Taurine Benefits - are they real or hype?

Supplements
#171

For cooking purposes, a teaspoonful is defined as 5 mL.

An international metric tablespoon is exactly 15 mL, about 0.53 imperial fluid ounce or 0.51 US fluid ounc

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#172

Yes, I use a normal silverware sized spoon. Not a soup spoon.

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#173

Because i didn’t know how much one should be taking until this thread… The bottle’s instructions said one a day…

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#174

I see.
I use bulk supplements powder from Amazon. Lasts a long time and cheap.

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#175

I just got a bulk pack in (1kg/2.2lbs) from amazon. you’re right, it is inexpensive.

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#176

I take taurine but have lowered the dose to ~2,000 mg/day because two 2025 papers directly challenge the foundational claims underlying the taurine geroprotective case.

A longitudinal study directly disputes the earlier Yadav/Singh et al. 2023 Science paper, which had found taurine declining with age in humans, mice, and monkeys and shown lifespan extension in mice with supplementation. C&EN

The key findings: in blood samples from humans, monkeys, and mice, including longitudinal data from the Baltimore Longitudinal Study of Aging (ages 26–100), found circulating taurine levels often increased or remained constant with age. Crucially, within-individual differences in taurine levels frequently exceeded age-related changes, and taurine levels were inconsistently associated with health outcomes across age, species, and cohorts. National Institutes of Health. In fact, taurine levels increased as women aged. The researchers concluded that the association between taurine levels and functional health status measures depended heavily on genetics and context. Inside Precision Medicine

A cell-based study, with all its strengths and limitations, found that circulating taurine levels were not associated with aging, muscle mass, strength, power, physical performance, body composition, insulin sensitivity, or mitochondrial function in humans Wiley Online Library. This is a comprehensive null result across exactly the outcomes that made the 2023 paper compelling. They concluded that taurine deficiency is therefore unlikely to be a primary driver of aging in humans, and these findings challenge its utility as a biomarker of aging and functional decline. This study does not rule out potential positive health impacts of taurine supplementation in older adults, especially in individuals with low circulating taurine levels and those with chronic diseases.

These studies warrant a meaningful downgrade of the case for taurine supplementation. The central pillar of the taurine geroprotective case was the Singh et al. finding of age-associated decline with the logic being that supplementation restores a deficient state. If circulating taurine does not reliably decline with age in humans (and may increase in women), the interventional rationale weakens considerably. Some resolution could be had by measuring taurine levels. Has anyone done that and do intelligent benchmarks exist?

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#177

Whether taurine declines with age is irrelevant. The question is whether supplementing taurine provides any benefit

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#178

Exactly… does it benefit?

My N=1 tested, says YES!

Going from a T score 4-years ago showing osteopenia… to a normal T score 2 years ago… after 1 full-year of daily taurine and now this year 2026… even deeper into normal T score… still daily spoonful of taurine in my morning coffee.

Glad I started.

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#179

I had titrated from1 to 2 to 3 grams. Experienced itching chest, upper arms. Somehow found study that said Taurine can cause itching. Went back to 1 gram and no more itching.

I must be very sensitive to some of these sides: had experienced ankle swelling and read that lithium (orotate) can cause it. Had moved up to 5 mg a day. Cut back to 5 mg a couple of times a week, and edema has resolved.

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#180

Edema can also be a side effect of Rapamycin.

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#181

A good friend of mine found that taurine upset his digestive track, so he discontinued taking it. Was only taking 2 g per day. It seems that some people have sensitivities to the supplement version. The same friend can down a steak and has no issues.

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#182

My mother also has gastrointestinal issues with Taurine. It is a thing.

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#183

https://www.sciencedirect.com/science/article/pii/S0753332226004300

Taurine inhibits apolipoprotein E4 aggregation

Highlights

• Impact of taurine on ApoE revealed through simulations, biophysical assays, and cerebral organoid models.

• Taurine inhibits ApoE4 aggregation, mimicking the protective effects of tramiprosate and its metabolite 3-sulfopropanoic acid.

• Taurine shifts ApoE4 phenotype toward the less harmful ApoE3 profile in cerebral organoids.

