Most people carry a private worry about their family history. A parent who had a heart attack at sixty. A grandmother who developed dementia. The unspoken question underneath is always the same: how much of this is already decided?
For a long time the honest answer was that we didn't know. Not because the question was unanswerable, but because nobody had measured both sides of it in the same population, at the same time, with the same rigour.
In March 2025, a team publishing in Nature Medicine did exactly that. And the result is worth understanding properly, because the headline version of it is being repeated everywhere and the headline version leaves out the half that matters most.
What the study actually did
The researchers worked with the UK Biobank, one of the largest health datasets in existence. For the mortality analysis they had records on 492,567 people.
They set out to compare two things. On one side, genetic risk — specifically, polygenic risk scores across 22 major diseases. On the other, the exposome: the accumulated environmental exposures of a life. Not a vague notion of "lifestyle", but 25 specific exposures they identified as independently associated with both mortality and biological aging.
Then they asked a direct question. Once you already know someone's age and sex, how much additional information does each side give you about when they will die?
The number people are quoting
Genetic risk across those 22 diseases added less than two percentage points of additional explanatory power. The exposome added seventeen.
That gap is large, and it is the finding that has travelled. It is also the point at which most coverage stops.
The half that usually gets left out
The same study found that genetics is not uniformly weaker. It depends entirely on what you are asking about.
For dementias and for breast, prostate and colorectal cancers, polygenic risk explained a greater share of the variation than the exposome did — between roughly 10 and 26 percent. For diseases of the lung, heart and liver, the exposome explained more, with a range running from around 5 to nearly 50 percent depending on the condition.
So the picture is not "environment beats genetics." It is that the two operate in different territories. Your inherited risk carries real weight for certain conditions. For overall mortality, and for a large portion of chronic organ disease, the accumulated environment carries more.
That distinction is not a technicality. It changes what you should do with the information.
Why this is more useful than it sounds
A polygenic risk score tells you something fixed. It is useful for screening decisions and for knowing where to pay attention, and it will not change between now and the end of your life.
The exposome is the opposite. It is made of things that are, in principle, modifiable — and it appears to carry more weight for the outcomes most adults are actually worried about.
The researchers also connected these 25 exposures to a proteomic aging clock built from blood proteins, in a subset of just over 45,000 people. On average, each exposure they identified was linked to more than twenty age-related biomarkers. In other words, these exposures are not abstract risk factors sitting in a statistical model. They show up in measurable biology.
What this does not mean
Two cautions, both of which the authors and independent commentators have raised.
First, this is an observational study. It identifies associations across an enormous population. It does not prove that changing a given exposure changes an individual outcome, and the analytical approach rests on assumptions that reasonable scientists can question.
Second, the UK Biobank cohort is not a perfect mirror of every population. Findings from it apply most directly to populations resembling the one studied.
Neither of those undermines the central result. They do mean the finding should be read as a map of where to look, not as a promise about any one person.
The practical version
If your family history worries you, this study does not tell you to ignore it. For some conditions it is exactly what you should be paying attention to.
What it does say is that for overall mortality, your genome describes a starting position rather than a conclusion. What accumulates on top of it — over decades, largely invisibly — carries more explanatory weight than the code you were born with.
And the part that accumulates is the part that can be measured.
At Biohax Medical, that is the layer we work in. Rather than reading a single result against a population average, we assess biomarkers across multiple systems and compare them against a person's own epigenetic profile, then measure again over time so the comparison is against themselves. What we are looking for is not a verdict. It is which system is moving fastest, and what appears to be driving it.
Your genome is the starting position. Almost everything after that is accumulation — and accumulation is something you can actually see.
Sources
Argentieri MA, Amin N, Nevado-Holgado AJ, et al. Integrating the environmental and genetic architectures of aging and mortality. Nature Medicine. 2025;31:1016–1025.
Science Media Centre. Expert reaction to study looking at genetic and lifestyle factors, and premature death, ageing and age-related diseases. February 2025.
This article is for general educational purposes and is not medical advice. It does not diagnose any condition, determine individual disease risk, or recommend treatment. Discuss your personal health questions with a qualified clinician.