# Taurine

Rating: Early — Mostly animal or cell studies; few or uncontrolled human data
Type: Compound
Updated: 2026-10-15
Canonical: https://heretic.bio/articles/taurine-the-aging-amino-acid.html

> Taurine is one of the body's most abundant free amino acids. A 2023 Science paper showed supplementation extends mouse lifespan 10-12% and improves healthspan in monkeys, but two 2025 studies overturned its core premise: blood taurine does not reliably decline with age. Human randomized trials show modest but real cardiometabolic benefits on blood pressure, glucose and lipids, and the dedicated TauAge aging trial finished primary completion in November 2025 with results pending.

> **Core thesis:** Taurine levels decline by ~80% with age across multiple species. Restoring youthful taurine levels extends lifespan in mice (10-12%), improves healthspan markers in monkeys, and associates with better health outcomes in humans. A 2023 _Science_ paper positioned taurine deficiency as a _driver_ of aging — not merely a correlate. Human clinical trials are now completing.  
  
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## What Is Taurine?

Taurine (2-aminoethanesulfonic acid) is an amino sulfonic acid — technically not used in protein synthesis, but one of the most abundant free amino acids in the body. It concentrates in **brain, retina, heart, muscle, and leukocytes**.

**Key physiological roles:** \- **Osmoregulation** — Maintains cell volume and hydration status \- **Membrane stabilization** — Modulates ion channels (Ca²⁺, Cl⁻, Na⁺) \- **Mitochondrial function** — Conjugates bile acids; regulates mitochondrial tRNA translation; protects against oxidative stress \- **Neurotransmission** — Acts as an inhibitory neuromodulator (GABA_A and glycine receptor agonist) \- **Calcium homeostasis** — Regulates intracellular Ca²⁺ flux

**Dietary sources:** Shellfish (mussels, scallops), dark meat poultry, beef, pork, seaweed. Not present in significant quantities in plant foods — vegans/vegetarians have significantly lower taurine levels.

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## The Singh et al. 2023 Landmark Study

### Taurine Deficiency as a Driver of Aging

The foundational paper: **Singh P, et al. "Taurine deficiency as a driver of aging."_Science_. 2023;380(6649):eabn9257.** PMID: [37262123](https://pubmed.ncbi.nlm.nih.gov/37262123/)

This study systematically demonstrated that taurine is not just a marker of aging but a causal factor:

### Key Finding 1: Age-Related Decline

Blood taurine concentrations decline dramatically with age: \- **Mice:** ~80% decrease from youth to old age \- **Monkeys:** ~85% decrease \- **Humans:** Serum taurine levels drop steadily — 60-year-olds have ~80% less than children

### Key Finding 2: Lifespan Extension in Mice

Intervention | Median Lifespan Increase | Absolute Benefit  
---|---|---  
Taurine supplementation (14-month-old mice) | **10-12%** | 3-4 extra months (~7-8 human years)  
Female mice | +12% | Greater effect than males  
Male mice | +10% | Significant  
  
### Key Finding 3: Healthspan Improvements in Mice

Taurine-supplemented mice (middle-age to old) showed: \- ↑ Bone mass and density \- ↑ Muscle endurance and strength \- ↑ Energy expenditure \- ↑ Immune system youthfulness \- ↓ Insulin resistance \- ↓ Age-associated weight gain \- ↓ Depression-like and anxious behaviors \- ↓ Cellular senescence markers \- ↓ DNA damage \- ↓ Mitochondrial dysfunction \- ↓ Telomerase deficiency effects

### Key Finding 4: Healthspan in Non-Human Primates

In cynomolgus monkeys (15-year-old, equivalent to ~45 human years), taurine supplementation for 6 months: \- ↑ Bone density (femur, tibia) \- ↑ Immune function (T-cell profiles) \- ↓ Oxidative stress markers \- ↓ Fasting glucose and insulin resistance markers \- ↑ Bone mineral content

### Key Finding 5: Human Epidemiological Associations

Analysis of 12,000+ participants across epidemiological cohorts: \- **Higher taurine levels** associated with ↓ type 2 diabetes prevalence \- **Higher taurine levels** associated with ↓ obesity \- **Higher taurine levels** associated with ↓ hypertension \- **Higher taurine levels** associated with ↓ inflammation \- **Exercise** acutely raises taurine levels — taurine may mediate some exercise benefits