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#184

What is/was recommended daily dosage?

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#186

Taurine: The Energy-Drink Amino Acid That Quiets Inflamed Blood Vessels — But Won’t Touch Your Blood Sugar

An 8-week Iranian randomized controlled trial gave 120 type 2 diabetics either 3 g/day of taurine or a starch placebo, both on top of a mild calorie-restricted diet. Taurine did not move the headline glycemic needles — fasting glucose, HbA1c, and lipids were statistically unchanged versus placebo — but it did significantly lower circulating insulin and insulin resistance (HOMA-IR), and produced consistent reductions across a panel of inflammation, oxidative-stress, and endothelial-adhesion markers (hs-CRP, TNF, MDA, ICAM-1, VCAM, E-selectin, MMP-9), while raising total antioxidant capacity. The authors frame this as the first clinical trial linking taurine to endothelial-dysfunction biomarkers in T2DM. The effect sizes are moderate, the study is short, and the biomarker data contain several internal inconsistencies that temper enthusiasm.

Taurine — the sulfur-containing amino acid best known as an energy-drink additive and a hot topic in aging research since a 2023 Science paper linked its decline to mammalian aging — has been put to a modest clinical test in people with type 2 diabetes. The result is a study of contrasts: taurine appears to calm the “vascular weather” of diabetes without meaningfully changing the disease’s defining feature, high blood sugar.

Researchers at Kermanshah University of Medical Sciences in Iran randomized 120 patients to 1 gram of taurine three times daily, or an identical-looking starch placebo, for eight weeks. Everyone also followed a 500-kcal/day deficit diet, meaning taurine’s effects sit on top of a background of gentle weight loss — a design choice that muddies interpretation, since caloric restriction alone improves most of these markers.

The clearest signal was in the endothelium, the single-cell lining of blood vessels that becomes dysfunctional early in diabetes and drives later heart attacks and strokes. Taurine reduced the “stickiness” molecules that let immune cells latch onto and inflame vessel walls — ICAM-1, VCAM, and E-selectin — alongside MMP-9, an enzyme that degrades vascular structure. Markers of oxidative stress (MDA) and inflammation (hs-CRP, TNF) fell, and antioxidant capacity rose. Taurine also cut circulating insulin and improved insulin resistance, suggesting the pancreas was working less hard.

Yet the metabolic story stops there. Fasting glucose, HbA1c, and every lipid fraction showed no significant advantage over placebo. The authors offer a reasonable defense for HbA1c — eight weeks is shorter than the ~120-day lifespan of a red blood cell, so the marker simply hadn’t had time to reflect any change. But the flat fasting glucose is harder to wave away and undercuts any claim that taurine is a glycemic agent.

The bigger picture is mechanistic plausibility meeting messy execution. Taurine’s biology — scavenging reactive oxygen species, neutralizing hypochlorous acid via taurine chloramine, supporting endothelial nitric oxide — makes vascular benefit believable. But this is a single, short, biomarker-only trial from one center, with no functional vascular endpoint (the authors admit they never measured flow-mediated dilation) and no clinical outcomes. It is a promising hypothesis-generator, not a practice-changer.

Actionable Insights (with effect-size magnitudes)

For a scientifically literate self-experimenter, the honest take-home is that **3 g/day taurine is a low-risk, low-cost vascular-and-inflammation intervention with moderate biomarker effects, but not a glucose-lowering tool.**Extracting standardized effect sizes (Cohen’s d, computed from end-of-study group means/SDs) puts the magnitudes in perspective:

  • hs-CRP reduction: d ≈ 0.67 (moderate) — arguably the most translationally meaningful, given CRP’s link to CV risk.
  • Serum insulin: d ≈ 0.64 (moderate).
  • TNF: d ≈ 0.57; ICAM-1: d ≈ 0.57 (moderate).
  • TAC (antioxidant capacity): d ≈ 0.45; HOMA-IR: d ≈ 0.41 (small-to-moderate).
  • MDA: d ≈ 0.36 (small).
  • Glycemic markers you might have hoped for: FBG d ≈ 0.37 but non-significant; HbA1c d ≈ 0.21 (trivial).

