Tyrosine and Men’s Lifespan: What the Study Shows, and What It Does Not
A headline now circulating warns that a popular “brain supplement” may shorten men’s lives. The supplement in question is the amino acid L-tyrosine, sold for focus, alertness, and mental performance under stress. The research behind the headline is real and worth attention, but the popular coverage leaves out the details a careful reader needs in order to decide whether anything in his own life should change.
It is also worth noting that the study is not new. It was published in October 2025 in the journal Aging by Jie V. Zhao and colleagues at the University of Hong Kong and the University of Georgia. It is simply receiving a second round of press.
What the researchers did
The team used the UK Biobank, a large British research cohort, and drew on data from roughly 272,000 participants. They asked two questions in two different ways.
First, in an observational analysis, they compared people’s measured blood levels of phenylalanine and tyrosine with their risk of death during follow-up. People with higher circulating tyrosine had higher all-cause mortality.
Second, they used Mendelian randomization. This method takes advantage of the fact that genes are assigned at conception, largely at random with respect to later lifestyle. If certain gene variants reliably raise a person’s blood tyrosine, and people carrying those variants have shorter lives, that pattern is harder to explain away by diet, smoking, income, or other lifestyle differences than an ordinary observational link would be. For the lifespan outcome, the researchers used large genetic studies of how long participants’ parents lived, a standard proxy in this kind of work.
Because the body converts phenylalanine into tyrosine, the two rise and fall together. To separate them, the researchers ran a combined analysis that held one constant while examining the other.
What they found
Once they accounted for phenylalanine, genetically higher tyrosine was associated with about 0.9 fewer years of life in men, and the statistical range around that estimate (roughly 0.2 to 1.6 years) did not include zero. In women, the estimate was smaller, about 0.4 years, and its range crossed zero, so it could not be distinguished from no effect. Phenylalanine showed no independent association with lifespan in either sex.
The authors noted that men tend to carry higher tyrosine levels than women and raised the possibility that tyrosine contributes, in part, to the familiar gap in life expectancy between the sexes. They were explicit that their data do not prove this.
Five things the headline leaves out
1. Blood tyrosine is not the same as supplement use. The study measured tyrosine circulating in the blood and the genes that influence it. It did not study anyone taking tyrosine capsules. The liver sets blood tyrosine mainly by converting phenylalanine into tyrosine and breaking tyrosine down. A man who takes tyrosine before a demanding afternoon raises his level for a few hours; a man whose genes nudge his baseline upward carries a slightly higher level every hour of his life. Mendelian randomization estimates the effect of the second situation, not the first. Whether occasional or even regular supplementation reproduces that lifelong exposure is unknown.
2. The difference between men and women is suggestive, not established. A result that reaches statistical significance in men and falls short in women does not by itself show that the two sexes differ. The women’s estimate still leaned in the same direction, and the ranges for the two groups overlap considerably. The honest reading is that the effect may be larger in men, not that women are exempt.
3. High tyrosine is a known marker of insulin resistance. Metabolic researchers have recognized for over a decade that elevated blood levels of the aromatic amino acids (tyrosine and phenylalanine) and the branched-chain amino acids (leucine, isoleucine, valine) accompany insulin resistance. In the Framingham Offspring Study, published in Nature Medicine in 2011, higher levels of these amino acids predicted the development of type 2 diabetes years before it appeared. Insulin normally helps clear amino acids from the blood into muscle; when tissues stop responding well to insulin, amino acids accumulate. Some of the association between tyrosine and early death may therefore reflect the metabolic disease behind the elevated tyrosine, rather than tyrosine acting as a cause. Mendelian randomization is designed to reduce this problem, but it cannot rule out that the chosen gene variants affect lifespan through some other pathway as well, such as broader liver or metabolic function.
4. The proposed mechanism is speculative. Popular coverage suggests that excess tyrosine could interfere with insulin signaling because that signaling depends on tyrosine. The insulin receptor works by attaching phosphate groups to tyrosine residues on signaling proteins, but that is a different matter from the amount of free tyrosine floating in the blood. No settled evidence shows that normal variation in free tyrosine disrupts the receptor. The authors offered insulin resistance and the brain’s stress chemicals (dopamine, norepinephrine, epinephrine, all made from tyrosine) as hypotheses to explore, not as findings.