### Mechanisms of Anti-Aging Action

Mechanism | Detail  
---|---  
**Reduced cellular senescence** | ↓ p16, p21 markers; see [Senolytics](senolytics.html)  
**Mitochondrial protection** | Preserves mitochondrial tRNA translation; ↓ ROS  
**Telomere maintenance** | Protects against telomerase deficiency–induced aging  
**Reduced DNA damage** | ↓ γH2AX foci; ↓ oxidative DNA damage  
**Reduced SASP/inflammation** | ↓ IL-6, TNF-α, other pro-inflammatory cytokines  
**Calcium signaling restoration** | Age-disrupted Ca²⁺ homeostasis normalized  
**Autophagy enhancement** | Promotes clearance of damaged proteins/organelles → see [Autophagy](autophagy.html)  
  
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## Human Clinical Evidence

### Completed RCTs

Trial | Population | Dose | Duration | Key Findings | PMID/Ref  
---|---|---|---|---|---  
**Meta-analysis: taurine on CV risk** | 29 RCTs, N=1,625 | Various | Various | ↓ Systolic BP (−3.8 mmHg), ↓ Diastolic BP (−2.0 mmHg); no effect on heart rate | [Waldman et al., 2023](https://pubmed.ncbi.nlm.nih.gov/36999619/)  
**Taurine + exercise** | Older women | 1.5 g/day | 14 weeks | ↑ Muscle strength, ↓ oxidative stress | Multiple  
**Taurine in metabolic syndrome** | Adults w/ MetS | 3 g/day | 8 weeks | ↓ Fasting glucose, ↓ HbA1c, ↓ triglycerides, ↓ atherogenic index | [PMID: 22583377](https://pubmed.ncbi.nlm.nih.gov/22583377/)  
**Taurine in type 2 diabetes** | T2DM patients | 3 g/day | 8 weeks | ↓ HbA1c, ↓ HOMA-IR, ↓ hs-CRP | [PMID: 33314884](https://pubmed.ncbi.nlm.nih.gov/33314884/)  
  
### Ongoing Clinical Trials

Trial | Registration | Population | Intervention | Status  
---|---|---|---|---  
**Taurine & biological aging** | [NCT06613542](https://clinicaltrials.gov/study/NCT06613542) | Healthy adults 55-75 | 4 g/day taurine × 6 months vs placebo | **Primary completion: Nov 2025** — results pending  
**Taurine & exercise in aging** | Multiple sites | Older adults | Taurine + resistance training | Ongoing  
  
> **The[NCT06613542](https://clinicaltrials.gov/study/NCT06613542) trial is critical.** This is the first RCT specifically designed to test taurine's effect on biological aging (epigenetic clocks, DNA methylation), physical fitness, and metabolic health in healthy older adults. Results were expected in late 2025 / early 2026 and will be the definitive test of taurine's human anti-aging potential.

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## Doses in studies

### Absorption & Pharmacokinetics

  * **Oral bioavailability:** Good — rapidly absorbed (peak serum in 1-2 hours)
  * **Half-life:** ~1 hour in plasma (but tissue accumulation occurs with chronic dosing)
  * **Steady state:** Achieved in 2-4 weeks of daily supplementation
  * **Excretion:** Renal — urine



### Safety Profile

Taurine has an **exceptionally strong safety record** : \- **EFSA:** No Observed Adverse Effect Level (NOAEL) of 3 g/day in human studies; Acceptable Daily Intake proposed at 6 g/day \- **Common side effects** (rare, mild): GI upset at high doses (>6 g) \- **No reported serious adverse events** in clinical trials at doses up to 6 g/day \- **Note:** Energy drinks contain taurine (typically 1-2 g per can), but adverse events associated with energy drinks are driven by caffeine and sugar content, not taurine itself

### Contraindications

  * **Bipolar disorder** — theoretical concern (taurine is neuroinhibitory; case report of mania exacerbation)
  * **Kidney disease** — reduced renal clearance may require dose adjustment
  * **Lithium therapy** — potential interaction (both affect renal function)



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## Combinations Discussed in the Literature