Practical framing: these are the magnitudes you’d expect from a supportive nutraceutical, not a drug. Taurine at this dose (well within the EFSA-cited safe ceiling of ~3000 mg/day) is a defensible adjunct if your goal is inflammation/endothelial support. It is not a substitute for anything moving your glucose. The vascular benefits are also confounded by concurrent calorie restriction, so real-world magnitude in a weight-stable person is likely smaller than these numbers.

Context / Source

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#187

Below is a study from 2024. It is a short-term study of four days, with low dose taurine, equivalent to 240 mg in humans. Footnotes 29 and 30, linked further below, tell a different story.

Assessing plaque vulnerability is crucial to preventing the harmful consequences of cardiovascular disease. Previous reports have shown that taurine may inhibit the rupture of atherosclerotic lesions.[29,30](javascript:void(0):wink: However, our study revealed that taurine treatment significantly reduced plaque stability in mice, which could increase the risk of plaque rupture. Supporting this, taurine treatment enhanced the expression of MMP-2 in vascular endothelial cells in vitro , which can reduce the collagen content in plaques. However, we did not find that taurine treatment significantly altered MMP-9 expression in vascular endothelial cells, expanding on previous reports that taurine inhibits MMP-9 activation in the glomerular basement membrane. Additionally, we only verified the mRNA transcripts, not the protein levels, of MMP-2 and MMP-9 in our experiment. As previous reports have shown, when plaques are unstable, protein levels of MMP-2 and MMP-9 are elevated.[31,32](javascript:void(0):wink: Since we have already confirmed that taurine increases plaque vulnerability, we hypothesize that the protein levels of MMP-2 and MMP-9 would also be upregulated after taurine treatment, though this has not yet been experimentally validated. Furthermore, long-term taurine treatment may stabilize artery plaques. In ApoE−/− mice fed a high-fat diet for 16 weeks, with 2% (w/v) taurine in drinking water for six weeks, taurine alleviated plaque vulnerability, as shown by quantification of the proportion of collagen, CD68, and α-actin.[28](javascript:void(0):wink: Therefore, we speculate that in the high-fat diet plus carotid artery ligation and cannula model used in our research, prolonging the taurine treatment period may reduce the risk of plaque rupture. This may be because the long-term taurine treatment lowers cholesterol levels.[33](javascript:void(0):wink: As cholesterol is the lipid core of plaques, reducing its levels may inhibit plaque growth. The fibrous cap on the plaque surface would then stop thinning, and the risk of plaque rupture would decrease.

Limitations

First, this study only explored the impact of short-term administration of taurine on atherosclerotic plaques. Long-term supplementation of taurine, which would better reflect the situation of people consuming energy drinks in daily life, is recommended in future studies. Second, oil red O staining is lack in our study as a direct evidence to determine the plaque area. [Footnote 29 quoted below, did O staining]

Third, carotid artery sections should display the longitudinal rather than the cross-sectional view of the blood vessel so that the size of the plaque and the thickness of the fibrous cap can be directly displayed and quantified. Forth, this study did not identify the targets and downstream pathways by which taurine reduces plaque area and stability.

There were ten (10) mice per arm in the mouse study. Dosage was low 50 mg/kg, equivalent to 240 mg in a 60 kg human.

The study’s footnote 29 says:

Similar to IMD (intermedin), taurine (Tau), a non-selective ERS inhibitor significantly reduced atherosclerotic lesion size and plaque vulnerability.

Similar to IMD, Tau significantly reduced lipid content and lesion area according to the quantification based on Oil Red O staining and H&E staining in the aortic root, as well as en face analysis (Supplementary Fig. 3). Moreover, Tau also significantly alleviated plaque vulnerability as shown by quantification of the size of necrotic cores, and collagen, VSMC, and macrophage contents (Supplementary Fig. 4).

