Despite their differences, all craving models assume that alcohol craving is a multifaceted phenomenon that is influenced by a variety of factors. Furthermore, animal experiments suggest that craving may be associated with certain brain regions (neuroanatomy) and neurotransmitters (neurochemistry). These relationships, however, have not yet been described in detail, and better clinical and laboratory models of craving are needed to address those issues. Such models likely will improve understanding of the neuroanatomical processes involved in craving, as well as of craving's role in abstinence and relapse, and may ultimately lead to improved psychosocial or pharmacological treatment approaches for alcoholism.

Most researchers and clinicians agree that a greater understanding of all aspects of craving is necessary in order to improve treatment. Models that attempt to merge psychological, behavioral, and brain mechanisms may be most useful for fostering the formulation and evaluation of new theories on craving. The next section discusses one such model, which attempts to explain craving in the context of phenomena frequently observed by clinicians. Although many aspects of this model remain speculative and more data are needed to support the concepts described, the model can help researchers link specific neurochemical systems to the processes that underlie the manifestation of craving.

A Neuroadaptive Model of Craving

Scientists believe that a gradual and, perhaps, permanent adaptation of brain function (neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence. Longterm alcohol consumption interferes with many brain functions. Because the body, including the brain, must maintain a balanced state (homeostasis) with respect to critical bodily functions (blood pressure, body temperature, and communication among cells), many cells - including nerve cells (neurons) in the brain - adapt their activities in response to the prolonged presence of alcohol. This neuroadaptation, or sensitization, leads to certain characteristics of alcohol dependence, such as tolerance and withdrawal, as well as to a condition that might be called reward memory, a memory that has its roots in certain brain cells and is dependent on chemical changes in those cells. The "reward memory," which may be unconscious, gives heightened attention, or salience, to environmental cues that are commonly paired with alcohol (the smell of alcohol or the sight of a beer bottle) or to alcohol consumption itself.

Neuroadaptation likely occurs to a greater extent and more permanently in people who are at increased risk for developing alcoholism, either because they have inherited a genetic predisposition from their parents or because they have acquired such a susceptibility through repeated experiences of severe stress. Such stress experiences, which can amplify the alcohol-induced neuroadaptation processes, can be mediated either by internal factors (a major psychiatric disorder) or by environmental insults (trauma or loss of a family member).

Animal models of addiction and craving, as well as pharmacological studies in humans, have indicated that several neurochemical systems contribute to neuroadaptation to alcohol. For example, the neurotransmitters dopamine, glutamate, gamma-aminobutyric acid (GABA), and endogenous opioids, as well as the neurons that respond to these molecules, may play a role in the development of reward memory. In addition, glutamate and GABA are thought to play a major role in alcohol withdrawal. Stress, which may influence neuroadaptation, also is modulated by neurochemical systems, primarily those involving the neurotransmitter serotonin. Consequently, medications that affect the serotonin system, such as fluoxetine (Prozac®) and sertraline (Zoloft®), are effective in the treatment of many psychiatric conditions (depression and various anxiety disorders). These medications also have been studied for the treatment of those conditions in alcoholics.

Given the diverse functions of neurotransmitter systems, abnormalities in any of the systems may result in the experience of craving. In alcoholics, such abnormalities can result from neuroadaptation to the presence of alcohol, which occurs insidiously over many years. In most cases, the drinker is unaware of the neuroadaptation, and many alcoholics - particularly those who are in the early stages of alcohol dependence - are likely to deny any craving for alcohol. In fact, Tiffany has suggested that craving emerges fully only when a person is prevented from access to AODs or consciously attempts to quit AOD use.

The neuroadaptive model of craving proposes that different mechanisms lead to craving during early alcohol withdrawal and during later recovery. During alcohol withdrawal, brain mechanisms that have adapted to the chronic presence of alcohol are left in an altered state. This imbalance can lead to physiological instability (anxiety and cardiovascular hyperactivity); sleep difficulties; and, possibly, subdued drive or reward states (depression, lack of motivation, and concentration problems). These symptoms are all associated with a subjective sense of discomfort, which may lead to a desire, urge, or craving for alcohol in order to "feel normal" again. Some of the mechanisms underlying the craving of early abstinence may persist for a considerable period (weeks to months). If the person remains abstinent or consumes very little alcohol, however, the altered brain mechanisms eventually return to their original state, leading to a renewed sense of well-being and a decrease in alcohol craving.

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Tags: Alcoholism

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