5. The effect is modest and averaged. Nine-tenths of a year is a population average attached to a genetic difference in baseline levels. It matters for public health and is worth understanding, but it is not a prediction for any individual, and it is small compared with the known effects of smoking, physical inactivity, and uncontrolled blood sugar.
The larger context: protein and aging
The authors framed their study within a long line of research showing that protein restriction extends lifespan in laboratory animals, and they were looking for which specific amino acids might be responsible. Methionine and the branched-chain amino acids have received most of the attention in that field; this study adds tyrosine as a candidate in humans.
That framing should be kept in proportion. Older adults face a real and well-documented danger from inadequate protein: loss of muscle mass and strength, falls, frailty, and slower recovery from illness. A general instruction to cut protein in order to lower tyrosine would trade a speculative benefit for a known harm, especially after age sixty. The authors themselves suggested dietary adjustment only for people with unusually high tyrosine levels, and no trial has tested whether doing so extends life.
What tyrosine supplements are actually good for
Tyrosine’s reputation is not unfounded. Controlled studies have found that it can modestly preserve working memory and mental performance under acute stress, such as sleep deprivation, cold exposure, or demanding multitasking, apparently by supplying raw material for the brain’s catecholamines when they are being depleted. The evidence for benefit in rested people under ordinary conditions is weaker. In other words, tyrosine appears most useful as a situational tool rather than as a daily tonic.
Tyrosine is also not appropriate for everyone. It should be avoided or used only under supervision by people taking MAO-inhibitor antidepressants (the combination can raise blood pressure dangerously), people taking thyroid hormone or with an overactive thyroid (tyrosine is a building block of thyroid hormone), and people taking levodopa for Parkinson’s disease (the two compete for absorption). On the other hand, people with phenylketonuria cannot make tyrosine from phenylalanine and depend on it in their diet or medical formula; nothing in this study applies to them.
A reasonable response
For a man who uses tyrosine or is considering it, the study supports a few sensible adjustments rather than alarm.
Reserve tyrosine for circumstances where it has shown benefit, rather than taking it every day indefinitely. If a daily need seems to be there, ask why focus and energy are flagging in the first place; sleep, blood sugar regulation, thyroid function, iron status, and depression are more common explanations than a tyrosine shortage.
Pay attention to insulin resistance. Whether elevated tyrosine turns out to be a cause, a marker, or both, the same metabolic picture drives a large share of early death in men. Waist circumference, fasting insulin, fasting glucose, hemoglobin A1c, and triglycerides tell a good deal about where a person stands, and regular exercise, particularly resistance training, is among the most effective ways to restore insulin sensitivity.
Do not abandon protein. Eggs, fish, poultry, meat, dairy, legumes, nuts, and seeds all contain tyrosine, and they also supply what the body needs to maintain muscle and repair tissue. Food-based intake has not been shown to shorten life.
A plasma amino acid panel can measure tyrosine, but no established target level for longevity exists, so the test is more useful for investigating a specific metabolic question than for routine screening.
The bottom line
A well-designed genetic study found that men whose genes give them higher lifelong blood tyrosine live, on average, slightly shorter lives. That is a useful clue about aging and possibly about lifespan differences between men and women. It is not evidence that tyrosine supplements shorten life, and it is not a reason to fear protein-rich food. The most practical lesson is an old one: the metabolic health that governs how the body handles amino acids, sugar, and fat matters far more than any single nutrient in a capsule.
As always, anyone taking prescription medication or managing a chronic condition should discuss supplement use with his physician.
References
Zhao JV, Sun Y, Zhang J, Ye K. The role of phenylalanine and tyrosine in longevity: a cohort and Mendelian randomization study. Aging (Albany NY). 2025. doi:10.18632/aging.206326
Wang TJ, Larson MG, Vasan RS, et al. Metabolite profiles and the risk of developing diabetes. Nature Medicine. 2011;17(4):448–453.