Worrying about getting old, it turns out, may not be a neutral psychological activity. In November 2025, Mariana Rodrigues, a PhD student at the NYU School of Global Public Health, and colleagues published a paper in the peer-reviewed journal Psychoneuroendocrinology analysing data from 726 adult women across the United States. The participants had completed standardised questionnaires assessing their anxiety about aging — broken into three specific dimensions: fears about declining health, fears about losing physical attractiveness, and fears about reproductive aging. They had also provided blood samples that the research team analysed using two of the most rigorous biological-age measurement tools currently available: DunedinPACE, which measures the current speed at which the body is aging, and GrimAge2, which estimates cumulative biological damage accumulated over a lifetime. The findings, presented as a cross-sectional snapshot rather than a clinical intervention, suggested that subjective fears about getting older may indeed have measurable effects on the underlying biology of aging itself.
According to the NYU School of Global Public Health’s press release on the study, the researchers found that women with higher aging anxiety showed accelerated epigenetic aging on the DunedinPACE clock — meaning their cells were aging measurably faster than would be expected for their chronological age. The effect was specific. Among the three dimensions of aging anxiety the team examined, only one was strongly associated with the biological-age acceleration: fears about declining health. Anxieties about appearance and fertility did not show a comparable association with the epigenetic clocks. The implication, in the researchers’ framing, is that not all aging fears are biologically equivalent. The specific worry that one’s body will fail in the future appears to be the one that does the most to accelerate the failure itself.
How the cellular measurement works
The two epigenetic clocks the NYU team used represent the current state of the art in biological-age measurement. Per PsyPost’s detailed coverage of the study’s methodology, DunedinPACE functions like a speedometer for cellular aging — it measures the rate at which the body is currently aging at the moment the blood sample was taken, expressed as a multiplier of normal aging (a DunedinPACE score of 1.0 indicates normal pace; higher values indicate faster aging). GrimAge2 functions differently, estimating cumulative biological damage accumulated across a lifetime, and has been validated as a strong predictor of mortality risk. Both clocks measure DNA methylation patterns — chemical modifications to the DNA that accumulate over time and that reflect, with substantial precision, the underlying biological state of the cells producing them.
The participants who scored higher on the aging-anxiety scale, particularly on the health-related dimension, showed faster DunedinPACE scores than participants with lower anxiety. The magnitude of the effect, while present, was modest in absolute terms — these are statistical patterns across hundreds of women, not dramatic personal accelerations visible to the individual. But the direction was consistent, the methodology was rigorous, and the use of two independent epigenetic clocks rather than one strengthened the basic finding. Rodrigues, in her summary of the work, described the implication directly: “Our research suggests that subjective experiences may be driving objective measures of aging. Aging-related anxiety is not merely a psychological concern, but may leave a mark on the body with real health consequences.”
Why women specifically
The study examined only women, and the researchers were explicit about why this population was chosen. As reported in the Sentinel Assam coverage of the NYU work, women may be especially vulnerable to aging anxiety because of the specific configuration of social expectations they navigate. Cultural pressures around youth and physical appearance, professional consequences of perceived aging, the timing of reproductive decisions, and midlife caregiving roles that often involve simultaneously watching one’s own parents age and become sick all combine to produce a particular intensity of aging-related psychological stress in women across the lifespan. Rodrigues noted in her commentary on the findings: “Women in midlife may also be juggling multiple roles, including caring for their ageing parents. As they see older family members grow older and become sick, they may worry about whether the same thing will happen to them.”
The decision to study women only also reflects a broader pattern in the aging-and-anxiety literature, where men and women appear to experience and process aging-related fears differently. Whether the basic finding — that fears about future health predict faster cellular aging — generalises to men, and whether the magnitude of the effect is similar across sexes, are questions that the present study cannot answer and that the research group identifies as priority topics for subsequent investigation.
What the study does not establish
The Rodrigues et al. 2025 paper is a cross-sectional observational study, not a randomised intervention. The researchers were careful to acknowledge several limitations that warrant honest framing. The most important is that the study captures a single point in time, which means it cannot determine the direction of causation. It is possible that aging anxiety accelerates cellular aging, as the popular framing of the finding suggests. It is also possible that women whose cells are already aging faster — for reasons unrelated to their anxiety — develop more aging-related health concerns as a result of subtle bodily changes they may not consciously recognise. Both directions are biologically plausible, and a single time-point study cannot distinguish between them. Longitudinal research that follows the same individuals across years and decades will be required to establish causation.
A second important limitation involves behavioural mediators. As reported in ScienceDaily’s coverage of the paper, when the research team adjusted their analysis to account for anxiety-related coping behaviours — particularly smoking and alcohol use — the association between aging anxiety and accelerated epigenetic aging weakened and lost statistical significance. This is a real finding that complicates the simple “fear ages you directly” narrative. It suggests that part of the biological effect of aging anxiety may be mediated through the behaviours people adopt to cope with the anxiety, rather than through a direct neuropsychological pathway. Women who worry intensely about declining health may smoke or drink more as a way of managing the anxiety, and those behaviours may then accelerate cellular aging through well-established mechanisms. The aging anxiety, in this account, is still consequential — but its consequence runs partly through behavioural channels that are themselves more directly addressable than the underlying psychological state.
Where this fits in the broader literature
The NYU finding does not stand alone. The Yale psychologist Becca Levy has been publishing on closely related territory for more than two decades, beginning with a 2002 paper in the Journal of Personality and Social Psychology showing that older adults with positive age stereotypes — those who viewed aging as a generally positive process rather than a feared decline — lived approximately 7.5 years longer on average than those with negative age stereotypes, after controlling for age, sex, socioeconomic status, loneliness, and functional health. Subsequent work in the Levy research programme has documented similar patterns across cardiovascular outcomes, dementia risk, recovery from disability, and a long list of other health indicators. The Rodrigues 2025 paper extends this body of work into the specific domain of epigenetic biological-age measurement, providing the first peer-reviewed evidence that the connection between aging-related psychological orientation and biological aging shows up directly in the molecular clocks researchers can now measure in blood.
What this means for ordinary readers is that the way a person thinks about aging may matter more than it has traditionally been treated as mattering. The implication is not that anyone can simply will themselves to age more slowly by adopting positive thoughts about getting older — the relationship is more complex than that, and the behavioural mediators identified in the NYU study suggest that the practical pathway runs partly through the daily habits that anxiety drives rather than through pure cognitive reframing. But the underlying observation — that subjective fears about the future are now measurable in the cells of the body that holds those fears — represents a substantive shift in how the boundary between psychology and biology can be understood. The mind-body connection, in the specific domain of aging, is no longer a metaphor. It is something that can be quantified in DNA methylation patterns, in a blood sample, in a laboratory in New York.
