Also, just to make clear, I am not urging anyone to not use metformin for any reason. Metformin has been cleared by the FDA, and if your physician prescribes it, you should follow your physician’s advice. I am not a doctor and I don’t offer medical advice.
I am explaining why I personally don’t take metformin at this time, and have no plans to do so, unless compelling research comes out that changes my mind.
As I understand it, the evidence is that metformin negatively affects exercise adaptations, and this is one of the reasons why I don’t want to take it. However if you see benefits, I am very happy for you. YMMV.
Thanks. I cannot understand what they did in your referenced study. It looks like only a portion was done in a live animal (vs. in a dish). And the part they did “in vivo” is hard to understand how the metformin got into the tissues that were tested.
This could all be true but if Ralph DeFronzo PhD, the guy who got metformin approved by the FDA is correct, metformin does not get into muscle of human beings. Any effects are occurring in liver (and maybe kidney, I can’t remember exactly)
That said I don’t know that means metformin doesn’t affect exercise adaptation, it just means it isn’t happening in the muscle. Perhaps the higher lactate (from the liver) is causing a stress signal that is too much…or some such indirect effect. Or, in my experience, metformin made hard exercise feel harder, which lowered how hard I could go, which no doubt lowered my adaptation to exercise because I didn’t exercise as hard.
But don’t worry. I’m not seeking your approval to take metformin. I’m just sharing potentially useful information for people to consider in their calculus.
I am puzzled (and should be given I am not a scientist), but does it matter that metformin doesn’t get into the muscle to explain metformin’s impact on exercise adaptation?
Metformin is a cost-effective oral medication generally administered twice daily to humans to reduce blood glucose levels. The molecular mechanisms by which acute metformin administration lowers blood glucose are not fully understood
Our data illustrate the necessity of mitochondrial complex I inhibition for the blood glucose–lowering effects of metformin
Any other glucose inhibitor discussed in the video such as SGLT1 or SGLT2, or not discussed like acabose would seem superior given the drawbacks to the holistic mitochondria inhibition. This same researcher in the video has published papers on acabose so I am puzzled (again) why he even mentions metformin other that for all practical purposes it is free. Too many drawbacks to it use, at least for active people.
"Long-term oral taurine (OT 3 g/d) ameliorates CHF,1 so it was desired to determine whether OT (1.0 g three times per day) relieves edema without causing hypotension in nonagenarians. Forty-nine residents of an extended-care nursing home (20 taking antihypertensive therapy) who developed edema (score ≥2, Appendix A) despite hospital-prescribed diuretics or excessive hypotension precluding effective diuretic usage were enrolled from March 1, 2007, to March 31, 2010.
The remarkable effects of OT on edema were apparent within the first month of treatment (Figure 1A); decreases in body weight occurred with some delay. Required doses of diuretics decreased after institution of OT in the majority of residents. Serum albumin levels increased in 32 hypoalbuminemic residents"
“Taurine is one of the major organic osmolytes that cells use to compensate for changes in extracellular osmolality to maintain cell volume. In the supraoptic nucleus of the hypothalamus, taurine is highly concentrated in astrocytes, and released in an osmo-dependent manner under hypoosmotic conditions.4 OT will increase interstitial fluid [taurine] that, acting through its agonist action on neuronal glycine receptors, will amplify the inhibition of the release of vasopressin and oxytocin that occurs physiologically only when hypoosmotic,4promoting diuresis independent from osmolality. The findings of the current study suggest that inadequate antidiuretic hormone secretion plays a major role in older adults. The improved hypoalbuminemia (Figure 1B) and OT-induced inhibition of vasopressin and oxytocin allowed greater diuresis with minimal Na+ involvement, thus not causing hypotension.”
Owen, thanks for your helpful post. Now that you have upped dosage to 5.5g, do you take that in divided doses? When during the day do you take Taurine? Do you take it with food or empty stomach?
A downside of taurine: It drives leukemia growth
Just saw this, not directly related to longevity but worth noting.
A downside of taurine: It drives leukemia growth | ScienceDaily
Original paper: 1. Sonali Sharma, Benjamin J. Rodems, Cameron D. Baker, Christina M. Kaszuba, Edgardo I. Franco, Bradley R. Smith, Takashi Ito, Kyle Swovick, Kevin Welle, Yi Zhang, Philip Rock, Francisco A. Chaves, Sina Ghaemmaghami, Laura M. Calvi, Archan Ganguly, W. Richard Burack, Michael W. Becker, Jane L. Liesveld, Paul S. Brookes, Joshua C. Munger, Craig T. Jordan, John M. Ashton, Jeevisha Bajaj. Taurine from tumour niche drives glycolysis to promote leukaemogenesis. Nature, 2025; DOI: 10.1038/s41586-025-09018-7
New research in Nature (14 May 2025) shows that acute myeloid leukaemia and blast-crisis CML stem cells over-express the taurine transporter SLC6A6 (TAUT), siphon taurine from the bone-marrow niche, activate mTOR-driven glycolysis, and accelerate disease; deleting taurine synthesis or blocking TAUT slows these cancers and lengthens survival in mouse and patient-derived models.
