Biology 202

2006 Second Web Paper

On Serendip

In my last paper, I explored the ways in which environment and genetic trends influence the disease of drug addiction. Using research on brain receptors, behavioral patterns, and neurotransmitter pathways, I found that, at the very least, genes and personal experiences may affect an individual's participation in the vicious cycle of addiction. Much of the research asserts that the seeming loss of free will during addiction is a direct result of the predisposing factors and the direct biochemical effects of the substances themselves. I followed these assertions without questioning IF the I-function and free will are inextricably linked to the problem of addiction.

Another assumption inherent in much of the research and intellectual debate was the fact that drug abuse is an abnormal or overriding force in contrast to 'normal'/healthy neuro-function. Again, while this assumption is a popular and comfortable one, the boundaries of 'normal' appear to be arbitrarily drawn, and the distinctive categories of normal biochemistry and normal behavior are either conflated or ignored. I plan to further our investigation into the realm of drug addiction by addressing these issues from the perspective of an amateur neurobiological scientist and a critic of the research constructs that frame the studies of drug addiction.

Does the I-function Have Any Autonomy "Under The Influence?":

Researchers have used the correlations between drug addiction and trends in genetic/receptors patterns in the brain in an attempt to establish causation between genetic 'predispositions' and the disease of addiction. While the biological trends are supported by strong data, there is little explanation for individuals who either follow the trend and avoid addiction or individuals who don't follow the trend and fall prey to the disease regardless.

Lab rats are more predictable than humans in their behavioral patterns under the influence. While rats have been used to justify many theories on addictive behavior, there have also been contradictory findings that are basically ignored compared to the data that supports the current party line. The current explanation for the slippery trajectory of addictive behavior states that the survival/decision-making parts of the brain become hijacked by the addictive substance and are therefore rendered useless. Why then have there been groups of rats, and more commonly/importantly humans, that are able to access the dopamine reward pathway with drugs and not become dependent on the substance? The dependence must be extricable from the addictive substance, and therefore, there must be mechanisms in the I-function that can either process or express immunity to the chemicals (1).

If we assume that the I-function (and thus the individual) can have some level of autonomy in the presence of psychotropic substances, then what divides users with "self-control" from users who seem to lose their sovereignty over the substance? A recent article's title inadvertently draws attention o this problematic distinction based on contemporarily codified patterns of psychology: "Drug Abuse A Preventable Behavior; Drug Addiction: A Treatable Disease" (2). Part of the definitions that divide abusers from addicts are dependent on researchers' attempts to loosely quantify a user's "motivational strength" by rating behavior based on categories of effort and desperation to obtain the relevant substance (1). Obviously these distinctions make sweeping assumptions about the relationship between a person's behavior and their relative feeling of desperation, but what about variations among and between populations? What about the variance among I-function autonomy? How can one possibly establish a gradation of usage behavior when we struggle to categorize quotidian behavior? (This issue arises later in the paper when the concept of normal behavior is challenged.)

Another issue with the causation arguments is the fact that almost all of the biochemical research is done on lab animals/rats. Lab animals are arguably much simpler biochemically then human beings, and our understanding of animal I-functions (if they exist) is more extensive than our limited understanding of our own I-function. Some of the lab animal experiments have shown that there are common neurochemical mechanisms at work in many animals that show addictive behavior. The findings include not only shared pathways but the effects the drugs have on those particular pathways (accelerating the firing rate of the neuron cells bodies/accelerating the rate of action potential transfer). Establishing similarities in genetic expression and action potential activity in lab rats does not automatically explain the connection between human neurochemistry and behavior with regard to drug addiction (1).

What Is Normal?:

"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?" (3).

Connecting the neuroscience of natural rewards to drug addiction can explain 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." (4) But 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 altered by the pattern of addiction, can not addiction be an inherent part of neurochemical infrastructure and fall into a category with other external stimuli that affect our homeostasis?

Could drug abuse have an exacerbating rather than a competitive effect on the reafferent loop? Is it not possible that addiction is an extreme example of reafferent neurochemical function? What justifies the categorization of addictive behavior as an outlier? My last paper in this series will focus on the issue of the reafferent loop, as well as on the role of central pattern generators. We will come full circle in our investigation by addressing the relationship between neurophysiology/neurochemistry and behavior/psychology.

Sources:
1)"Addiction controversies.", M.A. Bozarth (1990). Drug Addiction as a Psychobiological Process. In D.M. Warburton (Ed.)

2)HealthWise Newsletter, July 1997

3) Patzelt, Julia. Neurobiology Paper #1: "Drug Addiction: Which Comes First- Brain or Behavior- and Does it
Matter?"

4)A Behavioral/Systems Approach to the Neuroscience of Drug Addiction, The Journal of Neuroscience, May 1, 2002


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