In the twenty years spanning the September 11, 2001 terrorist attacks and the August 2021 withdrawal of United States Armed Forces from Afghanistan, approximately 4.9 million Americans served in the U.S. military and then transitioned to veteran status (U.S. Bureau of Labor Statistics, 2023). These two decades encompassed wars in both Afghanistan and Iraq across Operations Enduring Freedom (OEF), Iraqi Freedom (OIF), and New Dawn (OND), as well as numerous other deployments and military service around the world. Veterans from this period of service are known as the post-9/11 veteran cohort (alternatively, the Gulf War II cohort). This service period includes “signature wounds” (Kieran, 2019) comprised of high levels of mental health burden, particularly posttraumatic stress disorder and suicide (Kieran, 2019), exposure to toxic chemicals during deployment (Department of Veterans Affairs, 2023; National Academies of Science, Engineering, and Medicine, 2020; U.S. Congress, 2022), and traumatic brain injury (Kennedy et al., 2022; Reger et al., 2022). These hallmark exposures present a potent accumulation of risk factors linked to poor health outcomes as individuals grow older (Harper et al., 2022; Kennedy et al., 2022; Reger et al., 2022; World Health Organization, 2021). With a median age of approximately 40 years old, post-9/11 veterans are entering middle and older age and face increased risk for negative outcomes associated with aging: declining cognition, increased disability and loss of independence, the development and progression of chronic disease, and potential for premature mortality. However, there is an opportunity to prevent these outcomes if we can identify and treat veterans who are at risk for negative health consequences.

One promising approach to reduce future rates of disability, disease, and premature death among post-9/11 veterans is to develop interventions to slow the rate of their biological aging (López-Otín et al., 2013; Kaeberlein, 2013). This approach, termed geroscience, aims to understand the underlying physiology of aging in order to slow, or even reverse, the gradual decline in biological functions tied to growing older. In this framework, biological aging is the “common cause” of chronic disease and death (Kennedy et al., 2014), serving as a risk factor, putative mechanism, and surrogate clinical endpoint. By taking a disease-agnostic approach, the goal of geroscience is to slow aging through interventions to improve health outcomes across organ systems and diagnostic categories (Barzilai, Cuervo, and Austad, 2018; Justice et al., 2016; Sierra et al., 2021).

The development and maturation of geroscience as a field of study has come with technological advances in measuring biological aging using the epigenome (Belsky et al., 2018; Rutledge, Oh, and Wyss-Coray, 2022), specifically DNA methylation (DNAm). Measures of biological aging using DNAm are critical to the development of geroscience due to the ability to leverage epigenetic insights from deeply-phenotyped longitudinal cohorts, including some assessed over five decades (Belsky et al., 2015; Elliott et al., 2021; Poulton, Guiney, Ramrakha, and Moffitt, 2023), and apply them to new samples, cohorts, and populations. DNAm makes it possible to identify people with accelerated aging using a single measurement occasion and potentially test whether interventions can slow this aging in a shorter period of study, ideally avoiding decades of longitudinal study. As a result, epigenetic aging can act as an intermediate biomarker of aging and health that can be used in observational studies (e.g., Faul et al., 2023) and randomized controlled trials (e.g., Waziry et al., 2023). Although research using epigenetic measures of aging has advanced quickly in civilian populations (Rutledge et al., 2022), fewer studies have focused on the post-9/11 cohort of veterans, with most research instead focusing on specific veteran patient populations (e.g., veterans with PTSD; Wolf et al., 2018). It is important to both replicate the associations with biological aging found in civilian samples and identify veteran characteristics that may increase the risk for accelerated biological aging.

The post-9/11 cohort of veterans represents an ever-increasing proportion of the U.S. veteran population (Barroso, 2019), with concomitant increased levels of care expected as these veterans age into midlife and beyond. Notably, this cohort has important demographic differences when compared to prior cohorts. For example, the proportion of women who served in the post-9/11 period increased by a factor of eight compared to the 1970s, when women were limited by law to 2 % of the total military population (see U.S. Congress, 1948). The post-9/11 veteran population also includes an increasing number of veterans of color, particularly Black and Hispanic veterans (Barroso, 2019). These changing demographics necessitate a better understanding of which veterans might benefit most from intervention to prevent the emergence of poor health as this post-9/11 cohort of veterans grows older.

Slowing the biological aging of post-9/11 veterans, though a lofty goal, would have profound benefits to the health and wellbeing of millions of veterans and reduce costs associated with healthcare as they age. The post-9/11 cohort of veterans is entering a developmental period where slowing aging might provide notable future health benefits. To this end, new innovations in geroscience provide tools to assist in the identification of veterans at risk for accelerated aging (Moffitt, 2020), who could be treated to slow aging and improve health. However, supporting future geroscience-oriented prevention and intervention efforts requires discovering the characteristics associated with accelerated aging.

Our study sample was comprised of 2309 veterans from the Post-Deployment Mental Health Study (PDMH; Brancu et al., 2017)—a cohort of U.S. service members deployed following September 11, 2001. Participants completed self-report measures and provided blood samples that were used to derive DNAm aging scores. We examined whether veterans’ demographics—specifically sex, race/ethnicity, and age—were associated with differences in epigenetic aging scores, as assessed by DunedinPACE. We hypothesized that male, non-Hispanic Black, and older veterans would have faster aging than female, non-Hispanic White, and younger veterans.