This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.
1998 Second Web Reports
Neurobiology and Behavior
7 April 1998
Self Destructive Behavior and Role of the I function
The I function describes all behavior associated with the notion of self. Is there really a specific I function and what is its role exactly? Because the I function is linked to the self, one would think that it would prevent harmful behaviors. However, there are cases where the I function does not intervene to terminate detrimental actions for example addiction and a mental disorder called Lesch-Nyhan syndrome. In both cases, a person is harming themselves and can not seem to stop. Does the I function play a role in self-destructive behavior? By researching addiction, more specifically alcoholism, and Lesch-Nyhan syndrome, it is clear that the I function can be overruled by other structures of the brain even when harm to the body is one of the final outcomes.
Addiction is defined as a physical and psychological dependence on a substance or behavior (1). Initially the behavior simply satisfies the person but turns into addiction when strong urges accompany the behavior and the person feels that it is needed to avoid painful feelings. What is causing the urges? The brain can be divided into two parts, the primitive brain and the new brain or the neocortex (2). The primitive or beast brain is responsible for survival appetites which are associated with physical pleasure. However, in order to satisfy the urges, the beast brain must communicate to the neocortex and cause the necessary motions to get the drug or exhibit the behavior. According to Rational Recovery (2), the neocortex, or you can overcome the beast brain. Is this alluding to the I function? If this is true, why did the behavior become an addiction in the first place? Where was the I function during that first drink, or while biting that first nail? Why is it so hard to break an addiction?
Studies have shown that addictions such as alcohol abuse, smoking, cocaine, etc, change the chemistry of the brain. The three examples above increase the release of dopamine at synapses. This increase corresponds with satisfaction or reward (3). There is evidence of a mutation of the dopamine receptor gene (D2A1) in alcoholics. This mutation was present in 69% of severe alcoholics and 20% of non-alcoholics (4). This mutation does not mean that alcoholism is always genetic. The study was also done on Vietnam Veterans who had post-traumatic stress disorder due to severe combat conditions (4). This mutation was found in 40%-55% of these patients (4). Veterans were not born to go to war so the mutation could be caused by a chemical change due to the bodyis response to high stress. One hypothesis is that the D2A1 is affecting the degree of expression of the genes that are involved with addictive behaviors. The genes have not yet been identified (4).
Dopamine is associated with seratonin. Seratonin is affiliated with the part of the brain responsible for controlling emotions, paying attention, and thinking before acting (4). Research was done to determine whether or not alcoholics had seratonin abnormalities. A mutation of an enzyme, tryptophan oxygenase is hypothesized to be the cause of abnormal seratonin amounts in the blood stream of alcoholics and patients suffering from other mental disorders all of which exhibit addictive behaviors (4). Tryptophan oxygenase breaks down tryptophan. If the enzyme mutation causes the degradation of the amino acid to proceed too rapidly or too much, then sufficient amounts of seratonin (which is made from tryptophan) will not be produced. Further investigation using linkage analysis led researchers to believe that a gene causing early-onset hereditary alcoholism is located in the same band as tryptophan oxygenase, which indicates that they are the same gene (4).
Abnormal levels of dopamine and seratonin are present in individuals that have addictions. Addictions are self destructive behaviors that the self does not have complete control over. This lack of control stems from the chemical changes that the detrimental behaviors have on the individual. The part of the brain responsible for overcoming the urges may have to find new pathways because the old ones have been destroyed due to mutations or possibly absence of the necessary enzyme. Perhaps this is why recovery from an addiction is a long difficult process.
Lesch-Nyhan is a disease that is caused by a deficiency of hypoxanthine-guanine phosphoribosiltransferase (HPRT). (5) Lesch-Nyhan can be inherited or a spontaneous gene mutation can occur causing the disease. (8) HPRT is responsible for the break down of hypoxanthine and guanine to uric acid. Hypoxanthine and guanine are purines. When HPRT is deficient, purines build up and are not broken down into nucleotides. This pathway allows brain cells to regulate the synthesis of not only nucleotides that are necessary for normal functioning (6) but also limit the amount of uric acid that is produced (7). As in the case of Lesch-Nyhan, behavioral abnormalities occur when this pathway breaks down. Patients suffering from Lesch-Nyhan exhibit compulsive self-injurious behavior such as biting lips, fingers or hands and head banging (6). As the child ages, the behaviors can increase because the child is more capable of harming himself and more imaginative (8). This self nmutilation may be linked to abnormal levels of seratonin and dopamine due to defects with metabolism (8). There are abnormalities in dopamine functioning in the basal ganglia and levels of dopamine are approximately 10% of normal levels (7).
