20 seconds faster (8).

Even though there are studies proving that high school students benefit from later start times, the majority of the schools across the country are still starting around 7:00 a.m. There are many possible reasons for this. One being that companies employing students worry that they will lose their adolescent workstaff. Another reason is that schools are allowing afterschool time for sports teams, during daylight hours. Finally, school districts have an established system of high schools starting first, around 7:00, elementary, around 8:00, and middle, around 9:00. Considering that most public schools use the same fleet of buses for all ages, they worry about the difficulties, financially and authoritatively, of having to completely change their system (6).

Instead of focusing on the difficulties school districts would face while making the switch of start times of schools, it seems that it may be more rational to direct attention towards the positive effects such a change would have on the students. Some schools are indeed waking-up to the needs of teens. For example, a congresswoman from California, Zoe Lofgren, introduced legislation inticing high schools to begin at 9:00 a.m., by providing federal funding to offset the costs for such changes to take place. I believe it is no coincidence that she called this the Zzzz'a to A's Bill (6). Hopefully, all schools will eventually adopt this type of schedule, or other creative alternitives, allowing high school students to function as the Owls that they are. This would put an end to the stereotype of the lazy adolescent, as well as, enable them to be more alert, retain information better, and be more interested in school.

1) Are you a Lark, an Owl, or a Hummingbird?, site giving information on characteristics and differences between lark and owl chronotypes.

2) University of Surrey: School of Biomedical and Molecular Sciences. , site which defines Larks and Owls.

3) Canadian Sleep Society. , site explaining aspects of sleep.

4) Adolescent Brain Development. , site on the changes of sleep-wake cycle in adolescents.

5) Stanford University Article , site explaining difficulties in the sleep cycle and reasons for this.

6) Bay Weekly , online weekly journal article on sleep

7) When School Schedules Collide with Biological Clocks., a site explaining correlations between sleep difficulties and school start times.

8) Health on the Net Foundation , site discussing about the effect of sleep deprivation on student grades.

Full Name:  Claude Heffron
Title:  Orgasms: Why Some Women are Lucky Enough to Experience Them
Date:  2006-04-06 14:11:39
Message Id:  18877
Paper Text:


Biology 202

2006 First Web Paper

On Serendip

Orgasms are extremely beneficial to people, most notably the male orgasm is the single most important thing in perpetuating human life. It is no mystery that men have orgasms in order to reproduce, but biologists are divided over what the purpose of the female orgasm is. Two main viewpoints are represented in this debate, those who believe that the female orgasm has an evolutionary function, and those who believe that the female orgasm has no true purpose at all. Recent research on this natural event brings attention to competing theories of the female orgasm, particularly illuminating the theory that female orgasms do not serve a real purpose.

Dr. Elizabeth Lloyd, a professor at the University of Illinois, is the current representative of those who believe that the female orgasm is an accident of nature. This idea, which was originally put forth by Donald Symons in 1979, holds that a woman's ability to orgasm is a byproduct of anatomical development During development, before a fetus' sexual features are differentiated, neural pathways are laid out including the pathway that allows for reflexes such as an orgasm (7). The body is then differentiated with an influx of hormones, and the fetus becomes a male or a female (7). The fact that a woman does not need to orgasm in order to procreate is a strong indicator that orgasms are a residual feature left over from the undifferentiated fetus, and not something that has any evolutionary purpose. Lloyd's theory of the female orgasm has been one of the most widely supported in recent years.

An opposing theory, known as the upsuck theory, is supported by Dr. Mark Bellis and Dr. Robin Baker, who believe that the female orgasm is indeed functional. The upsuck hypothesis purports that when a women orgasms anytime between one minute before her partner ejaculates and 45 minutes after he does, she retains more sperm than she does if she orgasms at a different time or if she does not orgasm at all (7). When a woman orgasms, her cervix contracts and there is more suction in her uterus, forcing the semen inside her body (7). Believers of this theory claim that when women orgasm in the essential time frame, the increased suction causing sperm to enter her body increases the probability that she will conceive a child. Some even hypothesize that women may subconsciously favor one lover over another and orgasm while having intercourse with the preferred lover, increasing the probability that she will become pregnant (2). These scientists explain the female ability to orgasm multiple times is a function that evolved in order to increase a woman's chances of becoming pregnant since each orgasm increases the "upsuck" through cervical contractions (2). The "upsuck theory" is one of the major theories holding that female orgasms play an evolutionary role.

