Genes for higher blood tyrosine went with shorter lives. Supplements weren't studied.
A UK Biobank study found that people whose genes nudge up their blood tyrosine had parents who died somewhat sooner: about eight months per step up in tyrosine, for fathers and mothers alike. The robustness checks were mixed, the "men only" result depends on one statistical choice, and nobody in the study took a tyrosine pill.
8 October 2026 · How we rate evidence
- Claim
- Finding (Early, close to Speculative): In a genetic analysis, participants whose gene variants predict higher blood tyrosine had fathers who died younger: about 0.8 years earlier per standard deviation of tyrosine after allowing for phenylalanine (range 0.2 to 1.4 years; mothers 0.6). The years are calculated from hazard ratios, not observed. In the simpler analysis without that allowance (fathers 0.68 years), two of three robustness methods found no clear effect. Close to Speculative because the variants include some in genes with many jobs (one travels with APOE4, a major lifespan variant), and the paper screened them only against lifestyle traits.
Men vs women (Early): The paper says the effect was in men "but not in women." Its main genetic estimates were the same size in fathers and mothers (0.68 and 0.67 years per step), and the difference between the sexes was never shown to be clear of chance.
Blood levels and death (Early): Among 125,359 men followed from 2006-2010 to late 2022, each standard deviation higher tyrosine in a single blood sample went with a 3% higher death rate (relative), roughly 3 more deaths per 1,000 men over the period (our arithmetic). No clear link in women, though the difference between the sexes wasn't clear of chance (p = 0.16).
Popular claim (Overstated): "Popular brain supplement linked to shorter lifespan in men" and "higher tyrosine could shorten male lifespan by nearly one year" (ScienceDaily, 6 Sep 2026, reprinting the release from the journal's publisher, Impact Journals). Labroots: "higher levels of common, over-the-counter supplement tyrosine may shorten lifespan in men" - Studied in
- People: 272,475 UK Biobank participants aged 40 to 69 at recruitment, mostly of European ancestry, 23,964 of whom died during follow-up; the genetic analysis used the lifespans of their parents (about 389,000 to 415,000 participants reporting)
- Design
- Cohort study plus Mendelian randomization (gene variants used as a natural experiment), all in UK Biobank. Tyrosine instruments: 74 variants overall, 45 for men, 29 for women. Lifespan effects are calculated from parental survival statistics with a standard conversion. Not preregistered
- Status
- Peer-reviewed, Aging 17(10):2500-2533, published online 3 October 2025
- Replicated
- No. A check using genetic data from outside UK Biobank was inconclusive (main-method ranges spanning about two years either way). We found no independent study of tyrosine and lifespan using genetics, and no trial of supplements and survival
- Funding
- US National Institutes of Health (NIGMS) and the Hong Kong government's InnoHK initiative. The authors declare no conflicts of interest
- We read
- Full paper (free via PubMed Central, CC BY), including tables, the forest-plot figures and all 14 supplementary tables. Supplementary figures (spline curves, scatter and leave-one-out plots) seen as captions only. The release as ScienceDaily ran it (February, June and September 2026) and coverage by Labroots and Medical Dialogues
- Would change our mind
- Up: the men's effect holding in another biobank with sex-specific genetic data, using only variants that act on tyrosine itself, with a clear difference between men and women. Down: the effect vanishing once gene variants known to affect cholesterol, blood sugar or lifespan directly are set aside
Tyrosine is sold as a focus supplement, but the body gets it in other ways too: you eat it in protein, and the body makes it from another amino acid, phenylalanine. How much stays in circulation depends partly on genes that control that conversion and the breakdown afterward. A study of 272,475 people in UK Biobank asked whether people whose genes keep their tyrosine a little higher live less long.
The claim going around. The paper came out in October 2025. Coverage started in February, when ScienceDaily first ran the publisher's release as "Popular brain supplement linked to shorter lifespan in men," and resurfaced this month when ScienceDaily ran it again. It says "higher tyrosine could shorten male lifespan by nearly one year" and that "no significant effect appeared in women." Lower down, the release says the researchers "did not directly test tyrosine supplements." Labroots went further: "higher levels of common, over-the-counter supplement tyrosine may shorten lifespan in men."
What they did. Jie V. Zhao's team at the University of Hong Kong, with Kaixiong Ye's group at the University of Georgia, ran two analyses. First, a standard cohort study: they measured tyrosine once, in a blood sample taken between 2006 and 2010, and followed deaths to December 2022. Second, a genetic analysis called Mendelian randomization. They found variants that raise tyrosine, then checked whether people carrying them had parents who died younger. Parents are used because most participants are still alive, and a child shares half of each parent's genes.