In the case of Lesch-Nyhan, the disease is linked directly to genetics. When a person is born they either exhibit the symptoms or they do not. Addiction is very different. In the case of alcoholism, a person can be predisposed but may never become an alcoholic but a person born without a gene mutation may develop the addiction. In both cases, addiction and Lesch-Nyhan, the patient exhibits detrimental behaviors.
Dopamine levels are decreased in a Lesch-Nyhan patient but decreased in an alcoholic. It plays a major role in emotions, attention and motivation (4). Perhaps the patient sees self-injury as the only way to get attention or perhaps an inhibitory mechanism is absent which would prevent the patient from inflicting self-harm. In the case of the alcoholic, the increase in dopamine acts as a pleasurable sensation. Perhaps the Lesch-Nyhan patient only feels a sense of pleasure when he is in pain and to please himself he has to continue to inflict pain never being satiated.
Is this desire a function of the self or in opposition to it? In the case of harmful behaviors the primitive brain is overriding the I function. The limbic system is the predominate structure in the primitive brain. Apparently, the limbic system is in opposition to the neocortex. When the limbic system has a desire, it has to communicate its need to the neocortex in a way so that the need is met. This may happen with out the person consciously knowing about it. For example, does the Lesch-Nyhan patient realize after hurting himself continuously, that when he bangs his head on the wall yet again it will hurt. Can he stop himself? Or has the pattern become so habitual that the person can not stop it?
The limbic system is responsible for homeostatic life support, memory, learning, aggression and emotionality. It also has its own primitive form of intelligence and self-regulatory control (9). The limbic system is able to override neocortal control but is also inhibited by it (9). The neocortex is divided into two hemispheres. Sometimes the hemispheres do not communicate quick enough or efficiently and the limbic system responds to the needs of the body by causing a behavior (9).
So is the I function in the limbic system or in the neocortex? Because the limbic system is responsible for actions that are not always voluntary, the I function can not be located there. The I function only takes part in voluntary actions. If the I function is located in the neocortex, it can be overruled. The I function is unnecessary. The body could function without it. In fact, the I function may just be in the way most of the time. For example, sometimes I skip a meal. My entire body is begging for food but I continue to go about my errands without stopping to eat. By ignoring my desires, I am in this case harming myself. Perhaps the I function provides humans with a mechanism to ignore the desires of the nervous system on certain occasions. Can a person hold their breath until they die? My I function will not allow me to try this experiment for obvious reasons but is it possible?
Apparently, the brain is organized in a way so that if needed any part can override another. For example, the neocortex inhibits the desires of the limbic system, but when necessary the limbic system can ignore the inhibition. There are three structures previously mentioned, the neocortex, the limbic system and the I function. Certainly the first two exist and have specific locations. The I function is only a hypothetical at this point. It fits conveniently into hypotheses. It has not yet been proven wrong but at the same time more evidence is found indicating that the I function can not be included in the same category as structures like the limbic system or the neocortex. It does not have a definite location or a definite purpose. Does the I function exist or is it just wishful thinking that somewhere in the brain is the self or the soul which has some control over our actions whether or not the influence is beneficial.
1. Addictive Behavior -- Arnot Ogden Medical Center.
2. The Structural Model of Addiction
3. Neurochemical Systems Used to Study Brain and Behavior -- Jim Weber, Pacific Northwest National Laboratory
4. The Genetics of Addictive Behaviors: The Role of Childhood Behavioral Disorder -- Chemical Dependence, David E. Comings, M.D.
5. Lesch-Nyhan Syndrome -- The Association for Rare Diseases, Mauro Baschirotto, Italy
6. Lesch-Nyhan Syndrome -- Pediatric Database (PEDBASE).
7. New Approaches to Understanding Lesch-Nyhan Disease -- The New England Journal of Medicine. Vol. 334. No. 24 June 13, 1996
8. Lesch-Nyhan Disease -- Matheny School and Hospital, New Jersey
9. The Inside Story -- Robert Gilman.
| Course Home Page
| Back to Brain and Behavior
| Back to Serendip |