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(from https://twitter.com/theproof/status/1607622077879816192/photo/1 )

[low-fat vegetarians have better GLUCOSE than low-carb meat-eaters]. The only metrics vegetarians are worse on are triglycerides and free fatty acids (interestingly)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191896/

There were 2570 deaths among 73 308 participants during a mean follow-up time of 5.79 years. The mortality rate was 6.05 (95% CI, 5.82–6.29) deaths per 1000 person-years. The adjusted hazard ratio (HR) for all-cause mortality in all vegetarians combined vs non-vegetarians was 0.88 (95% CI, 0.80–0.97). The adjusted HR for all-cause mortality in vegans was 0.85 (95% CI, 0.73–1.01); in lacto-ovo–vegetarians, 0.91 (95% CI, 0.82–1.00); in pesco-vegetarians, 0.81 (95% CI, 0.69–0.94); and in semi-vegetarians, 0.92 (95% CI, 0.75–1.13) compared with nonvegetarians. Significant associations with vegetarian diets were detected for cardiovascular mortality, noncardiovascular noncancer mortality, renal mortality, and endocrine mortality. Associations in men were larger and more often significant than were those in women.

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epigenetic study below (it’s an isolated study so idk how generalizeable)

A gene list created by comparing the differentially methylated CpG sites observed in nonvegetarians and vegans was used to perform DAVID functional annotation clustering using its own Knowledgebase. This analysis revealed that out of 49 identified functional groups of genes (Table S4), the top cluster, as shown in Table 4, demonstrates enrichment of homeobox transcriptional factors. This enrichment is significant by a variety of statistical tests. The potential of these transcription factors to amplify differential activation may indicate that the presence or absence of animal proteins in the diet may lead to much larger differences in gene expression regulation than the relatively modest fold-changes detected by an epigenetics approach might suggest.

Table 4. Functional annotation cluster 1 report for vegans vs. nonvegetarians run with high classification stringency.

Table

Similar results were obtained when we performed the same analysis under the same conditions using the gene list based on differential methylation detected in pescatarians vs. vegans. Table 5 shows that homeobox transcription factors again form the top functional cluster among all the genes used in analysis. However, statistical characteristics for pescatarians are weaker (Table 5).

Table 5. Functional annotation cluster 1 report run for vegans vs. pescatarians run with high classification stringency.

Table

It is important to note that, out of 8 genes encoding homeobox transcription factors detected in pescatarians, 3 are found also in nonvegetarians, which indicate on nonrandom differences in methylation patterns (Table 6).

Table 6. CpG sites identified as differentially methylated in transcription factor genes in pescatarians.

Table

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Another Blagosklonny comment to think about
#2

Very interesting topic!
What to Eat & When to Eat for Longevity | Lifespan with Dr. David Sinclair #2 - YouTube at 48:35, 2013, adventist health group, big study

#3

https://www.google.com/url?q=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761449/&sa=U&ved=2ahUKEwihpcSF9JD8AhVVMlkFHUtCCm4QFnoECAsQAg&usg=AOvVaw2Sn714pKRePUDuhx9FHdYd says more hypomethylation, the opposite of OP

Esp in METTEC

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#4

Additionally, vegans and vegetarians have significantly higher counts of certain Bacteroidetes-related operational taxonomic units compared to omnivores. Fibers (that is, non-digestible carbohydrates, found exclusively in plants) most consistently increase lactic acid bacteria, such as Ruminococcus, E. rectale, and Roseburia, and reduce Clostridium and Enterococcus species. Polyphenols, also abundant in plant foods, increase Bifidobacterium and Lactobacillus, which provide anti-pathogenic and anti-inflammatory effects and cardiovascular protection

Vegetarians are more “separated” from pro-inflammatory western diet microbiota

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#5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8277109/

Protein quality impacts health and longevity

For many years, there has been interest in understanding if protein source plays a role in health, with the greatest focus on understanding if there is a difference between the effect of plant protein and animal protein. Several studies have suggested that plant-based protein is healthier. One study found that consumption of a plant-based vegan diet decreased all-cause mortality, coronary heart disease and a decrease in risk of developing obesity in humans (98); a more recent study showed that a plant based diet significantly lowered the incidence of cardiovascular disease (CVD), CVD mortality, and all-cause mortality in a cohort of middle-aged adults (99). Vegan diets have also been implicated in reducing the risk of developing metabolic syndrome, lowering triglycerides, blood pressure, glucose, waist circumference and body mass index (100), and decreasing fat mass and insulin resistance (101).

