What Is Craving? Models and Implications for Treatment - alcohol craving

Alcohol Research & Health,  Fall, 1999  by Raymond F. Anton

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Conditioning models are based on the tenets of classical conditioning. These tenets posit that alcohol-related cues (e.g., the sight of a bar or a beer bottle), after repeatedly being paired with alcohol consumption, become conditioned stimuli--that is, they elicit the same physiological and psychological response as alcohol consumption itself (e.g., release of certain brain chemicals [i.e., neurotransmitters]). If alcohol consumption does not occur immediately, these cue-induced responses result in craving, either to experience alcohol's pleasant, or reinforcing, effects or to avoid or alleviate the unpleasant, or aversive, effects of not drinking. Conversely, cognitive models are based on the assumption that responses to alcohol and alcohol-related cues involve various cognitive processes, such as expectations regarding the pleasant effects of alcohol and a person's belief in his or her own ability to cope with the desire to drink. Although some of these models may be more relevant to drugs other than alco hol, many characteristics (and, consequently, models) of craving overlap among various AODs.

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 (i.e., neuroanatomy) and neurotransmitters (i.e., 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 (i.e., neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence (Robinson and Berridge 1993; Koob and Le Moal 1997). Long-term alcohol consumption interferes with many brain functions. Because the body, including the brain, must maintain a balanced state (i.e., homeostasis) with respect to critical bodily functions (e.g., blood pressure, body temperature, and communication among cells), many cells--including nerve cells (i.e., 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 (see figure 1, p. 168), 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 unconsci ous, gives heightened attention, or salience, to environmental cues that are commonly paired with alcohol (e.g., the smell of alcohol or the sight of a beer bottle) or to alcohol consumption itself.