Comparison | Taurine | NAD+ Precursors | Rapamycin  
---|---|---|---  
**Mechanism** | Multi-target (mitochondria, senescence, Ca²⁺) | Sirtuin activation, DNA repair | mTOR inhibition  
**Lifespan in mice** | +10-12% | +5-10% | +14-26% (female)  
**Human RCT evidence** | CV/metabolic benefits; aging trial pending | Mixed; NAD+ market in crisis | PEARL trial; limited  
**Safety** | Excellent | Generally good | Immunosuppression risk  
**Cost** | Very low ($5-10/month) | Moderate | Moderate (generic)  
**Accessibility** | OTC, widely available | OTC | Prescription  
  
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## Critical Analysis

### Strengths of the Evidence

  1. **Causal data in mammals** — The Singh study demonstrated causation (supplementation → lifespan), not just correlation
  2. **Multi-species consistency** — Worms, mice, monkeys, and human epidemiology all align
  3. **Mechanistic plausibility** — Multiple aging hallmarks addressed simultaneously
  4. **Exceptional safety profile** — Among the safest candidate longevity interventions
  5. **Low cost and high accessibility** — Minimal barrier to adoption



### Limitations

  1. **No completed human lifespan/healthspan trial** — TauAge and TOP are the first direct intervention tests; as of August 2026, neither has posted results
  2. **The biomarker premise is broken** — de Cabo et al. _Science_ 2025 directly refutes the "circulating taurine falls ~80% with age" claim; any remaining human-benefit signal must come from the intervention, not from deficiency correction
  3. **Confounding in epidemiology** — Higher taurine levels correlate with meat consumption, exercise, and overall dietary quality — residual confounding is likely; biomarker ↔ age correlation no longer holds
  4. **Population specificity** — Vegans/vegetarians are biologically lower (synthesis only), but the post-2025 framework has not tested whether this translates to a supplement-response advantage
  5. **Young field, fast-moving** — Singh 2023 → de Cabo 2025 was a 2-year reversal in _Science_ ; replication of the lifespan finding is the highest-value next step



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## Critical Update: June 2025 — de Cabo et al. (NIH/NIA) Refute the Biomarker Premise

The Singh 2023 paper rested on a single empirical claim: **taurine levels fall ~80% with age, and this decline drives aging**. A 2025 _Science_ study from NIH/NIA directly tests that premise and largely overturns it.

**Citation:** de Cabo R, Fernandez ME, Ferrucci L, et al. "Is taurine an aging biomarker?" _Science_. 2025 Jun 5. [DOI: 10.1126/science.adl2116](https://www.science.org/doi/10.1126/science.adl2116)

### What they did

  * Longitudinal plasma taurine in **Baltimore Longitudinal Study of Aging (BLSA)** participants aged 26–100 (humans)
  * Longitudinal serum in **rhesus monkeys** aged 3–32 years
  * C57BL/6J mice aged 9–27 months (Study of Longitudinal Aging in Mice, SLAM)
  * Cross-sectional replication: Balearic Islands Study of Aging (n=20–85), Predictive Medicine Research cohort (Atlanta, n=20–68), cross-sectional arm of SLAM



### What they found

Finding | Result | Implication  
---|---|---  
Human taurine vs age | **Increased with age** (sex-specific) | Contradicts Singh's ~80% decline  
Monkey taurine vs age | Increased with age | Contradicts Singh's ~85% decline  
Mouse taurine vs age | Increased (female) / unchanged (male) | Contradicts Singh's ~80% decline  
Within-person variability | Often _exceeded_ age-related change | Single blood draw = unreliable biomarker  
Taurine vs muscle/weight | Inconsistent across cohorts, species, ages | Loose "functional aging" coupling at best  
  
### How this changes the picture

  * The headline Singh 2023 mechanism (restore youthful taurine → slow aging) **assumes a deficiency state**. If circulating taurine does not decline with age, the dosing rationale resembles _hormesis_ (pharmacological signal in an already-adequate pool) rather than _replacement_.
  * It does **not** falsify Singh's causal mouse lifespan data (high-dose supplementation did extend life). But it shifts the burden: any human benefit must be shown by direct intervention, not by biomarker correction.
  * It also reframes the TauAge, TOP, and other trials as **purely intervention tests of pharmacological taurine signaling** rather than deficiency-replacement studies.



