Demographic characteristics and epigenetic biological aging among post-9/11 veterans: Associations of DunedinPACE with sex, race, and age.

Measures of epigenetic aging derived from DNA methylation (DNAm) have enabled the assessment of biological aging in new populations and cohorts. In the present study, we used an epigenetic measure of aging, DunedinPACE, to examine rates of aging across demographic groups in a sample of 2,309 United States military veterans from the VISN 6 MIRECC's Post-Deployment Mental Health Study. As assessed by DunedinPACE, female veterans were aging faster than male veterans (ß = 0.39, 95 % CI [0.29, 0.48], p < .001), non-Hispanic Black veterans were aging faster than non-Hispanic White veterans (ß = 0.58, 95 % CI [0.50, 0.66], p < .001), and older veterans were biologically aging faster than younger veterans (ß = 0.21, 95 % CI [0.18, 0.25], p < .001). In secondary analyses, these differences in rates of aging were not explained by a variety of biopsychosocial covariates. In addition, the percentage of European genetic admixture in non-Hispanic Black veterans was not associated with DunedinPACE. Our findings suggest that female and non-Hispanic Black veterans are at greater risk of accelerated aging among post-9/11 veterans. Interventions that slow aging might provide relatively greater benefit among veterans comprising these at-risk groups.

Deployment-related toxic exposures are associated with worsening mental and physical health after military service: Results from a self-report screening of veterans deployed after 9/11.

Exposure to toxins-such as heavy metals and air pollution-can result in poor health and wellbeing. Recent scientific and media attention has highlighted negative health outcomes associated with toxic exposures for U.S. military personnel deployed overseas. Despite established health risks, less empirical work has examined whether deployment-related toxic exposures are associated with declines in mental and physical health after leaving military service, particularly among the most recent cohort of veterans deployed after September 11, 2001. Using data from 659 U.S. veterans in the VISN 6 MIRECC Post-Deployment Mental Health Study, we tested whether self-reported toxic exposures were associated with poorer mental and physical health. At baseline, veterans who reported more toxic exposures also reported more mental health, ß = 0.14, 95% CI [0.04, 0.23], p = 0.004, and physical health symptoms, ß = 0.21, 95% CI [0.11, 0.30], p < 0.001. Over the next ten years, veterans reporting more toxic exposures also had greater increases in mental health symptoms, ß = 0.23, 95% CI [0.15, 0.31], p < 0.001, physical health symptoms, ß = 0.22, 95% CI [0.14, 0.30], p < 0.001, and chronic disease diagnoses, ß = 0.15, 95% CI [0.07, 0.23], p < 0.001. These associations accounted for demographic and military covariates, including combat exposure. Our findings suggest that toxic exposures are associated with worsening mental and physical health after military service, and this recent cohort of veterans will have increased need for mental health and medical care as they age into midlife and older age.

Genome-wide DNA methylation analysis of cannabis use disorder in a veteran cohort enriched for posttraumatic stress disorder.

Cannabis use has been increasing over the past decade, not only in the general US population, but particularly among military veterans. With this rise in use has come a concomitant increase in cannabis use disorder (CUD) among veterans. Here, we performed an epigenome-wide association study for lifetime CUD in an Iraq/Afghanistan era veteran cohort enriched for posttraumatic stress disorder (PTSD) comprising 2,310 total subjects (1,109 non-Hispanic black and 1,201 non-Hispanic white). We also investigated CUD interactions with current PTSD status and examined potential indirect effects of DNA methylation (DNAm) on the relationship between CUD and psychiatric diagnoses. Four CpGs were associated with lifetime CUD, even after controlling for the effects of current smoking (AHRR cg05575921, LINC00299 cg23079012, VWA7 cg22112841, and FAM70A cg08760398). Importantly, cg05575921, a CpG strongly linked to smoking, remained associated with lifetime CUD even when restricting the analysis to veterans who reported never smoking cigarettes. Moreover, CUD interacted with current PTSD to affect cg05575921 and cg23079012 such that those with both CUD and PTSD displayed significantly lower DNAm compared to the other groups. Finally, we provide preliminary evidence that AHRR cg05575921 helps explain the association between CUD and any psychiatric diagnoses, specifically mood disorders.

