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All, Paul McGlothin and I have been having a discussion about the merits or risks of cider vinegar for longevity. Unfortunately the discussion is behind the CR Way paywall :( , so I won't post Paul's side of the discussion directly, but paraphrase him instead. Paul fears that the acetic acid in vinegar (cider or otherwise) gets converted into acetyl groups, which as discussed in this post, tend to unsilence genes by unwrapping them from histones in the nucleus so they can be transcribed into proteins. In particular, Paul is concerned that vinegar might reverse the effects of the Sirtuins, which are histone deacetylases, meaning they wrap genes tighter around histones, effectively silencing them. But when I questioned him about evidence for this specific effect of vinegar / acetic acid, he acknowledged that it's just a mechanistic hunch on his part. His hunch seems somewhat naive to me. Clearly some genes should be silenced and some expressed for effective aging, so its not clear a priori whether having more acetyl groups floating around would be good or bad from an aging perspective. In fact, the one piece of hard evidence I came across , seems to support the opposite of Paul's argument, i.e. it suggests vinegar / acetic acid may actually be an anti-aging agent, at least in C. Elegans. It found that acetic acid upregulated the expression of DAF-16 in C. Elegans, leading to a 25% increase in lifespan. It doesn't appear to be having this effect by directly unwrapping DAF-16 for increased expression, but by somehow interfering with another gene, DAF-2, which normally suppresses the expression of DAF-16. But whatever the mechanism, it suggests vinegar might not be so bad after all. Of course this is only a single study in worms, so there is no guarantee it is applicable to humans. But encouragingly, the human version of the DAF-16 gene upregulated by vinegar is the FOXO3 gene, the overexpression of which is well-known to be longevity-promoting in humans (e.g. ). BTW, 23andMe has a SNP for determining one's FOXO3 variant, rs2802292. From , the odds ratio for reaching 100 years of age for rs2802292(G;G) vs (T;T) carriers was 2.75 (p = 0.00009; adjusted p = 0.00135). One's odds of living to 100 with one copy of 'G' for rs2802292 (i.e. G:T), appears to be about 1.5-2 times greater than people with T:T. I'm G:T for rs2802292, so I've got that goin' for me :) Does anyone have and thoughts on vinegar, and whether you include it in your diet? --Dean ----------------  Bioorganic & Medical Chemistry. 2009 Nov 15;17(22):7831-40. doi: 10.1016/j.bmc.2009.09.002. Epub 2009 Sep 6. The lifespan-promoting effect of acetic acid and Reishi polysaccharide. ChuangMH(1), Chiou SH, Huang CH, Yang WB, Wong CH. Author information: (1)Genomics Research Center, Academia Sinica, Taipei 115, Taiwan. Using Caenorhabditis elegans as a model organism, various natural substances and commercial health-food supplements were screened to evaluate their effects on longevity. Among the substances tested, acetic acid and Reishi polysaccharide fraction 3 (RF3) were shown to increase the expression of the lifespan and longevity-related transcription factor DAF-16 in C. elegans. We have shown that RF3 activates DAF-16 expression via TIR-1 receptor and MAPK pathway whereas acetic acid inhibits the trans-membrane receptor DAF-2 of the insulin/IGF-1 pathway to indirectly activate DAF-16 expression. In addition, a mixture of acetic acid and RF3 possesses a combined effect 30-40% greater than either substance used alone. A proteomic analysis of C. elegans using 2-DE and LC-MS/MS was then carried out, and 15 differentially expressed proteins involved in the lifespan-promoting activity were identified. PMID: 19837596 -------------  Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13987-92. doi: 10.1073/pnas.0801030105. Epub 2008 Sep 2. FOXO3A genotype is strongly associated with human longevity. Willcox BJ(1), Donlon TA, He Q, Chen R, Grove JS, Yano K, Masaki KH, Willcox DC, Rodriguez B, Curb JD. Author information: (1)Pacific Health Research Institute, 846 South Hotel Street, Honolulu, HI 96813, USA. firstname.lastname@example.org Human longevity is a complex phenotype with a significant familial component, yet little is known about its genetic antecedents. Increasing evidence from animal models suggests that the insulin/IGF-1 signaling (IIS) pathway is an important, evolutionarily conserved biological pathway that influences aging and longevity. However, to date human data have been scarce. Studies have been hampered by small sample sizes, lack of precise phenotyping, and population stratification, among other challenges. Therefore, to more precisely assess potential genetic contributions to human longevity from genes linked to IIS signaling, we chose a large, homogeneous, long-lived population of men well-characterized for aging phenotypes, and we performed a nested-case control study of 5 candidate longevity genes. Genetic variation within the FOXO3A gene was strongly associated with human longevity. The OR for homozygous minor vs. homozygous major alleles between the cases and controls was 2.75 (P = 0.00009; adjusted P = 0.00135). Long-lived men also presented several additional phenotypes linked to healthy aging, including lower prevalence of cancer and cardiovascular disease, better self-reported health, and high physical and cognitive function, despite significantly older ages than controls. Several of these aging phenotypes were associated with FOXO3A genotype. Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype. Further exploration of the FOXO3A gene, human longevity and other aging phenotypes is warranted in other populations. PMCID: PMC2544566 PMID: 18765803