Addiction and the Brain Term Paper

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Psychosocial Ramifications of Drug & Alcohol Abuse

A Japanese proverb in its pithiness adequately accounts for the entire process of drug and alcohol abuse. To wit: "Man takes Drink. Drink takes Drink. Drink takes Man." One of the problems with understanding drug or alcohol abuse is the psychosocial ramifications associated with the problem. Moral associations cloud the behavioral and physiological factors. For some time now, alcohol and drug addiction have been identified as disease. It is however, not viewed as such by many who have a special stake in the matter. One of the common misconceptions associated with addiction is that it uni-dimensionally fulfills physical needs; and, withdrawal consists mainly of physical symptoms. Treating addiction as such is often therefore, fraught with pitfalls.

Essentially, drug (and alcohol) abuse and addiction can be viewed as a behavioral issue with psychological and physiological consequences. Simply put (clinical and neurological factors will also be discussed), substance abuse points to motivation. The motivation for all living beings at the most intrinsic level is self-sustenance and procreation. Once these motivational needs are met, higher order motivations such as a career, self-sufficiency and self-actualization can also be sought. Once motivational needs are met, the feeling of fulfillment and the "feel good" effect are associated with the stimulation of pleasure centers in the brain. In this sense therefore, motivation can be classified into two parts: appetitive and aversive. Appetitive is the fulfillment of what some call hedonistic needs. Epicurism and the need for sex are examples of appetitive motivations. Aversive motivations are associated with self-preservation. Protecting oneself against cold or even attempting to rid oneself of a headache are aversive motivations.

These neurological pleasure centers can also be stimulated by chemicals. By replacing the normal secretions, these chemicals disrupt the neurological processes associated with feelings of well-being. Narcotics mimic these chemicals, creating artificial feelings of well-being. For instance, powerful narcotics such as heroin and cocaine initially create a high. This high is also stored in the users' subconscious memory. Subsequent administrations of drugs however, cannot replicate the first euphoric feeling. The addict attempts to replicate the high, which he or she does by escalating the dose. This is one reason why withdrawal is difficult and physiologically (and psychologically) demanding. Researchers call this "well-being" locus in the brain the reward center. This system of rewards is the fundamental concept in understanding addiction. (Addiction-Science, The Primer on Drug Addiction, 2000)

From the above therefore, a new motivational perspective of drug abuse emerges. It can be classified as two fold: extreme motivational strength and extreme motivational toxicity. Motivational strength is associated with the extent to which addiction can replace other basic motivations such as food, sex and the need to maintain a career. Motivational strength is also associated with to what lengths an addict will go to procure drugs. The psychosocial ramifications (as mentioned above) are a consequence of motivational strength. Motivational toxicity, on the other hand, can be defined by how it can be disruptive.

Cocaine affects the user differently than heroin and methamphetamines. Typically, addiction can be towards anything. Most people are addicted to mild sedatives, cigarettes (though some aver that it is more addictive than cocaine), coffee, shopping, chocolate and gambling. Any of these addictions can be measured based on motivational strength and motivational toxicity. (Addiction-Science, The Nature of Addiction, 2000) The withdrawal from substance abuse is difficult because physiological processes are affected, and not merely emotional ones.

To understand addiction from a physiological, and more specifically, neurological standpoint, one must turn towards the brain. Indeed, one might refer to environmental factors or even genetic factors -- such as an addictive personality or that, children of alcoholics tend to be alcoholics. These are non-pharmacological issues. Indeed, non-pharmacological factors often combine with pharmacological factors to exacerbate the problems due to addiction. The central nervous system however, remains the primary determinant for drug and alcohol addiction. Dopamine is a neurotransmitter secretion that is implicated in drug addiction. There are different dopamine types and different dopamine secretions and reception centers. Dopamine has even been thought of as having something to do with Alzheimer's disease. The dopamine that is considered responsible for addiction is specifically located in the mesolimbic dopamine system. (Goldstein, 1991) Dopamine is the secretion that determines moods and hence, feelings of well-being. Mesolimbic dopamine secretions are known to be self-activating. They are secreted in small amounts to maintain normal mood balances. It has been found that lower (than normal) dopamine levels are associated with depression.

