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The physical structure of the brain remains constant, but the addition of a tiny chemical drastically alters brain function and ultimately behavior. Understanding how alcohol affects our brain also offers insight into how our brains work in general. So the next time you drink, even though you may be killing some valuable brain cells, you can toast to the fact that you’re contributing to neuroscience.

What is a High-Functioning Alcoholic?

This concept is consistent with that of Oscar-Berman and Marinkovich (Oscar-Berman & Marinkovic, 2007) in noting that achieving normal performance in one function can occur at the expense of other functions (cf., Sullivan & Tapert, 2013). This concept cast a long shadow on cognitive rehabilitation efforts and has been eschewed by those who believe that recovery means a return to a premorbid state. Rather, a head injured patient might undergo restitution and recuperation, achieving “new normal” where health “is restored if a relation between preserved and disturbed performances is reached (page 331)” (Goldstein, 1995). But such adaptation could result in a brain-injured patient’s adapting to the deficit state and rejecting change.

Meaning of Neuroadaptation to the Recovering Alcoholic

Disruptions of the normal inhibitory functions of prefrontal networks often have the interesting effect of releasing previously inhibited behaviors. As a result, a person may behave impulsively and inappropriately, which may contribute to excessive drinking. Understanding what motivates people to drink abusively involves knowing their drinking behaviors and patterns and their perceptions, or cognitions, about themselves and about alcohol. Cognitive-behavioral psychology incorporates all of these elements, expanding the basis of traditional behavior theory beyond an exclusive focus on observable behaviors to include thoughts and emotions.

Postmortem Studies: Then and Now

Studies of motivational interviewing, which is a relatively new technique, have provided early indications of effectiveness (Bien et al. 1993). Cue exposure therapy is still in the experimental stages and is not ready for widespread clinical application. The alcohol industry invests heavily to make themselves ubiquitous—from billboards to the commercial breaks of your favorite streaming shows. You may see ads with scenes from lively barbecues, glamorous holiday parties, casual after-work drinks at a local pub, or even relaxed gatherings at book clubs, all suggesting that this is the norm at every gathering. Imagine sipping a beer and suddenly landing your dream job, or a glass of wine doubling your bank balance. Yet, alcohol ads craft these fantastical scenarios to sneak into our subconscious, subtly shifting our perceptions and decisions.

The expansion of the fluid-filled spaces of the brain was interpreted as a sign of local tissue shrinkage rather than as irreversible tissue loss (i.e., atrophy) (Ron et al. 1982). One prescient idea was that the primary breakdown product of alcohol, acetaldehyde, rather than the alcohol itself (i.e., ethanol), may have a key role in brain changes produced by chronic alcohol consumption. These ideas first were developed in a series of articles from the laboratory of Virginia Davis, including articles published in Science and Nature (Davis and Walsh 1970; Yamanaka et al. 1970). The idea that alcohol is only a “pro-drug” and that acetaldehyde is the effective agent has a boomerang quality because it is discarded every few years, only to return later.

Frequent reviews of previously taught skills will enhance the clients’ mastery and help to counter problems they may have in retaining the skills. In addition to the view of alcoholism as a learned phenomenon, other theories have been developed to account for its origins. One of these focuses on genetics as a factor in the development of alcohol dependence.

• Understanding how alcohol affects our brain also offers insight into how our brains work in general.
• This set of results led to the speculation that low insular CBF impairs connectivity among functional salience network nodes and reduces ability to switch from interoceptive desires, such as cravings (impulsive system), to cognitive control over these desires (executive system).
• Family members generally require education about alcohol and its effects as well as opportunities to discuss the impact that a loved one’s alcoholism has had on their lives.
• Drinking doesn’t just affect the individual; it affects the entire family unit.
• With repeated heavy drinking, however, tolerance develops and the ability of alcohol to produce pleasure and relieve discomfort decreases.

For practical, evidence-based tips on supporting your patients with AUD, see the Core articles on treatment, referral, and recovery. Degradation of brain structure appears to underlie alcoholism-related alterations in the selection of cognitive strategies to execute a task, and the new neural pathways taken can be identified with fMRI. These analyses found that a change in processing strategy occurs, where alcoholics use inefficient high functioning alcoholic neural systems to complete a task at hand because the preferred neural nodes or connecting fiber tracks are compromised. Such compensatory activation may be crucial for adequately completing a task but curtails available capacity to carry out multiple activities in parallel. Ultimately, structural abnormalities impose a fundamental change in the choice of cognitive operations possible for the alcoholic (see figure 5).

• When a dose of a radioactively labeled glucose (a form of glucose that is absorbed normally but cannot be fully metabolized, thus remaining “trapped” in a cell) is injected into the bloodstream of a patient performing a memory task, those brain areas that accumulate more glucose will be implicated in memory functions.
• Age, family history, and how much or how often an individual drinks are other important variables when considering someone’s relationship with alcohol.
• If any of the factors below are familiar with you or someone you love, you might be at higher risk of becoming a functioning alcoholic.
• But there is strong evidence of a genetic component of addiction; it arises not only because someone has a weak will.

Innovative Frontiers in Addiction Recovery