Taurine itself is still FDA-GRAS and non-mutagenic, so it probably doesn’t initiate cancer - but for TAUT-positive clones it functions as high-octane fuel. This explains why taurine extended lifespan in healthy mice without increasing their usual lymphomas: those tumours don’t depend on TAUT. For us, ordinary dietary doses remain low-risk, yet gram-level self-experiments deserve caution, particularly if you carry clonal haematopoiesis, odd blood counts, or a past marrow malignancy.
Taurine’s longevity promise survives, but context now matters - make sure you know which engine you’re fueling.
Worth mentioning that taurine levels in the bone marrow/BM interstitial fluid were 5,000ng/mL (rising 1.7-fold in leukemia), which is much lower than serum levels in mice. For example, in Taurine deficiency as a driver of aging they were shown to peak at 100-150ng/mL in early life, falling to ~50ng/mL by 55 weeks old.
We know that a causatively significant portion of taurine in the BM niche/microenvironment is paracrine-derived, since cysteine dioxygenase type 1/CDO1-inhibition in osteolineage cells could attenuate leukemia growth. Additionally, the 100-fold concentration gradient (using a serum value of 50 since most acute myeloid leukemias/AMLs arise in late life) suggests that supplementation wouldn’t significantly affect niche levels.
One study in humans showed 1.5g taurine/day for 2 weeks could increase serum levels by 50%, but this wouldn’t be expected to raise niche levels much, as the concentration gradient opposing net diffusion into the BME would still be massive. It’s also unclear how taurine would enter the BME, if at all. ChatGPT suggests non-specific anion channels (e.g pannexins) and facilitated diffusion via a hypothetical taurine uniporter as possibilities, but both of these would promote taurine efflux from the BME due to the concentration gradient. TauT wouldn’t reverse at these concentrations either, so even if it was expressed on the basolateral endothelium, it would also promote taurine efflux from the BME.
Overall, I think it’s unlikely taurine supplementation would significantly impact BME levels, at least not directly. Also, taurine’s sulfur is in the fully oxidized sulfonic acid (-SO3H) state, and this oxidation is irreversible in humans, so taurine won’t directly increase cysteine levels either.
One thing this paper does do is provide further support for diets low in sulfur-containing amino acids like cysteine and methionine. AML is rare enough that the lifespan increase from methionine restriction probably isn’t mediated via a reduction in AML risk, but a potential reduction in AML risk would be a nice secondary benefit nonetheless.
Taurine (Tau) has modulatory effects on inflammatory and oxidative stress biomarkers; however, the results of clinical studies are not comprehensive enough to determine the effect of different durations and doses of Tau supplementation on inflammatory and oxidative stress biomarkers. The current study was conducted based on the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. For this purpose, PubMed/Medline, Scopus, and Embase databases were systematically searched to obtain the relevant studies published before 30th March 2021. Meta-analysis was performed on controlled clinical trials by using the random-effects method. Non-linear relationship between variables and effect size was performed using dose-response and time-response analyses. The Cochrane Collaboration’s tool was used to evaluate the quality of included studies. Tau supplementation can reduce the levels of malondialdehyde (MDA) (SMD = -1.17 µmol/l; 95% CI: -2.08, - 0.26; P = 0.012) and C-reactive protein (CRP) (SMD = -1.95 mg/l; 95% CI: -3.20, - 0.71; P = 0.002). There have been no significant effects of Tau supplementation on the levels of tumor necrosis factors-alpha (TNF-α) (SMD = -0.18 pg/ml; 95% CI: -0.56, 0.21; P = 0.368), and interleukin-6 (IL-6) (SMD = -0.49 pg/ml; 95% CI: -1.13, 0.16; P = 0.141). Besides, Tau has more alleviating effect on oxidative stress and inflammation on 56 days after supplementation (P < 0.05). Tau can decrease the levels of CRP and MDA. Based on the currently available evidence, Tau has no significant effect on the level of TNF-α and IL-6. Eight-week of Tau supplementation has more beneficial effects on inflammatory and oxidative stress biomarkers.
I’m a healthy 40-ish-year-old experimenting with taurine for general cardiometabolic and longevity benefits. I’m trying to decide between:
Split dosing: 2 g with breakfast, 2 g with lunch, 2 g before bed (total = 6 g/day)
Single bolus: taking the full dose at once to hit a high plasma peak
From what I’ve read, oral taurine peaks ~1–2 h after ingestion, the half-life is ~1 h, and levels drop back to baseline in ~6 h. That makes me wonder whether a steadier exposure (higher AUC) is more useful than chasing a short-lived spike.
