★ Could Your Weekly Wine Be Fueling Cognitive Decline?
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Could Your Weekly Wine Be Fueling Cognitive Decline?
A 313,000-participant study found no safe level of alcohol - even seven drinks a week can shrink brain mass, promote tau tangles, and quietly impair memory and thinking.
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Unfortunately, my beloved father died from alcohol use.
Alcohol use disorder (AUD) is associated with a progressive decline in cognitive function. According to some studies, up to 80% of patients with AUD may have mild to severe cognitive impairment. These impairments interfere with the acquisition of new learning (e.g., memory) and improved decision-making (e.g., executive functioning (EF)), hindering recovery. Alcohol-related brain defects and alcohol-associated cognitive impairments may contribute to the progression of AUD by impairing an individual's ability to benefit from treatment and by impairing their daily functioning in the community, which in turn increases stress and subsequent relapse. In a large-scale study, with a mixed sample of substance use disorder (SUD) patients with a mean age of 40 years (SD = 13.9) (N = 656 patients; 391 used alcohol, 123 used cannabis, 100 used stimulants, 26 used opioids), the prevalence of cognitive impairment was 31%. Patients who used alcohol had lower total and memory domain scores on the Montreal Cognitive Assessment (MoCA) than those who used cannabis. They also reported an association between older age and greater impairment, the strongest association being for the AUD sample. Not surprisingly, younger patients scored higher than older patients on all SUDs, which may suggest that greater continuous exposure to the effects of substances over time leads to greater cognitive decline over time. A review of cognitive impairments in SUD concluded that "altered cognitive function can be considered a hallmark of substance use disorders, and particularly of EDs, with documented impairments in the so-called 'executive' areas of attention, inhibition/regulation, working memory, and decision-making." The authors added that these deficits regulate subsequent motivational processes and constitute core impairments in addiction.
A National Institute on Alcohol Abuse and Alcoholism (NIAAA)-funded study (RO1AA029075) of cognitive training and donepezil in alcohol use disorder (AUD), for which ATEC is one of the cognitive assessments, and a separate study of ATEC itself that includes several participants with AUD, are currently underway. A review article on alcohol-related dementia (ARD) found 72 articles supporting the strong association between EDs and cognitive decline, concluding that chronic alcohol use impairs visuospatial functions, memory, and executive tasks, with the potential for partial recovery if abstinence is maintained. Our ATEC findings support this conclusion, with 43% displaying mild or greater overall impairment, with the highest frequency of impairment in embodied memory and self-regulation. Construct validity was also found for ATEC working memory and embodied delayed recall. HVLT list-learning immediate memory was not associated with ATEC memory domains, but HVLT delayed recall was related to ATEC working memory, though not to embodied delayed recall. Visual memory on the BVMT was much more strongly related to our ATEC memory scores. Finally, our findings with ATEC support the argument that younger age, higher educational level, and higher premorbid IQ are protective factors against cognitive decline in this ED sample. Education is a complex variable, as it can also reflect socioeconomic status and parental income, but the significant relationship with premorbid IQ appears to support the interpretation that cognitive reserve is involved.
https://www.mdpi.com/2076-3425/15/3/228 (2025).--
Wish these alcohol studies took diet of participants into account. Meaning, is alcohol interacting with high LA and PUFA levels to create "lesions"? Would it be different in a low LA and natural fats subject?