One possibility that has been advanced to explain the beneficial effects of plant protein is that there is a difference in protein quality – the specific amino acid composition of the protein. Plant-based diets have a reduced level of methionine as compared to animal sources, and humans consuming a vegan diet have reduced plasma levels of methionine compared to humans who eat animal proteins (102, 103). As discussed below, significant data now suggests that the level of methionine – as well as of several other dietary amino acids – has a profound effect on health and longevity, not only in rodents, but also in humans. An overview of recent studies is provided in Table 1 and Table 2).

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#6
#7

I just learned who Walter willet of hsph!! He advocates vegetarian diets! Maybe not at the analytical forefront anymore but of high social importance

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9839575/

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#8

TMAO link to heart disease is probably confounding or reverse causality:

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Diet and Healthspan - Uncertain but High Value
#9

Thanks for posting. The relationship between TMAO and cardiovascular diseases has been a bit confusing because on one hand there are indications that TMAO is harmful while on the other hand fish is a very rich source of TMAO and fish intake is certainly not associated with increased risk of cardiovascular diseases.

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#10

The Health Debates Over Plant-Based Meat

4.2. Long Term Health Outcomes

Estimating the long-term health outcomes of eating certain things is difficult because food is highly bound up in the culture we live in and culture correlates to just about every health outcome you could possibly imagine. Even less conveniently, nutritional science is highly anti-inductive; if a particular food group is identified as being healthy people with an interest in being healthy flock to that food group, and people with an interest in being healthy are likely to be healthy for a bunch of reasons regardless of diet.

So here’s a nice headline result: vegetarians have less heart disease with extremely high certainty, and probably less cardiovascular disease and cancer too. Most of the studies in that meta-analysis have had some of the really obvious stuff adjusted away (race, income, etc.) but not all studies adjust for all confounders, and we should be cautious about trusting studies that ‘adjust for confounders’. If you ignore confounders then the answer is clear; eating vegetarian is good for you in every single way we can measure (including, possibly, circulating testosterone in defiance of stereotypes about meat eaters!).

If you are interested in confounders: There are a handful of cool natural experiments, taking groups with reasons to eat certain food but not bother with the associated healthy lifestyles, which are the closest we are likely to come to a true experiment in this area. In particular, the American Adventist Health Studies are pretty much state of the art in the field from what we can see. Adventists have quite unique dietary habits, brought about by religious prohibitions on certain foodstuffs which some Adventist churches follow and some don’t. Consequently, if you are an Adventist you are functionally ‘randomized’ into different food-eating conditions depending on which church you attend, and this randomization can be exploited by researchers.

Based on the Adventist Health Studies, a vegetarian diet increases life expectancy by around 3.6 years. The less meat you eat, the healthier your BMI and the less likely you are to get diabetes.

Overall we might expect lacto-ovo vegetarians to have a health related quality of life around 10% better than a meat eater, with most of this benefit being apparent 20 years after making the switch to a vegetarian diet.

You could complicate this picture a lot (especially by introducing future discounting) but we think the general principle that if you value life-years towards the end of your life you should likely go vegetarian is well demonstrated by the data:

One final point on how meat might affect your lifespan; there is a growing awareness of the fact that industrially produced meat is an ideal breeding ground for zoonotic disease, and that those diseases can mutate and jump to humans very quickly. Previous pandemics such as H1N1 (‘swine flu’) and H5N1 (‘bird flu’) may have originated with farmed animals, and were rapidly spread by the close contact of unhealthy animals and global nature of the meat supply chain. At the margin, eating meat probably increases the probability of a global pandemic but there isn’t good evidence on how much your individual consumption affects things at the margin.

In the model we take the Adventist study result at almost face value, estimating that eating vegetarian will increase your lifespan by 3 years, and include constant low costs due to possible nutritional deficiency and moderate benefits to health that appear later in life.

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#11
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#12
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#13

https://glycanage.com/glycanhub/podcast/season-1/should-you-stop-eating-red-meat-glycans-inflammation-and-cancer-with-prof-vered-padler-karavani

#14

as expected, vegan healthier…

they forgot to mention increase telomere length on vegan diet.