The mice in the study in footnote 29 were given “high-fat diet plus taurine group (HF + Tau group): mice were fed a high-fat diet for 16 weeks, and 2% (w/v)Tau was added into drinking water for 6 weeks”

Plaque composition of lipid-rich cores, collagen, smooth muscle cell, and macrophage contents was analyzed by Oil red O staining, trichrome staining, immunofluorescence staining for α-SMA and CD68, respectively. The stainings were assessed and quantified blindly by two independent observers.

https://www.nature.com/articles/s41419-021-03712-w

Footnote 30

https://www.sciencedirect.com/science/article/abs/pii/S0306987704002877?via%3Dihub

Says the following:

Abstract

The rupture of atherosclerotic plaque, responsible for triggering the majority of myocardial infarctions, presumably requires proteolysis of collagen fibers and other protein components of the intercellular matrix. This is achieved by activated matrix metalloproteases (MMPs) secreted by intimal macrophages and foam cells. MMPs are synthesized as inactive pro-enzymes in which coordinate binding of the thiol group of a key cysteine residue to the active-site zinc atom blocks proteolytic activity. Physiological activation of MMPs is mediated, in large measure, by phagocyte-derived hypochlorous acid (HOCL), which can oxidize the zinc-bound thiol to sulfinic acid, thus freeing the active-site zinc. HOCL also encourages proteolysis of ground substance by inactivating proteins such as TIMP-1 that are physiological inhibitors of MMPs. In vivo, the unrestrained oxidant activity of HOCL is opposed by taurine, which reacts spontaneously with HOCL to generate taurine chloramine, much more stable than HOCL. Taurine chloramine has less impact than HOCL on MMP activation, and does not impair the activity of TIMP-1. Since tissue levels of taurine can be boosted via supplementation, taurine may thus have potential for stabilizing plaque and thereby warding off infarction – an effect that should be reinforced by taurine’s platelet-stabilizing activity. In light of recent epidemiological evidence that increased expression of myeloperoxidase - the enzyme which generates HOCL – is an important risk factor for coronary disease, supplemental taurine may indeed have broader utility for suppressing both the genesis and the rupture of atherosclerotic plaque.

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#188

Sorry if this is a repeat, but I’m sharing that Claude Fable found:

What the paper actually is — Biomedicine & Pharmacotherapy 2026 (Sciencedirect s0753332226004300), preprint Aug 2025. Lab and organoid, not human, not even mouse.

Taurine is a chemical cousin of tramiprosate, a drug that blocks ApoE4 clumping. The study shows taurine does the same in a test tube and in lab-grown brain tissue from ApoE4/E4 donors, nudging ApoE4 toward the safer ApoE3 behaviour.
• Concentrations: 100 µM in the organoid dish over 50 days; test-tube effects needed millimolar levels, roughly 10x higher. Normal human blood taurine is about 50–100 µM (from memory). So the dish dose is around normal blood levels — not a signal that more is better.
• The related mouse work (5XFAD, Sep 2025) used 1000 mg/kg — an absurd human equivalent, tens of grams a day. Not a dose guide.

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#189

10 characters needed

Incidentally it is the ellipsis.

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#190

I was doing some independent research of Taurine for my specific circumstances, reviewed this long thread with many links and incorporated them into my research. Then attempted to make a general guide on taurine and came up with the following:

Taurine: A Clinical Use Guide

What the evidence actually supports, what it doesn’t, and at what dose.

Evidence key: ★★★★ multiple RCTs/meta-analysis or regulatory approval · ★★★ consistent RCT signal, limited size or duration · ★★ preliminary (single trial or biomarkers only) · ★ mechanism/animal/observational only · ✗ not supported or refuted

What it is

A sulfonic β-amino acid — not proteinogenic. Concentrated in heart, retina, skeletal muscle, leukocytes, and brain. Acts as an osmolyte, membrane and calcium stabilizer, bile-acid conjugator, scavenger of hypochlorous acid (forming taurine chloramine), and an essential modifier of mitochondrial tRNA-Leu(UUR).

Humans synthesize it from cysteine (CDO/CSAD, B6-dependent), but synthesis is modest; most intake is dietary, from meat, fish, and shellfish. Plants contain essentially none — vegans run measurably lower plasma and much lower urinary taurine [1]. Absorption via TauT/SLC6A6 is efficient (>90%); renal reabsorption exceeds 95%.

