From what I know, people take from 1 to 6g.
I chose 6g based on being vegan and knowing I was probably deficient… and hoping it would give me Agetron bone results… which it didn’t.
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Your bone scan results intrigue me.
I have also been taking a teaspoon of taurine in my coffee every morning for about 3 years. Never had a bone scan before, though. I need to book one in to see what’s going on.
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Yes…I’d say its about 15 grams.
So cheap… why not go with a big dose
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Ahhhhh, so when you say teaspoon, you don’t mean an actual tsp… you mean silverware tsp… I was wondering why you were taking such a tiny dose…. 1/2 a tablespoon (a measuring spoon) is 6g (it might vary slightly from brand to brand based on how fluffy) .
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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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Yes, I use a normal silverware sized spoon. Not a soup spoon.
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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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I see.
I use bulk supplements powder from Amazon. Lasts a long time and cheap.
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I just got a bulk pack in (1kg/2.2lbs) from amazon. you’re right, it is inexpensive.
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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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Whether taurine declines with age is irrelevant. The question is whether supplementing taurine provides any benefit
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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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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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Edema can also be a side effect of Rapamycin.
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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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My mother also has gastrointestinal issues with Taurine. It is a thing.
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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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What is/was recommended daily dosage?
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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
- Open Access Paper: 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, 2022 Jul 23.
- Institution / Country: Kermanshah University of Medical Sciences, Iran (with co-authors from Iraqi institutions and Tabriz University of Medical Sciences).
- Journal: Nutrition & Metabolism (BMC / Springer Nature).
- Impact Evaluation: The impact score of this journal is approximately 4.0 (Clarivate JIF ~3.9; Scopus-derived metric 4.35; SJR 1.243, Q1–Q2), evaluated against a typical high-end range of 0–60+ for top general science, therefore this is a Medium impact journal.
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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)
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)
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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