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Just steve's avatar

Alcohol, seed oils and - Corn Sugar all negatively affecting the liver and being processed like alcohol, would suspect Corn Sugar would too. A one, two, three punch. Then glyphosate to disrupt Gut Health and causing direct throughout the body through circulation along with Leaky Gut deposits outside of the circulatory system. Bam. A one two punch. No wonder so many are just limping through their day.

Guillermou's avatar

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. This impairment interferes with acquiring new learning (e.g., memory) and with better decision-making (e.g., executive functioning [EF]), hindering recovery. Alcohol-related brain damage and alcohol-associated cognitive impairments can contribute to the progression of AUD by affecting an individual's ability to benefit from treatment and by impairing their daily functioning in the community, which in turn increases stress and the risk of relapse. In a large-scale study with a mixed sample of patients with substance use disorder (SUD) with a mean age of 40 years (SD = 13.9) (N = 656 patients; 391 used alcohol, 123 used cannabis, 100 used stimulants, and 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. An association was also reported between older age and greater impairment, with the strongest association observed in the AUD sample. Not surprisingly, younger patients scored higher than older patients across all SUDs, suggesting that greater continuous exposure to the effects of substances over time leads to greater cognitive decline. A review of cognitive impairments in substance use disorders (SUDs) concluded that “impaired cognitive function can be considered a hallmark of substance use disorders, and particularly of eating disorders, with documented impairments in the well-known ‘executive’ areas of attention, inhibition/regulation, working memory, and decision-making.” The authors added that these deficits regulate subsequent motivational processes and constitute fundamental impairments in addiction.

A study funded by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) (RO1AA029075) of cognitive training and donepezil in alcohol use disorder (AUD) is currently underway, for which ATEC is one of the cognitive assessments, along with another study of ATEC itself that includes several participants with AUD. A review article on alcohol-related dementia (ARD) found 72 articles supporting the strong association between alcohol use disorder (AUD) and cognitive impairment, concluding that chronic alcohol consumption affects visuospatial functions, memory, and executive tasks, with the potential for partial recovery if abstinence is maintained. Our ATEC findings support this conclusion, with 43% showing mild or greater overall impairment, most frequently in embodied memory and self-regulation. Construct validity was also found for ATEC working memory and embodied delayed recall. Immediate memory on HVLT list learning 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 attainment, and better premorbid IQ are protective factors against cognitive decline in this eating disorder 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).--

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