Posttraumatic stress disorder, trauma, and accelerated biological aging among post-9/11 veterans.

People who experience trauma and develop posttraumatic stress disorder (PTSD) are at increased risk for poor health. One mechanism that could explain this risk is accelerated biological aging, which is associated with the accumulation of chronic diseases, disability, and premature mortality. Using data from 2309 post-9/11 United States military veterans who participated in the VISN 6 MIRECC's Post-Deployment Mental Health Study, we tested whether PTSD and trauma exposure were associated with accelerated rate of biological aging, assessed using a validated DNA methylation (DNAm) measure of epigenetic aging-DunedinPACE. Veterans with current PTSD were aging faster than those who did not have current PTSD, ß = 0.18, 95% CI [0.11, 0.27], p < .001. This effect represented an additional 0.4 months of biological aging each year. Veterans were also aging faster if they reported more PTSD symptoms, ß = 0.13, 95% CI [0.09, 0.16], p < 0.001, or higher levels of trauma exposure, ß = 0.09, 95% CI [0.05, 0.13], p < 0.001. Notably, veterans with past PTSD were aging more slowly than those with current PTSD, ß = -0.21, 95% CI [-0.35, -0.07], p = .003. All reported results accounted for age, gender, self-reported race/ethnicity, and education, and remained when controlling for smoking. Our findings suggest that an accelerated rate of biological aging could help explain how PTSD contributes to poor health and highlights the potential benefits of providing efficacious treatment to populations at increased risk of trauma and PTSD.

Which Types of Stress Are Associated With Accelerated Biological Aging? Comparing Perceived Stress, Stressful Life Events, Childhood Adversity, and Posttraumatic Stress Disorder.

OBJECTIVE: Stress and stressful events are associated with poorer health; however, there are multiple ways to conceptualize and measure stress and stress responses. One physiological mechanism through which stress could result in poorer health is accelerated biological aging. This study tested which types of stress were associated with accelerated biological aging in adulthood. METHODS: Studying 955 participants from the Dunedin Longitudinal Study, we tested whether four types of stress assessed from ages 32 to 45 years-perceived stress, number of stressful life events, adverse childhood experiences, and posttraumatic stress disorder-were associated with accelerated biological aging. RESULTS: Higher levels of all four measures of stress were significantly associated with accelerated aging in separate models. In a combined model, more perceived stress and more stressful life events remained associated with faster aging, and the stress measures explained 6.9% of the variance in aging. The magnitudes of the associations between the four measures of stress and biological aging were comparable to associations for smoking and low education, two established risk factors for accelerated aging. People with high levels of perceived stress, numerous adverse childhood experiences (4+), high stressful life event counts, or posttraumatic stress disorder were aging an additional estimated 2.4 months, 1.1 additional months, 1.4 months, and 1.4 months per year, respectively. CONCLUSIONS: Assessing stress, particularly perceived stress, could help identify people at risk of accelerated aging. Intervening to treat stress or the health-relevant sequelae of stress could potentially slow the rate at which people are aging, improving their health as they age.

Childhood Adversity and Midlife Health: Shining a Light on the Black Box of Psychosocial Mechanisms.

Adverse childhood experiences (ACEs) are associated with poorer health, which has spurred public health efforts to reduce the number of adverse events children experience. Unfortunately, it is unlikely that all ACEs can be prevented. For adults who already experienced ACEs in childhood, what psychological, social, and behavioral intervention targets might reduce risk for negative health outcomes? To provide insight into the "black box" of psychosocial mechanisms linking ACEs to poor health, our study used data from the Dunedin Study, a longitudinal cohort assessed from birth to age 45. Mediation models (N = 859) were used to examine whether candidate psychosocial variables in adulthood explained the association between childhood ACEs and health in midlife. Potential psychosocial mediators included stressful life events, perceived stress, negative emotionality, and health behaviors. Children who experienced more ACEs had poorer health in midlife. They also had significantly more stressful life events, more perceived stress, more negative emotionality, and unhealthier behaviors as adults. These mediators were each independently associated with poorer health in midlife and statistically mediated the association between ACEs and midlife health. Health behaviors evidenced the strongest indirect effect from ACEs to midlife health. Together, these psychosocial mediators accounted for the association between ACEs in childhood and health three decades later. Public health efforts to mitigate the health consequences of ACEs could aim to reduce the stressful life events people experience, reduce negative emotionality, reduce perceived stress, or improve health behaviors among adults who experienced childhood adversity.