Tier 1 — Strongest evidence

MELAS ★★★★ (highest impact)

The one true disease-modifying indication. The m.3243A>G mutation causes a taurine-modification defect in mitochondrial tRNA-Leu(UUR); taurine corrects it. In a 52-week open-label phase III trial, 9 g/day (<50 kg) or 12 g/day (≥50 kg) in three divided doses completely prevented stroke-like episodes in 6 of 10 patients and significantly cut annual relapse rates, with a measurable rise in tRNA taurine modification [2]. Approved for this use in Japan. Narrow indication, large effect — the opposite of everything else on this list.

Hypertension / prehypertension ★★★★

The best-supported general-population use. Meta-analyses converge on roughly −3 to −4 mmHg systolic and −1.5 to −2.5 mmHg diastolic at 1–6 g/day [3,4]. The cleanest single trial randomized 120 prehypertensives to 1.6 g/day for 12 weeks: clinic SBP fell 7.2 mmHg vs 2.6 on placebo, with improved endothelial function and a rise in plasma H₂S that tracked the BP change [5].

Effects are larger at higher baseline BP and mechanistically distinct from ARBs and calcium blockers (H₂S signaling, TRPC3 inhibition, aquaresis), so they appear additive. Modest but real, cheap, and safe.

Heart failure (adjunct) ★★★

Old but reproducible. A double-blind crossover trial in CHF improved NYHA class, pulmonary crackles, and chest film findings vs placebo — no patient worsened on taurine, four worsened on placebo [6]. A 2024 meta-analysis of 20 RCTs (n=808) found LVEF +4.98%, NYHA −0.40, HR −3.6 bpm [4]. Small trials, mostly 3 g/day, none powered for mortality. Reasonable adjunct, not a substitute for guideline therapy.

Metabolic syndrome, lipids, insulin resistance ★★★

25 RCTs, 1,024 participants, 0.5–6 g/day: triglycerides −18.3 mg/dL, total cholesterol −8.3, LDL −6.5, plus the BP effects above [3]. In overweight/obese adults, 3 g/day improved HbA1c (−0.37%) and fasting glucose (−7.1 mg/dL); lower doses did not [7]. Fasting insulin and HOMA-IR fall consistently.

Caveat: in type 2 diabetics, 3 g/day for 8 weeks moved insulin, HOMA-IR, and endothelial adhesion markers but left fasting glucose and HbA1c unchanged [8]. Treat it as a lipid/insulin-sensitivity and vascular agent, not a glucose-lowering drug. It does not reduce body weight or BMI [9].

Tier 2 — Moderate or narrow

Inflammation & oxidative stress markers ★★★ — Meta-analysis: CRP and MDA fall significantly; TNF-α and IL-6 do not. Largest effects around 8 weeks. Heterogeneity is high, so point estimates are soft [10]. Practical corollary: taurine lowers CRP, so it can obscure an inflammatory trend you’re trying to interpret.

Cirrhosis: cramps and portal pressure ★★★ — Two of the better-designed taurine trials in medicine. A crossover RCT at ≤2 g/day cut muscle cramps by 7 per fortnight and reduced severity [11]. A separate RCT at 6 g/day for 4 weeks lowered HVPG ~12%, with 58% achieving >10% response vs 0% placebo [12].

Exercise performance and soreness ★★ — Real but small. Endurance meta-analysis g ≈ 0.40 [13]. A 2025 meta-analysis of acute single doses across 23 trials: g ≈ 0.25, best ~1 h pre-exercise, no dose-response between 1 and 6 g — a threshold effect, not a ladder [14]. Anyone selling taurine as a muscle-building or lean-mass-preserving agent in humans is ahead of the data; that work is animal-only.

Vegetarian/vegan repletion ★★ — A genuine dietary-shortfall argument rather than a pharmacologic one: vegans show lower plasma taurine (≈45 vs 58 µmol/L) and roughly one-third the urinary excretion of omnivores [1]. No trial has shown correcting this changes a clinical outcome.

First-episode psychosis ★★ — One phase 2 double-blind RCT: 4 g/day for 12 weeks alongside low-dose antipsychotics improved BPRS, depression scores, and global functioning — but not cognition [15]. Never replicated.