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Raghav 'RV' Sehgal

Raghav ‘RV’ SehgalRaghav ‘RV’ Sehgal • 1st • 1st Venture Consultant @ Longevitytech.fund | PhD @ Yale | AI-driven Investment StrategiesVenture Consultant @ Longevitytech.fund | PhD @ Yale | AI-driven Investment Strategies
3h •


3h •

Very excited to share that the Netflix documentary “You are what you eat: A twin study” is the same research study that used, System Age (my first, first author publication) to show that vegan diets can slow aging in heart, liver and other specific organs. Grateful to Varun Dwaraka, PhD from TruDiagnostic for using Systems Age for this work!

Alex K. Chen



[

Varun Dwaraka, PhDView Varun Dwaraka, PhD’s profile (He/Him) • 1st Bioinformatician | Aging and Longevity Investigator

](https://www.linkedin.com/in/ACoAAAnc2ycB_0DdCI66UZhslqRW-nezY0WYDKM)

3h

Thanks for creating a very nifty tool!



[

Shahaf PelegView Shahaf Peleg’s profile • 1st Group leader at FBN and co-founder of Luminova Biotech

](https://www.linkedin.com/in/ACoAAA17bY8BMRk6flKbXcF6AaJHPTM8VzxwP_o)

3h

Cool

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#15

Great find Alex. It would be interesting to see the study conducted over much longer time frames though.

#16

@AlexKChen any sense of adding taurine supplementation to vegan diet?

#17

^just do it, it’s easier than eating shellfish

Excessive methionine dietary intake produces higher vascular organ damage than any other amino acid. This toxicity can be due to various mechanisms including increases in iron levels (Kumagai et al., 2002), or in methionine metabolites like S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), cysteine or homocysteine. Methionine can also induce damage by increasing liver lipid peroxidation and oxidative stress (Park et al., 2008), or by oxidation of methionine residues in proteins to methionine sulfoxide leading to their loss of biological function (Ciorba et al., 1997). Overexpression of methionine sulfoxide reductase, which repairs methionine sulfoxide in proteins, protects against oxidative stress and increases longevity in Drosophila melanogaster (Lim et al., 2012), and long-lived Ames dwarf mice have increased activity of the transulfuration pathway (Uthus and Brown-Borg, 2006).

There is evidence that methionine itself is responsible for some of the adverse effects produced by the excess of this amino acid in the diet (Troen et al., 2003). Direct addition of methionine to isolated mitochondria in vitro increases the rate of mitROSp in liver and kidney (Gómez et al., 2011). Therefore, part the effect of methionine supplementation on mitROSp can be due to direct interaction of methionine with mitochondria.

Several studies indicate that methionine is an important factor affecting rodent longevity. Furthermore, protein and methionine supplementation increase plasma levels of its metabolites such ass-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH) and homocysteine in rodents (Velez-Carrasco et al., 2008; Gómez et al., 2009) and homocysteine in humans (Verhoef et al., 2005). Based on the following examples, it is plausible that some products of methionine metabolism are responsible for part of the detrimental effects of methionine on health: i) increased homocysteine levels in blood can induce both atherosclerosis and hypertension (Troen et al., 2003); ii) elevated plasma homocysteine levels may accelerate aging of the vascular system (Fau et al., 1988) and possibly in the brain (Algaidi et al., 2006); iii) cysteine, a product of methionine metabolism, can be responsible for part of the pro-aging effect of methionine on longevity; iv) plasma cysteine levels have been found to be related to fat mass increasing adiposity in humans (Elshorbagy et al., 2008). Furthermore, various beneficial changes induced by MetR including decreases in mitROSp, mitDNA damage, body weight gain, body fat, subcutaneous fat, visceral fat, and serum hormones associated with adiposity are reversed by cysteine dietary supplementation (Elshorbagy et al., 2011; Gómez et al., 2015).

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#18

Does anyone know what steps / protocol Bryan uses for his homocysteine? (@AnUser ?)

Does anyone have good results with modifying their homocysteine?

Per Peter Attia protocol I tried upping methylated B12 and Folate, and also take some activated B6 (P5P) 3 times a week. That lowered my homocysteine by 4-5 points or so to 9.5, but I’d ideally get it down to 8ish or below.

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#19

Creatine can help, it’s good for intelligence and weightlifting as well.

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#20

Interesting. Any thoughts on optimal doing? I’ve taken 2.5-5g sometimes around weightlifting days.