Tyrosine is sold as a cognitive enhancer. It synthesizes dopamine. The marketing is simple: more dopamine precursor, better brain function. People take it voluntarily.
A study of 270,000 UK Biobank participants used Mendelian randomization to test whether genetically elevated tyrosine levels affect lifespan. Mendelian randomization exploits genetic variants as natural experiments. If a variant that increases tyrosine also predicts shorter life, the link is causal, not confounded by diet or lifestyle.
The result: genetically elevated tyrosine shortens male lifespan by approximately eleven months. No effect in women.
The mechanism runs through insulin resistance. Men have naturally higher baseline tyrosine levels. The additional load tips them into metabolic territory that accelerates aging. Women, with lower baselines, stay below the threshold where tyrosine becomes harmful. The same molecule is neutral in one body and toxic in another.
What matters here is the method. Observational studies of tyrosine supplementation face a standard problem: people who take supplements differ from people who do not in ways that correlate with health outcomes. Mendelian randomization strips this away. The genetic variants are assigned at conception. They correlate with tyrosine levels but not with the decision to take supplements. When the causal lens replaces the observational lens, the cognitive enhancer becomes a lifespan cost.
This is not a rare inversion. It is what happens when you apply a method capable of separating cause from association to a substance whose reputation was built on association. The supplement was never proven to help cognition through causal methods either. The entire framework — take precursor, get neurotransmitter, improve function — was plausible mechanism without causal evidence. When causal evidence arrives, it points the other way.