Questions
Has anyone here compared split vs single-dose taurine in practice or seen data on which gives better real-world benefits (BP, exercise performance, sleep, etc.)?
Does a higher peak confer any unique advantage, or is it mostly wasted because the kidneys dump the excess?
Any side-effects you noticed when moving from 3–4 g/day up to 6 g/day?
All insights, anecdotes, and links to papers are welcome—thanks!
I have a friend that also dropped taurine because it gave him gas and an upset stomach. He eats plenty of meat, so he’s getting it there but the supplemental version didn’t agree with him.
This says you can’t use taurine as a marker of age, as levels don’t decline with age, unlike previous claims. A serious dent in the taurine for longevity story.
Taurine Might Not Be the Anti-Aging Miracle We Hoped For
“They analyzed long-running data from past human, mice, and monkey studies, finding that taurine levels didn’t change much over time and widely varied between individual animals. The results suggest that taurine isn’t a good marker for age and throw into doubt the idea that it can prolong healthy aging.
“Circulating taurine doesn’t decline with age in healthy individuals of these three mammalian species across the adult lifespan,” said lead study researcher Maria Emilia Fernandez, a postdoctoral fellow in the Translational Gerontology Branch of the NIH’s National Institute on Aging, in a press conference Tuesday announcing the findings.“
De Cabo’s study is “more convincing” than the previous one, says geneticist David Sinclair at Harvard University in Boston, Massachusetts. In recent years, there has been an over-reliance on cross-sectional data sets, such as those used in the earlier study, he says — and those are highly variable. That variability, he says, can lead to misinterpretations and false-positive conclusions.
I am not in David Sinclair’s fan club, but it is worth reporting his statement here. I never thought Taurine was a miracle molecule, but I had bought some and it was in my stack. Whether I will replace this or not is not currently clear. I will decide when I have finished eating it. I haven’t noticed any identifiable effects, but I don’t always manage to.
My stack “in the round” is doing quite well at the moment. But it does get quite complex with numerous factors.
Regardless of whether taurine levels decline with age - per the study I posted above perhaps not - there may still be reasons to supplement. One such reason might be its impact on blood pressure and other aspects of CV health. If not longevity, perhaps healthspan? FWIW, my blood pressure started to creep up in the last few years and so I have boosted my taurine intake to 3-4g/day.
Functional Role of Taurine in Aging and Cardiovascular Health: An Updated Overview
Perhaps you are one of the group that is low on taurine. Personally, I saw no noticeable effect on my blood pressure even on 10 grams a day.
Apparently, with many people, taurine levels increase with age.
“The amino acid taurine was once thought to decline with age, and animal research suggested that taurine supplements could delay ageing. But a new study shows that the decline doesn’t happen consistently. In fact, taurine levels tend to increase in people over time, suggesting that low levels of the nutrient aren’t a driver of ageing.”
@desertshores Am I hallucinating or did you at some point have a major breakthrough by taking a huge dose of taurine? I seem to recall you saying there were no effects at all that you could feel until you went past a certain threshold that was pretty high, at which point angelic choirs broke out? Or was that a nothingburger?
Yes.
On any given day I can feel euphoric and attribute it something that actually has nothing to do with it.
I have no objective or subjective reason to believe taurine is doing anything for me
They analyzed long-running data from past human, mice, and monkey studies, finding that taurine levels didn’t change much over time and widely varied between individual animals. The results suggest that taurine isn’t a good marker for age and throw into doubt the idea that it can prolong healthy aging.
Unless you’re in the business of storytelling, whether a factor increases/decreases with age is irrelevant.
The only question we should be concerned with regarding taurine supplementation is: does it increases lifespan (and/or some other measure of good health/healthspan) relative to a control group. It did that in mice relative to long-lived controls, although they weren’t genetically heterogenous. It also showed some healthspan benefits in primates as well.
Nobody was getting excited about taurine because it allegedly declined with age, it was because of the promising RCT results. So while this new paper provides valuable information about taurine’s value as a longevity biomarker, it’s a red herring with respect to taurine’s value as a longevity supplement.
Yes but the fact that Taurine declines with age in mice was a finding that made sense that supplementing with Taurine might make up for a deficiency as they aged. If that is true, and it doesn’t decline with age in humans then it may mean that we shouldn’t expect the mouse result to translate to humans.
The new paper also found an age-dependent increase in taurine levels for female C57BL/6J mice (male levels unchanged). This is the same mice strain that lived longer with taurine supplementation and where taurine levels were (perhaps erroneously) suggested to decline with age.
