Half of the people who die by suicide never say a word about wanting to die. The silence around them feels ordinary right up until the moment it isn’t, and a new study from University of Utah Health suggests that this absence of signs is not simply a failure of screening or a missed diagnosis. It may reflect a different kind of biological risk altogether.
The study, published in JAMA Network Open, examined genetic data from 2,769 Utahns who died by suicide. Researchers split them into two groups. One had documented suicidal thoughts or behaviors before death. The other had no such record in clinical notes or diagnostic codes. That division seems simple enough, but what followed was not. When the team compared polygenic scores for 12 neuropsychiatric traits, the two pathways looked startlingly different.
Two Paths, One Outcome
The usual assumption is that people who die without obvious warning signs were still depressed or anxious but never came to clinical attention. Yet the Utah group found something else entirely. People with no evidence of prior suicidality, the SD-N group, carried lower genetic liabilities for major depressive disorder, depressed affect, anxiety, neuroticism, posttraumatic stress disorder, and even Alzheimer’s disease than those with known suicidal histories.
For several traits, the SD-N profiles were not different from nearly 20,000 population controls at all. That makes the common refrain of “we must have missed the depression” feel less like a clinical oversight and more like a misunderstanding of risk itself.
“There are a lot of people out there who may be at risk of suicide where it’s not just that you’ve missed that they’re depressed, it’s likely that they’re in fact actually not depressed,” says Hilary Coon, PhD, the study’s first author.
This pulls the ground a bit. The field has long leaned on the idea that better depression screening would catch most people at risk. That logic works for the SD-S group. It falters in the SD-N group, where depression-related genetic risks are muted and sometimes absent. Screening harder for something that is not there will not save the people it misses.
Polygenic scores explain only the faintest sliver of risk, and no one in the study suggests genes are destiny. Still, when hundreds of thousands of genetic variants are summarized across thousands of individuals, the patterns can be telling. In this case, they drew a line between two groups who reach the same outcome for different reasons.
The Traits That Cut Across Both Groups
Not everything diverged. Genetic liabilities related to attention deficit hyperactivity disorder and alcohol use were elevated in both suicide subtypes. That overlap hints at shared vulnerabilities tied to impulsivity or disinhibition, the kinds of traits that rarely appear in a depression screen but shape behavior in quieter ways.
Schizophrenia polygenic scores stood out too. They were consistently higher in both groups than in controls, even though actual schizophrenia diagnoses appeared far more often in SD-S. In SD-N, the genetic signal rose without a matching rise in clinical records. It’s an odd mismatch. It may suggest undiagnosed symptoms. Or that the schizophrenia polygenic score is picking up other behavioral or cognitive traits that matter for suicide risk, even when no one in a clinic used the word schizophrenia.
The demographic picture shifted as well. SD-N deaths involved a higher share of men and tended to occur at older ages. When the researchers sliced the data by sex or age at death, the genetics fractured again. Some differences flipped direction. Others vanished. A few sharpened. The overall impression is messy and more realistic than any clean narrative: suicide mortality does not follow a single genetic script.
Rethinking Prevention
The temptation after a study like this is to imagine a new test or a clever predictive score. That is not what the data offer. The researchers are careful about this. The numbers are too small, the effects too faint, the influences too intertwined with environment, illness, and circumstance.
But the study does challenge a core assumption in suicide prevention: that psychiatric conditions form the central pillar of risk. For about half of suicide deaths, especially those without documented suicidality, the vulnerabilities may lie elsewhere. Chronic pain. Inflammation. Respiratory disease. Social conditions that never prompt a mental health visit. Those are areas Coon’s group is already exploring.
“We hope our work will begin to define subsets of individuals at risk, and also the contexts in which these risk characteristics may be important,” Coon says. “If people have a certain type of clinical diagnosis that makes them particularly vulnerable within particular environmental contexts, they still may not ever say they’re suicidal.”
The takeaway is uneasy but clarifying. Some people who die by suicide really do leave no psychiatric trail, not because their suffering was ignored, but because their risk did not resemble the pattern clinicians are trained to look for. That demands a broader approach to identifying vulnerability and a more nuanced understanding of what suicide risk actually looks like in the population.
Citation: Coon H, Shabalin AA, Monson ET, et al. “Genetic Liabilities to Neuropsychiatric Conditions in Suicide Deaths With No Prior Suicidality.” JAMA Network Open. Published October 20, 2025. DOI: 10.1001/jamanetworkopen.2025.38204.
ScienceBlog.com has no paywalls, no sponsored content, and no agenda beyond getting the science right. Every story here is written to inform, not to impress an advertiser or push a point of view.
Good science journalism takes time — reading the papers, checking the claims, finding researchers who can put findings in context. We do that work because we think it matters.
If you find this site useful, consider supporting it with a donation. Even a few dollars a month helps keep the coverage independent and free for everyone.
People might be overlooking another factor. Not all suicides are actual suicides. They can be homicides that were covered up for whatever reason.