Longitudinal analysis of Alcohol Use Disorder (AUD) and cohort interactions between comparing chronological age and AUD by measuring the brain’s precentral and superior frontal regions with age-associated cortical volume decline observed in the control participants. According to the authors, these evaluations occurred up to 8 times during the 10 year observational phase. This represents the largest and longest-studied group to date. Overall, the authors conclude that the results support the hypothesis that AUD accelerate aging and cortical volume deficits independent of drug dependence and comorbidity associated with hepatitis C infection.

Alcoholism or Addiction Use Disorder (AUD) is commonly conceptualized as a 3-stage cycle:

1.) Binge/intoxication—Loss of behavioral control

2.) Withdrawal/negative affect—Remorse, addressing harmful consequences

3.) Preoccupation/anticipation—A Pavlovian conditioned response that involves dysregulation of

  • incentive salience/conditioned response, craving
  • negative emotional states, e.g. sorrow, guilt & self-loathing
  • executive function, e.g., sustained attention, planning, impulse control, etc.

These functions are mediated by the neurocircuitry of the basal ganglia, extended amygdala, and prefrontal cortex, respectively. Excessive alcohol use (binging to achieve rapid intoxication) results in frontal cortex impairment, failure to inhibit hedonic drives, impulsivity and risk-taking behavior, especially among teens and young adults (< 25), whereas the prefrontal cortex is not fully developed and thus persistent alcohol consumption can cause allostatic dysregulation of the brain’s reward systems and the ability to problem solve and mediate stress in an age appropriate manner. The disruption of emotional homeostasis results in negative affect, hastening the preoccupation and reward seeking behavior.

As the onset of alcohol initiation trends downward, the functional ability of the adolescent is compromised, leading to hedonically driven choices to mediate disruptions in frontal homeostasis and negative affect.

As adults age, incremental deficits in the frontal cortex are expected. A lifetime alcohol abuser’s premature deficits in this area would be expected, leading to further dysregulation of basic motivational systems, attention, reward salience and continued alcohol use. Brain imaging studies reveal extensive regional volume deficits in the lateral and medial frontal, parietal, and insular cortices, with additional deficits in temporal and cingulate regions.

Why Does This Matter?

The golden years, as they are often described, are anything but for lifelong drinkers. It is the frontal areas of the brain that contain their unique humanity, creativity, problem solving abilities and sustained self-efficacy. Deficits in the frontal brain associated with alcohol use disorder are associated with anhedonia, poor motivation, memory deficits, and problems with ordering one’s life.

Educating adults, particularly seniors, regarding the risks of alcohol abuse is a worthy endeavor that could truly make retirement years golden once again.

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Reference:

Koob GF. Age, Alcohol Use, and Brain Function: Yoda Says, “With Age and Alcohol, Confused Is the Force”. JAMA Psychiatry. 2018 Mar 14. doi:10.1001/jamapsychiatry.2018.0009. [Epub ahead of print]