Psychosocial Ramifications of Drug and Alcohol Abuse

Introduction: Understanding Drug and Alcohol Abuse

A Japanese proverb captures the entire process of drug and alcohol abuse with striking economy: "Man takes Drink. Drink takes Drink. Drink takes Man." One of the central problems in understanding drug or alcohol abuse is the psychosocial ramifications associated with it. Moral associations tend to cloud the behavioral and physiological factors. For some time now, alcohol and drug addiction have been identified as diseases — yet this view is not shared by many who have a personal stake in the matter. One of the most common misconceptions surrounding addiction is that it uni-dimensionally fulfills physical needs, and that withdrawal consists mainly of physical symptoms. Treating addiction on those terms alone is therefore fraught with pitfalls.

Drug and alcohol abuse and addiction can more accurately be viewed as a behavioral issue with psychological and physiological consequences. Simply put, 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 career, self-sufficiency, and self-actualization — can also be pursued. When motivational needs are satisfied, the resulting feeling of fulfillment and the "feel good" effect are associated with the stimulation of pleasure centers in the brain.

In this sense, motivation can be classified into two parts: appetitive and aversive. Appetitive motivation involves the fulfillment of what some call hedonistic needs — epicurism and the desire for sex are examples. Aversive motivations are associated with self-preservation: protecting oneself from cold, or attempting to rid oneself of a headache, are aversive motivations. These neurological pleasure centers can also be stimulated by chemicals. By replacing normal secretions, such chemicals disrupt the neurological processes associated with feelings of well-being. Narcotics mimic these chemicals, creating artificial feelings of well-being.

Motivational Framework and the Brain's Reward System

Powerful narcotics such as heroin and cocaine initially create a high that is stored in the user's subconscious memory. Subsequent administrations, however, cannot replicate the first euphoric feeling. The addict attempts to recreate the high by escalating the dose — one reason why withdrawal is both physiologically and psychologically demanding. Researchers refer to this "well-being" locus in the brain as the reward center. This system of rewards is the fundamental concept in understanding addiction (Addiction-Science, The Primer on Drug Addiction, 2000).

From this framework, a new motivational perspective of drug abuse emerges, one that can be classified as twofold: extreme motivational strength and extreme motivational toxicity. Motivational strength refers to the extent to which addiction can replace other basic motivations such as food, sex, and the need to maintain a career. It also describes the lengths to which an addict will go to procure drugs. The psychosocial ramifications of addiction are a direct consequence of motivational strength. Motivational toxicity, on the other hand, can be defined by the degree to which addiction is disruptive to normal functioning.

Cocaine affects the user differently than heroin and methamphetamines. Addiction, typically, can develop toward almost anything. Many people are addicted to mild sedatives, cigarettes (which some argue are more addictive than cocaine), coffee, shopping, chocolate, or gambling. Any of these addictions can be measured based on motivational strength and motivational toxicity (Addiction-Science, The Nature of Addiction, 2000). Withdrawal from substance abuse is difficult because physiological processes are affected, not merely emotional ones.

Neurochemical Mechanisms of Addiction

To understand addiction from a physiological and neurological standpoint, one must look to the brain. Environmental and genetic factors — such as an addictive personality, or the tendency for children of alcoholics to become alcoholics themselves — represent non-pharmacological issues that often combine with pharmacological factors to exacerbate the problems caused by addiction. The central nervous system, however, remains the primary determinant of drug and alcohol addiction.

Dopamine is a neurotransmitter implicated in drug addiction. There are different dopamine types, secretions, and reception centers; dopamine has even been associated with Alzheimer's disease. The dopamine considered responsible for addiction is specifically located in the mesolimbic dopamine system (Goldstein, 1991). Dopamine determines moods and, therefore, feelings of well-being. Mesolimbic dopamine secretions are self-activating, secreted in small amounts to maintain normal mood balance. Lower-than-normal dopamine levels have been associated with depression.

Dopamine neurons originate in the ventral tegmental area of the brain. Dopamine receptors are present in the nucleus accumbens, located in the forebrain and postsynaptic to the dopamine neurons (Fibiger and Phillips, 1979). Gamma-aminobutyric acid (GABA) is shown by researchers to inhibit dopamine neurons, thereby regulating the amount of dopamine secreted. Along that pathway lies the amygdala, also known as the pleasure center of the brain. The precise roles of each of these structures are based on hypotheses drawn from neurological and behavioral studies on laboratory animals. This mechanism of dopamine disruption is typical for psychomotor stimulants such as methamphetamines and cocaine. The other major category of drugs, opiates, includes heroin and morphine as typical examples.

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

For alcohol addiction, the amygdala is known to play an important role. Alcohol increases GABA neurotransmission in the amygdala. From a mechanistic standpoint, a hormone called corticotrophin releasing factor (CRF) is especially relevant. Like alcohol, CRF increases GABA secretions in the amygdala. CRF is found in different parts of the brain and is secreted in response to stress, anxiety, and depression. It works by stimulating the hypothalamic-pituitary-adrenal stress response and, in the amygdala, stimulates behavioral responses to stressors (Nie et al., 2004).

It appears that alcohol increases GABA neurotransmissions by stimulating CRF to do so. Studies have shown that CRF secretions increase not only with alcohol consumption, but also when the animal brain is deprived of alcohol. This points to the difficult withdrawal effects from alcohol, because CRF continues to signal the brain that alcohol is being consumed. Researchers believe that CRF antagonists may help people with alcohol abuse problems. When CRF receptors were removed in animal studies, the combined effects of CRF and alcohol were lost, as they no longer stimulated GABA secretions.

Heroin increases the release of dopamine by increasing the firing of dopamine neurons, inundating postsynaptic neuronal receptors to levels far higher than normal. Heroin usage is therefore associated with mood elevation and euphoria. When the brain metabolizes the heroin, subconscious recollection of the high increases cravings. Cocaine, a psychomotor stimulant, acts differently. A constant secretion and reuptake of dopamine is necessary to maintain a normal, cyclic flow for mood sustenance. While heroin increases dopamine secretion, cocaine inhibits and disrupts the cycle by preventing the reuptake of dopamine. This causes abnormally high levels of dopamine to accumulate in the synapses, producing euphoria — an effect that 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). Ions such as sodium, potassium, calcium, and chloride constitute the electrical signal flows in the brain. Drug and alcohol metabolites are also implicated in problems during withdrawal, remission, and craving (Smith, n.d.). These metabolites are residual substances that remain from drug and alcohol metabolism in the liver. Under normal circumstances they would be removed from the body, but they can remain trapped in fatty tissues. Once released, they stimulate the same brain centers that the drugs did, giving rise to reward-flashbacks with the same stimulatory effects, which only intensify cravings.

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