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Resveratrol vs. alcohol


KHashmi316
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I recall but can't find -- those damned lost Archives!! -- a few CR List discussions on what the stuff ( in certain boozes ) may be that's of bennie. 

IIRC, Micheal Rae (??) noted the alcohol molecule itself as a key bennie. That's all I remember! 

Any one have better memory? Journal/paper links probably most useful.

(Note: This was well before Resveratrol  and the whole longevinex.com/Bill Sardi thing).

Thanks!! 

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I just did a deep dive in this and there are a couple studies on the polyphenols in red wine specifically, which include catechin and quercetin in addition to resveratrol:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407993/
https://pubmed.ncbi.nlm.nih.gov/23408240/

And here's my deep dive: https://www.longevityadvice.com/alcohol-life-expectancy/

Turns out there's actual in vivo animal studies showing life extension from small amounts of alcohol. I always thought that advice was only based on epidemiological studies which I tend to distrust.

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I'd take a lot of these studies with a grain of salt, and be suspicious of cultural/social bias and industry. And resveratrol appears to actually be detrimental, on the whole, as discussed elsewhere on this forum.

Some of the longest-living studied populations, like the Okinawans and the Adventists, don't drink red wine or don't drink at all. Just like with olive oil, you can get the good stuff like polyphenols more efficiently from other sources, without the detrimental effects. And yes, I have drunk a wide variety of alcohol since I was 15 or 16, spirits when young and mostly red wine and sake when not so young :)

 

All cause mortality and the case for age specific alcohol consumption guidelines: pooled analyses of up to 10 population based cohorts

Results In unadjusted models, protective effects were identified across a broad range of alcohol usage in all age-sex groups. These effects were attenuated across most use categories on adjustment for a range of personal, socioeconomic, and lifestyle factors. After the exclusion of former drinkers, these effects were further attenuated. Compared with self reported never drinkers, significant protective associations were limited to younger men (50-64 years) and older women (≥65 years). Among younger men, the range of protective effects was minimal, with a significant reduction in hazards present only among those who reported consuming 15.1-20.0 units/average week (hazard ratio 0.49, 95% confidence interval 0.26 to 0.91) or 0.1-1.5 units on the heaviest day (0.43, 0.21 to 0.87). The range of protective effects was broader but lower among older women, with significant reductions in hazards present ≤10.0 units/average week and across all levels of heaviest day use. Supplementary analyses found that most protective effects disappeared where calculated in comparison with various definitions of occasional drinkers.

Conclusions Beneficial associations between low intensity alcohol consumption and all cause mortality may in part be attributable to inappropriate selection of a referent group and weak adjustment for confounders. Compared with never drinkers, age stratified analyses suggest that beneficial dose-response relations between alcohol consumption and all cause mortality may be largely specific to women drinkers aged 65 years or more, with little to no protection present in other age-sex groups. These protective associations may, however, be explained by the effect of selection biases across age-sex strata.

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