Pair bond accounts, first put forth by zoologist Desmond Morris in 1967, present another set of ideas about the evolutionary function of the female orgasm. These theories postulate that the female orgasm evolved to increase the bond between two sexual partners, which would in turn increase the chances that their offspring would survive. If both partners are sexually satisfied, they are more likely to remain together and are more capable of ensuring their offspring's survival (8). Morris and his followers believe that the bonding effects of the female orgasm show that humans have genetic tendencies towards family values (6). Many variations of the pair bond theory have been put forth, but they all share a common belief that there is an evolutionary purpose explaining why women orgasm.

There are number of other ideas about the female orgasm, but the three discussed above are among the most widely supported. I tend to believe Elizabeth Lloyd's idea that there is no evolutionary function for the female orgasm based on newer research about female orgasms. A study done just last year in Australia, revealed a strong genetic factor contributing to why the regularity with which women experience orgasm varies so greatly. The research involved a survey of the frequency with which female twins reached orgasm in different scenarios including during sexual intercourse, during other forms of sexual activity, and during masturbation. Over 3000 pairs of identical twins participated in the survey and behavioral geneticist Khytam Dawood concluded that when women masturbated, their genes were 51% responsible for their ability to climax. For other methods the figures are lower, with genes accounting for 31% of success during regular sex and 37% in other forms of sex (5). Dr. Gemma O'Brien theorizes that genes influence a woman's ability to orgasm indirectly, by shaping the limbic system, a more primitive area of the brain that is believed to play a major role in creating the orgasm experience (5). Some would say that because orgasms have a genetic basis, they actually do serve an evolutionary purpose. Lloyd defends her ideas against this attack by explaining that if the genetic variation which makes it difficult for many women to reach orgasm were crucial to procreation, those who posses this gene would have been eliminated through natural selection long ago.

This study has reframed some of the common theories in the female orgasm debate. Tim Spector, one of the leaders of the research, explains that "The theory goes that if a man is considered powerful enough, strong enough or thoughtful enough, in bed or in the cave, then he's likely to hang around as a long-term partner and be a better bet for bringing up children" (3). It could actually be that sperm is flushed higher into the reproductive tract when women orgasm, as the upsuck theory states, which is more likely to occurr when a woman has an attractive and attentive partner (3). Others say that the twin study further supports the pair bond theories described earlier by improving the relationship between sexual partners.

The most basic reason why I am in agreement with Elizabeth Lloyd's hypothesis that female orgasms are functionless is because procreation occurs in the absence of orgasm. Only about 14% of women always have orgasms during sexual intercourse, 32% were unable to orgasm at least one quarter of the times they had sex, and 16% never reached orgasm during sex (4). If orgasms serve an evolutionary function, and evolutionary functions are those things that are intended to increase survival and reproduction, why aren't orgasms necessary for procreation? Furthermore, why is there such variation in the frequency with which women experience orgasms on the level of both the individual and the population?

At this time there is still much controversy over the evolutionary function of the female orgasm. Dozens of theories are being contested and new research is being compiled which supports any number of these theories, sometimes applying to more than one. While it is not entirely possible to know for sure why wo men orgasm, it does appear that there is a genetic factor contributing to the likelihood of the female orgasm. If scientists are able to discover with more certainty why women orgasm, it may be possible to develop methods that allow more women to experience orgasms, but until then, only the lucky genetically programmed few will experience this state of ecstasy.

Works Cited

1)George Mason University Stats

2)Global Ideas Bank

3)London Times

4)New Scientist

5)News in Science

6)The Boston Globe, COMMENTS ABOUT IT

7)The New York Times


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