What they found. In the cohort, each standard deviation higher tyrosine went with a 3% higher death rate in men (a relative figure) and no clear change in women, though the gap between the sexes wasn't clear of chance. Among the 125,359 men, 14,230 died, so 3% is roughly 3 more deaths per 1,000 men over about 12 to 17 years (our arithmetic, after the study's adjustments). The paper doesn't say how big a standard deviation is in blood-test units.
In the genetic analysis, higher genetically predicted tyrosine went with shorter parental lives: 0.68 years less per step for fathers and 0.67 for mothers. After allowing for phenylalanine, the figures were 0.80 years for fathers and 0.59 for mothers, both clear of chance. These years are converted from survival statistics with a standard formula, not counted. The raw material is good of its kind: deaths came from linked registry records rather than memory, and the gene variants were strong predictors of tyrosine, which guards against one common way these analyses go wrong.
| Genetic estimate, life years per SD of tyrosine | Fathers | Mothers |
|---|---|---|
| Main method | −0.68 | −0.67 |
| Main method, allowing for phenylalanine | −0.80 | −0.59 |
| MR-Egger, allowing for phenylalanine (in the abstract) | −0.91 | −0.36 (not clear of chance) |
| Weighted median (robustness check, simpler analysis) | −0.47 (not clear) | −0.16 (not clear) |
Men only? The abstract's "men but not women" comes from the third row, a method the paper's own methods section says to treat as the main result only if a test finds the variants' side effects lean one way. That test didn't find it, for men or women. By the paper's main method, mothers were affected too. The paper reports one direct test of the sex difference, in the cohort, and it wasn't clear of chance (p = 0.16). Our calculation from the genetic estimates finds no clear difference either. The authors write that low statistical power "may explain" this; it may, but that means the difference is unproven, not that it exists. The release also says men "generally have higher levels of tyrosine"; the paper's source for that is an older study of young adults in Mexico, and this study didn't report levels by sex.
What it doesn't show. The biggest gap is the supplement. Nobody took one. The variants act on how the body makes and clears tyrosine, and they shift levels slightly for a lifetime. A pill raises blood tyrosine within hours of a dose, as a small dosing study cited by the paper shows; whether years of pills raise resting levels is unknown. The authors write that their study "is not directly related to tyrosine supplement." On supplements, the paper is cautious; the release headline was not.
Second, the robustness checks were mixed. Two of the three extra methods found no clear effect in anyone, and a repeat using genetic data from outside UK Biobank was inconclusive: only one of four methods, in the whole group, was clear of zero. Among the 74 variants is one usually inherited together with APOE4, one of the strongest known lifespan variants and a top hit in the parental data the study used; it is among the 45 variants for men too. If it was used, its direction would push against the result, and the paper doesn't show what it did. Either way, the list includes variants with big effects of their own. The authors screened variants against smoking, drinking, exercise, education and deprivation, not against cholesterol, blood sugar or heart disease.
Third, the cohort link is small and, at below-average tyrosine levels, reversed: there, higher tyrosine went with lower mortality. Tyrosine tracks insulin resistance, as the paper notes, and the analysis didn't adjust for it.
What it means beyond the study. For people, the question is whether a lifelong tendency to carry more tyrosine costs time, and whether anything you can change moves that. This study hints at the first and says nothing about the second. The paper's suggestion that protein-restricted diets "will be helpful for prolonging lifespan" goes beyond its data; no diet was tested.
Why it's still interesting. Cutting protein extends life in flies and rodents, and fly experiments cited by the paper point to tyrosine specifically. This is one of the first attempts to ask the same question in people with genetics, and the answer wasn't a flat no: the main estimate was about eight months per step, for fathers and mothers alike. Some of the variants sit in HPD and SLC16A10, genes that handle tyrosine directly. Testing those alone is the obvious next step.
Open questions.
Is it tyrosine, or other jobs the same genes do? Re-run the analysis using only variants in genes that break down or transport tyrosine, or adjust for cholesterol and blood-sugar genetics. If the effect holds, tyrosine becomes a plausible target for research on ageing; if it fades, high tyrosine is a marker of metabolic health, not a cause.
Is there any difference between men and women? Test the contrast directly, in a biobank outside the UK with genetic data split by sex. The answer decides whether tyrosine says anything about why women outlive men.
Do years of supplements change resting tyrosine? Compare fasting blood tyrosine in long-term users and non-users, or measure it in a months-long trial. If resting levels don't move, this study is irrelevant to supplement users; if they do, a longer safety study is worth running.
A note on timing. The paper was published online on 3 October 2025. ScienceDaily first ran the release on 26 February 2026 and re-ran it in June and again on 6 September, eleven months after publication. The study hadn't changed.