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## Newly Identified Mechanism (2025): Taurine Restrains Inflammaging via NLRP3 Inactivation

**Citation:** Guan C, Ryu S, Dong M, Youm YH, Mohanty S, Maeda R, et al. "Hormetic elevation of taurine restrains inflammaging by deactivating the NLRP3 inflammasome." 2025. PMID: [40501605](https://pubmed.ncbi.nlm.nih.gov/40501605/) (preprint: [bioRxiv 2025.05.27.656381](https://www.biorxiv.org/content/10.1101/2025.05.27.656381v1))

This Yale/Buck-aligned group demonstrated that taurine is an **upstream metabolic sensor of cellular perturbations** that control NLRP3 inflammasome activation. Key findings:

  * Taurine acts in a **hormetic dose-response** — low/normal physiological pools buffer stress; pharmacological elevation switches the NLRP3 inflammasome off
  * Reduces age-related **IL-1β, IL-18** release (the canonical NLRP3 outputs)
  * Provides a mechanistic explanation for why taurine lowers hsCRP, IL-6, TNF-α in human RCTs (Maleki 2020, multiple others)
  * Frames NLRP3 as one of the specific molecular targets taurine uses to act on the **inflammaging** hallmark of aging



This complements the Singh 2027 mechanistic package (mitochondrial tRNA translation, ER stress, etc.) with a discrete, druggable inflammasome target.

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## Updated Meta-Analyses (2024–2025)

### Tzang et al. 2024 — Cardiovascular Trial-Level Meta-Analysis

Tzang CC, Lin WC, Lin LH, et al. _Nutr J_. 2024;23:93. PMID: [39148075](https://pubmed.ncbi.nlm.nih.gov/39148075/) · PMC: [PMC11325608](https://pmc.ncbi.nlm.nih.gov/articles/PMC11325608/)

  * Search to 2 Jan 2024, multiple databases, PRISMA-2020 compliant
  * Primary outcomes: HR, SBP, DBP, LVEF, NYHA class
  * **Taurine significantly reduced HR, SBP, DBP, and NYHA class; improved LVEF**
  * **Dose-dependent relationship** : lower HR and DBP with higher total taurine dose (meta-regression)
  * Updated and larger than the older Waldman 2023 analysis (PMID [36999619](https://pubmed.ncbi.nlm.nih.gov/36999619/))



### Nie et al. 2025 — Cardiometabolic Risk Factors

Nie Z, Liu Y, Zhang M, et al. "Effects of Oral Taurine Supplementation on Cardiometabolic Risk Factors: A Meta-analysis and Systematic Review of Randomized Clinical Trials." _Nutrition Reviews_. 2025;nuaf220. [DOI: 10.1093/nutrit/nuaf220](https://academic.oup.com/nutritionreviews/advance-article-abstract/doi/10.1093/nutrit/nuaf220/8340615)

  * PROSPERO CRD42024577852
  * **≥8 weeks** for glucose/lipid effects; **< 8 weeks** sufficient for blood pressure and inflammation
  * Significant reductions in fasting glucose, HOMA-IR, triglycerides, MDA; increases in HDL and TAC



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## New / Updated Human Trials (2025–2026)

### Doses in studies

**Citation:** Chu MH, Lai JK, Lee A, Wu WK, Huang Z, Wong HM, et al. "Effects of taurine supplementation on metabolic health and biological aging in healthcare workers: A protocol for a triple-blinded, Bayesian-optimized phase II randomized controlled trial." _PLOS ONE_. 2026;21(5):e0350389. DOI: [10.1371/journal.pone.0350389](https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0350389)

  * Registration: ChiCTR2500102879 (Chinese Clinical Trial Registry)
  * Design: stratified, parallel-arm, triple-blinded Phase II, Bayesian-optimized (BOP2)
  * Arms: 3 g/day vs placebo, 6 months
  * Primary endpoint: **HbA1c reduction** at 6 months
  * Secondary endpoints: LDL-C, triglycerides, BP, biological age (validated epigenetic/clinical clocks), AGE accumulation (skin autofluorescence: SAF-age)
  * Pre-specified interim analyses allow futility/superiority stopping (Type I error controlled)
  * Population: adult healthcare workers (occupational-health rationale)



This trial tests **whether the animal/NHANES-style benefits translate into a hard clinical endpoint** (HbA1c) within the gold-standard design space.

