05 June 2020 In Diabetes

We aimed to elucidate the effect of chronic alcohol consumption on fatty liver. We assessed the consumption of alcohol in 2429 Japanese males (mean age: 54.2 +/- 9 years); they were classified according to average consumption into non-drinkers (ND), light drinkers (LD), moderate drinkers (MD), and heavy drinkers (HD).

The prevalence of fatty liver was the lowest in the MD and highest in the ND group (p < 0.001), while obesity was not significantly different among the groups (p = 0.133). Elevated levels of alanine aminotransferase (ALT) were the lowest in the MD group (p = 0.011) along with resistance to insulin (homeostasis model assessment-insulin resistance (HOMA-IR)), which was highest in the ND group (p = 0.001).

Chronic consumption of alcohol was independently and inversely associated with fatty liver and insulin resistance after adjusting for obesity, hypertension, fasting hyperglycemia, habit of drinking sweet beverages, physical activity, and age (odds ratios are as follows: ND, 1; LD, 0.682; MD, 0.771; HD, 0.840 and ND, 1; LD, 0.724; MD, 0.701; HD, 0.800, respectively).

We found that regardless of the type of alcoholic beverage, chronic consumption of alcohol is inversely associated with insulin resistance and fatty liver in Japanese males. This study had limitations, most notably the lack of investigation into diet and nutrition.

04 May 2020 In Diabetes

We aimed to determine the association between alcohol consumption change on fasting serum glucose, insulin resistance, and beta cell function.

The study population consisted of 55,858 men from the Kangbuk Samsung Health Study. Participants were divided into non-, light, moderate, and heavy drinkers for each of the first and second health examinations based on a self-reported questionnaire on alcohol consumption. The adjusted mean values for change in fasting serum glucose (FSG), homeostatic model assessment of insulin resistance (HOMA-IR), and beta cell function (HOMA-beta) levels were determined according to alcohol consumption change by linear regression. Compared to sustained initial drinkers, those who increased alcohol intake to moderate (p < 0.001) and heavy (p < 0.001) levels had increased FSG levels.

In contrast, reduction in alcohol intake to light levels among initial heavy drinkers was associated with reduced change in FSG levels (p = 0.007) compared to sustained heavy drinkers. No significant associations were observed between changes in alcohol intake with HOMA-IR levels. Compared to sustained light drinkers, those who increased alcohol intake to moderate (p < 0.001) and heavy (p = 0.009) levels had lower increases in HOMA-beta levels.

Finally, compared to sustained heavy drinkers, those who reduced alcohol consumption to light levels had greater increases in HOMA-beta levels (p = 0.002). Increases in alcohol consumption were associated with higher blood glucose levels and worsened beta cell function. Heavy drinkers who reduce alcohol intake could benefit from improved blood glucose control via improved beta cell function.

27 March 2020 In Dementia

INTRODUCTION: Observational studies have suggested that light-to-moderate alcohol consumption decreases the risk of Alzheimer's disease, but it is unclear if this association is causal.

METHODS: Two-sample Mendelian randomization (MR) analysis was used to examine whether alcohol consumption, alcohol dependence, or Alcohol Use Disorder Identification Test (AUDIT) scores were causally associated with the risk of Late-Onset Alzheimer's disease (LOAD) or Alzheimer's disease age of onset survival (AAOS). Additionally, gamma-glutamyltransferase levels were included as a positive control.

RESULTS: There was no evidence of a causal association between alcohol consumption, alcohol dependence, or AUDIT, and LOAD. Alcohol consumption was associated with an earlier AAOS and increased gamma-glutamyltransferase blood concentrations. Alcohol dependence was associated with a delayed AAOS.

DISCUSSION: MR found robust evidence of a causal association between alcohol consumption and an earlier AAOS, but not alcohol intake and LOAD risk. The protective effect of alcohol dependence is potentially due to survivor bias.

27 March 2020 In Dementia

BACKGROUND: Alzheimer's disease (AD), the most threatening neurodegenerative disease, is characterized by the loss of memory and language function, an unbalanced perception of space, and other cognitive and physical manifestations. The pathology of AD is characterized by neuronal loss and the extensive distribution of senile plaques and neurofibrillary tangles (NFTs). The role of environment and the diet in AD is being actively studied, and nutrition is one of the main factors playing a prominent role in the prevention of neurodegenerative diseases. In this context, the relationship between dementia and wine use/abuse has received increased research interest, with varying and often conflicting results.

Scope and Approach: With this review, we aimed to critically summarize the main relevant studies to clarify the relationship between wine drinking and AD, as well as how frequency and/or amount of drinking may influence the effects.

Key Findings and Conclusions: Overall, based on the interpretation of various studies, no definitive results highlight if light to moderate alcohol drinking is detrimental to cognition and dementia, or if alcohol intake could reduce risk of developing AD.

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