Tier 3 — Claimed, poorly supported

Claim Grade Status
Slows aging / extends lifespan ✗/★ The 2023 Science paper extended mouse lifespan 10–12% and reported taurine falling with age [16]. Two 2025 papers dismantled the human premise: longitudinal cohorts (incl. BLSA) show circulating taurine does not decline with age and often rises, with within-person variation exceeding any age effect [17]; a second found no association with muscle mass, strength, performance, or mitochondrial function [18]. The mouse data stand; the human rationale does not.
Cognition, dementia, ApoE4 ★ In vitro/organoid work shows taurine inhibits ApoE4 aggregation, but oral taurine crosses into brain/CSF poorly and animal doses were ~1000 mg/kg. No human trial.
Sleep quality ★ Plausible via GABA-A/glycine receptors; essentially no human RCT. Glycine 3 g pre-bed has actual polysomnographic data — use that instead if sleep is the target.
Anxiety, depression, mood ★ Animal and mechanistic only.
NAFLD/MASLD, lowering ALT/AST ★ Consistent in rodents; no dedicated human RCT reporting transaminase outcomes. Human hepatic data are limited to cirrhosis and post-transplant settings.
Kidney protection ★ Review-level and preclinical. No outcome trials.
Tinnitus, epilepsy, retinal disease ★ Old, tiny, or animal studies. Retinal taurine depletion is real (vigabatrin, taurine-free formula), but that’s deficiency correction, not therapy.
Bone density, sarcopenia ★ Cell and rodent data only.
Hangover, “energy,” immunity ✗ Energy-drink effects belong to caffeine and sugar. Taurine alone is not a stimulant.
Weight loss ✗ Meta-analysis shows no effect on BMI or body weight [9].

Dosing & pharmacokinetics

  • General adult range: 1.5–3 g/day. Most positive BP and metabolic trials sit here; 3 g/day is where glycemic and lipid effects appear most reliably [7].
  • MELAS: 9–12 g/day in three divided doses with meals — a disease-specific dose, not a wellness dose [2].
  • No benefit ladder above ~3 g for BP, metabolic, or performance endpoints. Exercise data show a threshold, not dose-response [14].
  • Split dosing is rational: after a 4 g oral dose, peak plasma is ~1.5 h and half-life ~1 h, returning to baseline by 6–8 h [19]. Twice daily beats once daily.
  • Form: plain L-taurine powder or capsules. Powder costs pennies per gram. Choose USP/NSF or Informed Choice third-party tested, single-ingredient. Food timing is irrelevant.
  • Skip piperine “bioenhancers.” Taurine is already >90% absorbed, and piperine inhibits CYP3A4, P-glycoprotein, and UGT — a real interaction risk with calcium blockers, PDE5 inhibitors, statins, and many others.
  • Blood taurine testing is not useful. Within-person variability swamps the signal and no validated benchmarks exist for guiding supplementation [17].

Safety

Among the better-characterized supplements. A formal risk assessment of 30 controlled trials (245 supplemented subjects) set an Observed Safe Level of 3 g/day, the highest RCT dose being 10 g/day for 6 months without significant adverse effects [20]. EFSA separately places the observed safe level at 6 g/day [21]. These two figures are frequently conflated; both are real and come from different bodies. GI upset is the main dose-dependent complaint, uncommon below 6 g.

Cautions worth naming:

  • Additive hypotension. Stacked on antihypertensives, PDE5 inhibitors, or SGLT2 inhibitors, watch for orthostasis. Taurine is also aquaretic — it promoted diuresis in nonagenarians without causing hypotension or significant sodium loss, apparently by suppressing vasopressin [22].
  • Leukemia niche signal. A 2025 Nature paper showed AML and blast-crisis CML stem cells import bone-marrow taurine via SLC6A6 to fuel glycolysis [23]. Entirely preclinical, marrow taurine is locally synthesized, and there is no human link between taurine intake and hematologic cancer. Reasonable to be conservative with gram-level dosing if there’s known clonal hematopoiesis or a personal history of myeloid malignancy; otherwise not actionable.
  • Plaque stability. One short-term mouse study reported reduced plaque stability; it contradicts stronger prior animal work and has no human correlate. Human CV meta-analyses show benefit.
  • Marker masking. Because taurine lowers CRP and is hepatoprotective, hold it during an active workup of unexplained transaminase elevation or inflammation so the trend stays interpretable.