### TauAge ([NCT06613542](https://clinicaltrials.gov/study/NCT06613542)) — Updated Trial Architecture

  * Sponsor: Technical University of Munich (Karolina Starzynska, responsible party)
  * Design: RCT, parallel, quadruple-blinded
  * Arms: **4 g/day** vs placebo, 6 months
  * **Three primary objectives** (the trial is unusually rigorous): 1\. Plasma **proteomic** organismal and organ-age clock change 2\. **DNA methylation** epigenetic clock change 3\. Acute and chronic taurine/metabolome changes in plasma and urine
  * Deep phenotyping: blood, stool, urine; physical + cognitive function; lifestyle
  * Funding: DFG project 574580611
  * Enrollment: 91 men and women aged 55–75



TauAge is the **causal-test trial** — if proteomic and epigenetic biological-age clocks both shift in the taurine arm, that is the first intervention-grade evidence in humans. Until those numbers post, the field is in a holding pattern.

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## Updated Critical Analysis (2026)

### What survived the 2025 NIH challenge

  1. **Causal mouse lifespan data** (Singh 2023) — the supplementation-without-deficiency still works; high-dose taurine extends life in rodents.
  2. **Cardiometabolic RCT effects** — modest but real (Tzang 2024, Nie 2025) for HR, BP, lipids, glucose.
  3. **NLRP3 mechanism** — there is a coherent molecular target (Guan 2025).
  4. **Safety profile** — unchanged; exceptional across all doses tested.



### What no longer holds

  1. **Blood taurine as a biomarker of aging** — explicitly refuted by de Cabo 2025 (Science)
  2. **Vegans / elderly are "deficient"** — partially undermined; supplementation is now best framed as **hormetic signaling** , not replacement therapy
  3. **The 80% decline narrative** in marketing materials — directly contradicted by NIA's three-species longitudinal data



### Open questions for 2026–2027

  * Will any trial enroll beyond 6 months? (Hormetic mechanisms raise the question of **duration-of-effect vs. washout**.)



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## Independent Refutation (2025): Marcangeli Aging Cell

A second, independent refutation of the "taurine-deficiency-drives-aging" thesis appeared August 2025 from a Canadian group (UQAM/McGill), strengthening the de Cabo NIH/NIA conclusion.

**Citation:** Marcangeli V, Cefis M, Hammad R, Granet J, Leduc-Gaudet J-P, Gaudreau P, Aubertin-Leheudre M, Bélanger M, Robitaille R, Morais JA, Gouspillou G. "Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans." _Aging Cell_. 2025 Aug 11;24(10):e70191. PMID: [41061678](https://pubmed.ncbi.nlm.nih.gov/41061678/) · PMCID: [PMC12507425](https://pmc.ncbi.nlm.nih.gov/articles/PMC12507425/) · DOI: [10.1111/acel.70191](https://doi.org/10.1111/acel.70191)

### Design

  * Cross-sectional + functional assessment, **137 men aged 20–93** , stratified by physical-activity status (SenseWear Mini Armband accelerometer + PASE interview)
  * DXA whole-body lean/fat mass; pQCT thigh cross-sectional area; grip strength; gait speed; 6-min walk; mitochondrial respiration (permeabilized fibers)
  * Fasting serum taurine measured by standard clinical chemistry



### Findings (clean null result)

  * **No association** between circulating taurine and **chronological age** in the full cohort (R² ≈ 0; p > 0.05)
  * **No association** between circulating taurine and lean mass, grip strength, thigh CSA, gait speed, 6-min walk distance
  * **No association** between circulating taurine and mitochondrial respiratory states (complex I, complex I+II, leak, ETS capacity) in permeabilized muscle fibers
  * Active and inactive subgroups showed identical null patterns
  * Authors conclude: taurine deficiency is **unlikely to be a primary driver of aging in humans** — directly concordant with de Cabo et al. _Science_ 2025.



### Why this matters beyond de Cabo

de Cabo 2025 was a cross-sectional biomarker study; Marcangeli 2025 added **functional and mitochondrial endpoints** and used activity stratification to address the "exercise confound" (exercise raises taurine, exercise extends healthspan — could the Singh cross-species decline be an exercise-decline artifact?). The Marcangeli data say **no** : even after stratifying, the null holds. The biomarker premise is now refuted on two independent cohorts with two independent endpoint families.

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## Taurine as Part of Multi-Amino-Age Biological Clocks (2026)

Counterpoint to the "taurine is not informative" line: taurine is now embedded in modern biological-age clocks, suggesting it carries **state-dependent** (not chronological) aging information.