Dopamine neurons originate in the ventral tegmental area of the brain. Dopamine receptors are present in the nucleus acumbens, which is in the forebrain area and postsynaptic to the dopamine neurons. (Fibiger and Phillips, 1979) Gamma-amino butyric acid (GABA) is shown by researchers to inhibit the dopamine neurons, which also regulates the amount of dopamine secretions. Along that pathway lies the amygdala, also known as the pleasure center of the brain. The actual roles of each of these are subject to hypotheses based strictly on neurological and behavioral studies on laboratory animals. This mechanism of dopamine disruption is typical for psychomotor stimulants. Examples of these stimulants are methamphetamines and cocaine. The other types of drugs belong to the category of opiates. Heroin and morphine are typical examples.

Research has shown that the ventral tagmental area contains a center for opioid peptides. Other brain regions involved in this mechanism. "aqueductal gray area, arcuate nucleus, amygdala and locus coeruleus," often use peptides as a response to pain. Opiates mimic these secretions and disrupt the normal processes. (NIDA, 2004)

There are several possible models to determine the brains response to external (narcotic) stimulation. For alcohol addiction, the amygdala is known to play an important role. Alcohol is shown to increase GABA neurotransmission in the amygdala. From a mechanistic standpoint, it is worth looking at a hormone called corticotrophin releasing factor (CRF). Like alcohol, CRF increases GABA secretions in the amygdala too. CRF is found in different parts of the brain. According to researchers, it is secreted in response to "stress, anxiety and depression." CRF works by stimulating the hypothalamic-pituitary-adrenal stress response. In the amygdala, it stimulates behavioral response to stressors. (Nie et al., 2004)

It appears therefore that alcohol increases GABA neurotransmissions by actually stimulating CRF to do that. Studies have shown that CRF secretions increase with not only alcohol, but also when the brain of the animal is deprived of alcohol. This points therefore, to the difficult withdrawal effects from alcohol, because CRF continues to "inform" the brain that alcohol is being consumed. Researchers believe that CRF antagonists will actually be used to help people with alcohol abuse problems. They showed that when the CRF receptors were removed in animals, the effect of CRF and alcohol were lost since they did not stimulate the secretions of GABA.

Given the broad definitions of putative mechanisms of addiction, it is important to recognize how the more known (and dangerous drugs) influence neurochemistry. Heroin increases the release of dopamine by increasing the firing of dopamine neurons. The postsynaptic neuronal receptors are then inundated (to levels far higher than normal). Therefore, heroin usage is associated with the feelings of mood elevation and euphoria. When the brain processes and metabolizes the heroin, the subconscious recollection of the "high" increases cravings. The psychomotor stimulant cocaine on the other hand acts a differently. A constant secretion and uptake of dopamine is necessary to maintain a normal and cyclic flow for mood sustenance. While heroin increases dopamine secretion, cocaine inhibits and disrupts the cycle by preventing the reuptake of dopamine. This means that the synapses contain abnormally high levels of dopamine that give the feeling of euphoria. This effect, and the resulting high, is short-lived. (Addiction-Science, The Biological Basis of Addiction, 2000)

In addition to dopamine, the hormones serotonin and norepinephrine are also implicated in the reward mechanism of addiction. (Pratt, 1991) It is these ions like sodium, potassium, calcium and chloride that constitute the electrical signal flows in the brain.

Drug and alcohol metabolites are also implicated in problems during withdrawals, remission and craving. (Smith, n.d.) These metabolites are residual substances of drugs that remain during drug and alcohol metabolism that takes place in the liver. These substances that should, under normal circumstances, be removed from the body remain trapped in fatty tissues. Once released, they stimulate the same centers that the drugs did. These give rise to instances of erward-flashbacks with the same stimulatory affects, which only result in greater cravings.

Media and current knowledge have shown the ill effects of drugs are known. In the context of this work, they bear repeating. Some of the behavioral and psychological problems range from "agitation, irritability, dysphoria (unpleasant mood), mood swings, hostility, and violence to anxiety and panic attacks." Drug and alcohol addiction causes dysfunction in the family. Depression and divorce are all too common, as are decline in performance in school or the careers. Denial is an important aspect of drug and alcohol abuse. Because of the societal stigma associated with it,…[continue]

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