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Higher Risk of Brain Deficits in Older Alcoholics

Higher Risk of Brain Deficits in Older Alcoholics

Action Points

  • Alcohol use disorder may confer greater risks of deficits in frontal lobe function, specifically a prominent alteration in frontal cortex volumes, and prefrontal and frontal cortical tissues.
  • Note that drug dependence with cocaine, cannabis, amphetamines, or opiates and HCV infection compounded the deleterious effects of alcohol dependence on frontal cortical volumes.

Alcohol use disorder (AUD) may confer greater risks of deficits in frontal lobe function, specifically a prominent alteration in frontal cortex volumes, and prefrontal and frontal cortical tissues, according to a longitudinal study.

In terms of systemic damage, the following volume deficits were reported via atlas-based, quantitative MRI of 222 men with alcoholism compared with 199 age-matched controls:

  • Frontal: t= -5.732 (P<0.001)
  • Temporal: t= -3.151 (P=0.002)
  • Parietal: t= -5.063 (P<0.001)
  • Cingulate: t= -3.170 (P=0.002)
  • Insular: t= -4.920 (P<0.001)

Accelerated aging occurred in the frontal cortex (t= -3.019, P<0.02), and precentral (t= -2.691, P<0.05), and superior gyri (t= -2.763, P<0.05), reported by Edith V. Sullivan, PhD, of Stanford University School of Medicine in Stanford, California, and colleagues.

These relationships were particularly pronounced in adults ages ≥65, and were observed regardless of whether or not excessive drinking was a consistent life-long pattern or one initiated later in life, they wrote in JAMA Psychiatry.

Further aims of the study were to examine if the deleterious effects of alcohol on the aging brain are compounded or augmented by drug dependence or hepatitis C virus comorbidity.

The group found 54.5% of those with alcoholism and concomitant substance abuse issues — alcohol plus cocaine (t = −2.310, P=0.04) and alcohol plus opiate (t = −2.424, P=0.04) groups — had smaller frontal volumes than the drug-dependence-free alcoholism group. This was marked by deficits in precentral (t = −2.575, P=0.01), supplementary motor (t = −2.532, P=0.01), and medial (t = −2.800, P=0.01) volumes endured in drug-dependence-free participants with alcoholism compared with control participants.

These relationships also extended to those with HCV infection, displayed by greater deficits than those without HCV infection in frontal (t = 3.468, P=0.01), precentral (t = 2.513, P=0 .03), superior (t = 2.533, P=0.03), and orbital (t = 2.506, P=0.03) volumes. Yet total frontal (t = 2.660, P=0.02), insular (t = 3.526, P=0.003), parietal (t = 2.414, P=0.03), temporal (t = 3.221, P=0.005), and precentral (t = 3.180, P=0.01) volume deficits persisted in the uninfected participants with alcoholism, compared with control participants with known HCV status.

The study was conducted from April 2003 to March 2017. DSM-IV criteria were used to determine alcohol and drug diagnoses and serology testing determined HCV status.

Although the volume of the frontal context in normal adults continued to decline over time, these results confirmed “the older brain [is] especially vulnerable to insult from other factors” including “comorbid licit and illicit drug dependence, which is a frequent concomitant factor of alcohol misuse; and acquired medical conditions such as hepatitis C virus (HCV) infection, which is prevalent in individuals who misuse alcohol,” thus hastening the process of brain degradation, wrote Sullivan’s group.

They highlighted the importance of this investigation given the aging U.S. population, with projections suggesting that by 2050 nearly one in five people in the U.S. will be ages ≥65, compared with one in seven now.

In addition to aging, people are drinking more alcohol, including “an increase in binge drinking among women 60 years and older,” wrote George F. Koob, PhD, director of the National Institute on Alcohol Abuse and Alcoholism in Rockville, Maryland, in an accompanying editorial.

To contextualize the study and the development of the “pathological state known as AUD,” Koob identified a kind of symmetry between the developing and aging brain in terms of the formation of the three major neurocircuitry agencies involved in addiction: the prefrontal cortex, basal ganglia, and extended amygdala.

“The hypothesis is that the top-down prefrontal cortex control to reduce impulsivity and compulsivity is underdeveloped in adolescence and compromised in aging, thus opening the possibility of greater vulnerability to AUD in early and late in life,” he wrote.

Study limitations included the recruitment methods, where alcohol-dependent participants were selected from community-based treatment centers, which account for less than 25% of individuals needing treatment, thereby causing a barrier to generalizability. Additionally, there was also uncertainty over whether or not sex-differences came into play, as well as a lack of a non-alcohol dependent drug or HCV comparison groups.

Further research directions may include analyses of functional correlates and the possibility of ameliorative or retraining efforts for compromised individuals, the authors stated.

The study was funded by the National Institute on Alcohol Abuse and Alcoholism and the Moldow Women’s Hope and Healing Fund.

Sullivan and co-authors, as well as Koob, disclosed no relevant relationships with industry.

  • Reviewed by
    Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco

1969-12-31T19:00:00-0500

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