**Citation:** "Amino acid-based biological age clock and its implications for human health and aging." _Nature Communications_. 2026;17:6733. DOI: [10.1038/s41467-026-73371-y](https://www.nature.com/articles/s41467-026-73371-y)

### AmiAge architecture

  * Random Forest regressor trained on **18 amino acids** in plasma across 11,000+ in-house samples and 270,000+ public samples, ages 1–89
  * Strong correlation between AmiAge Gap (biological − chronological) and: frailty index, telomere length, age-related disease incidence, all-cause mortality
  * Distilled to an **8-amino-acid clinical panel** : alanine, glutamine, glycine, histidine, leucine, phenylalanine, tyrosine, valine



### Where taurine fits

  * Taurine is **one of the 18 input features** in the full AmiAge model and contributes measurable regression weight in the gap-prediction branch
  * In the distilled 8-AA panel taurine drops out — suggesting taurine's aging signal is **redundant with the BCAAs and other large-neutral amino acids** at the population level
  * **Interpretation:** taurine is not a _primary_ aging biomarker (consistent with de Cabo + Marcangeli), but taurine is one of several correlated amino-acid features that **collectively** track biological age. The failure of the _single-marker_ hypothesis does not mean taurine is uninvolved in aging biology — it means a **panel approach** captures more variance.



### Practical implication

  * Self-tracking enthusiasts should not monitor serum taurine as a personal aging metric (high within-person noise, no cross-sectional signal in two independent cohorts)
  * An amino-acid panel (AmiAge-style) may be more informative than any single amino acid, but commercial availability is limited to research-grade metabolomics
  * Trials like TOP that combine taurine supplementation with **SAF-age** (skin autofluorescence AGE accumulation) and validated epigenetic clocks are testing exactly this panel-vs-single-marker question



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## Sources

1. Singh P, et al. "Taurine deficiency as a driver of aging." Science . 2023;380(6649):eabn9257. PMID: 37262123 (PubMed 37262123)
2. Waldman W, et al. "The effect of taurine on cardiovascular risk factors: a systematic review and meta-analysis." 2023. PMID: 36999619 (PubMed 36999619)
3. PubMed 22583377 (PubMed 22583377)
4. Maleki V, et al. "Taurine supplementation improves glycemic and lipid profiles, and reduces inflammation in adults with metabolic syndrome." 2020. PMID: 33314884 (PubMed 33314884)
5. NCT06613542 (TauAge). Technical University of Munich; Starzynska KA responsible party; DFG 574580611 funding. Last update 2025-11-21. ClinicalTrials.gov (NCT06613542)
6. de Cabo R, Fernandez ME, Ferrucci L, et al. "Is taurine an aging biomarker?" Science . 2025 Jun 5. DOI: 10.1126/science.adl2116 — NIH/NIA longitudinal BLSA/SLAM/rhesus refutation of the Singh 2023 "80% decline" premise. (DOI 10.1126/science.adl2116)
7. Guan C, Ryu S, Dong M, et al. "Hormetic elevation of taurine restrains inflammaging by deactivating the NLRP3 inflammasome." 2025. PMID: 40501605 — preprint at bioRxiv 2025.05.27.656381 (PubMed 40501605)
8. Tzang CC, Lin WC, Lin LH, et al. "Insights into the cardiovascular benefits of taurine: a systematic review and meta-analysis." Nutr J . 2024;23:93. PMID: 39148075 · PMCID: PMC11325608 (PubMed 39148075, PMC11325608)
9. Nie Z, Liu Y, Zhang M, et al. "Effects of Oral Taurine Supplementation on Cardiometabolic Risk Factors: A Meta-analysis and Systematic Review of Randomized Clinical Trials." Nutrition Reviews . 2025;nuaf220. DOI: 10.1093/nutrit/nuaf220 (DOI 10.1093/nutrit/nuaf220)
10. Marcangeli V, Cefis M, Hammad R, et al. "Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans." Aging Cell . 2025;24(10):e70191. PMID: 41061678 · PMCID: PMC12507425 — Independent UQAM/McGill refutation with functional + mitochondrial endpoints; n=137 men, ages 20–93. (PubMed 41061678, PMC12507425)
11. DOI 10.1111/acel.70191 (DOI 10.1111/acel.70191)
12. Vu TT, et al. "Taurine as a possible therapy for immunosenescence and inflammaging." Int J Mol Sci . 2023. PMC: PMC10757708 (PMC10757708)