Bottom line

Worth taking for MELAS (disease-modifying, 9–12 g/day), and as a cheap, safe adjunct for elevated blood pressure, dyslipidemia with insulin resistance, or heart failure — 1.5–3 g/day split twice daily.

Defensible as dietary replacement on a plant-based diet, and for cramps or portal hypertension in cirrhosis.

Not worth taking for longevity, sleep, cognition, weight loss, or energy.

Expect a few mmHg and a modest lipid shift, not a transformation.

References
  1. Laidlaw et al. Plasma and urine taurine levels in vegans. Am J Clin Nutr 1988;47:660–3.
  2. Ohsawa et al. J Neurol Neurosurg Psychiatry 2019;90:529–36. pubmed.ncbi.nlm.nih.gov
  3. Tzang et al. Nutr Diabetes 2024. Taurine reduces the risk for metabolic syndrome: a systematic review and meta-analysis of randomized controlled trials | Nutrition & Diabetes
  4. Tzang et al. Nutr J 2024. pubmed.ncbi.nlm.nih.gov
  5. Sun et al. Hypertension 2016;67:541–9. pubmed.ncbi.nlm.nih.gov
  6. Azuma et al. Clin Cardiol 1985;8:276–82. pubmed.ncbi.nlm.nih.gov
  7. Sun Q et al. Nutrients 2024. https://doi.org/10.3390/nu17010055
  8. Moludi et al. Nutr Metab 2022. Protective and therapeutic effectiveness of taurine supplementation plus low calorie diet on metabolic parameters and endothelial markers in patients with diabetes mellitus: a randomized, clinical trial | Nutrition & Metabolism | Springer Nature Link
  9. Guan & Miao. Eur J Pharmacol 2020. pubmed.ncbi.nlm.nih.gov
  10. Faghfouri et al. Eur J Clin Nutr 2021. Profiling inflammatory and oxidative stress biomarkers following taurine supplementation: a systematic review and dose-response meta-analysis of controlled trials | European Journal of Clinical Nutrition
  11. Vidot et al. Aliment Pharmacol Ther 2018. https://doi.org/10.1111/apt.14950
  12. Schwarzer et al. Aliment Pharmacol Ther 2018. pubmed.ncbi.nlm.nih.gov
  13. Waldron et al. Sports Med 2018;48:1247–53. pubmed.ncbi.nlm.nih.gov
  14. Deng et al. Scand J Med Sci Sports 2025. pubmed.ncbi.nlm.nih.gov
  15. O’Donnell et al. J Clin Psychiatry 2016. pubmed.ncbi.nlm.nih.gov
  16. Singh et al. Science 2023. https://doi.org/10.1126/science.abn9257
  17. Fernandez et al. Science 2025. https://doi.org/10.1126/science.adl2116
  18. Marcangeli et al. Aging Cell 2025. https://doi.org/10.1111/acel.70191
  19. Ghandforoush-Sattari et al. J Amino Acids 2010. pubmed.ncbi.nlm.nih.gov
  20. Shao & Hathcock. Regul Toxicol Pharmacol 2008. pubmed.ncbi.nlm.nih.gov
  21. EFSA FEEDAP Panel 2012. https://www.efsa.europa.eu/en/efsajournal/pub/2736
  22. Miyamoto et al. J Am Geriatr Soc 2011. https://doi.org/10.1111/j.1532-5415.2010.03207.x
  23. Sharma et al. Nature 2025;644:263–72. pubmed.ncbi.nlm.nih.gov

Evidence current as of September 2026. Informational synthesis, not medical advice.

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#191

My initial question was whether to increase dose from 1g to 3g. Vegetarian with BP controlled by Telmisartan (80mg) and Amlodipine (2.5mg) along with a couple other supplements if questionable efficacy. Will be increasing my dose to 3g total per day, 1g AM and 2g PM (hour before bed).

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