Association of Pace of Aging Measured by Blood-Based DNA Methylation With Age-Related Cognitive Impairment and Dementia.

BACKGROUND AND OBJECTIVES: DNA methylation algorithms are increasingly used to estimate biological aging; however, how these proposed measures of whole-organism biological aging relate to aging in the brain is not known. We used data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the Framingham Heart Study (FHS) Offspring Cohort to test the association between blood-based DNA methylation measures of biological aging and cognitive impairment and dementia in older adults. METHODS: We tested 3 "generations" of DNA methylation age algorithms (first generation: Horvath and Hannum clocks; second generation: PhenoAge and GrimAge; and third generation: DunedinPACE, Dunedin Pace of Aging Calculated from the Epigenome) against the following measures of cognitive impairment in ADNI: clinical diagnosis of dementia and mild cognitive impairment, scores on Alzheimer disease (AD) / Alzheimer disease and related dementias (ADRD) screening tests (Alzheimer's Disease Assessment Scale, Mini-Mental State Examination, and Montreal Cognitive Assessment), and scores on cognitive tests (Rey Auditory Verbal Learning Test, Logical Memory test, and Trail Making Test). In an independent replication in the FHS Offspring Cohort, we further tested the longitudinal association between the DNA methylation algorithms and the risk of developing dementia. RESULTS: In ADNI (N = 649 individuals), the first-generation (Horvath and Hannum DNA methylation age clocks) and the second-generation (PhenoAge and GrimAge) DNA methylation measures of aging were not consistently associated with measures of cognitive impairment in older adults. By contrast, a third-generation measure of biological aging, DunedinPACE, was associated with clinical diagnosis of Alzheimer disease (beta [95% CI] = 0.28 [0.08-0.47]), poorer scores on Alzheimer disease/ADRD screening tests (beta [Robust SE] = -0.10 [0.04] to 0.08[0.04]), and cognitive tests (beta [Robust SE] = -0.12 [0.04] to 0.10 [0.03]). The association between faster pace of aging, as measured by DunedinPACE, and risk of developing dementia was confirmed in a longitudinal analysis of the FHS Offspring Cohort (N = 2,264 individuals, hazard ratio [95% CI] = 1.27 [1.07-1.49]). DISCUSSION: Third-generation blood-based DNA methylation measures of aging could prove valuable for measuring differences between individuals in the rate at which they age and in their risk for cognitive decline, and for evaluating interventions to slow aging.

Cardiovascular reactivity, stress, and personal emotional salience: Choose your tasks carefully.

Both greater cardiovascular reactivity and lesser reactivity ("blunting") to laboratory stressors are linked to poor health outcomes, including among people who have a history of traumatic experiences. In a sample of recently separated and divorced adults (N = 96), this study examined whether differences in cardiovascular reactivity might be explained by differences in the personal emotional salience of the tasks and trauma history. Participants were assessed for trauma history, current distress related to their marital dissolution, and cardiovascular reactivity during two tasks, a serial subtraction math stressor task and a divorce-recall task. Participants with a greater trauma history evidenced less blood pressure reactivity to the serial subtraction task (a low personal emotional salience task) when compared to participants with less trauma history. In contrast, participants with a greater trauma history evidenced higher blood pressure reactivity to the divorce-recall task, but only if they also reported more divorce-related distress (high personal emotional salience). These associations were not significant for heart rate reactivity. Among people with a history of more traumatic experiences, a task with low personal salience was associated with a lower blood pressure response, whereas a task with higher personal emotional salience was associated with a higher blood pressure response. Future studies examining cardiovascular reactivity would benefit from determining the personal emotional salience of tasks, particularly for groups that have experienced stressful life events or trauma.

Association of Treatable Health Conditions During Adolescence With Accelerated Aging at Midlife.

IMPORTANCE: Biological aging is a distinct construct from health; however, people who age quickly are more likely to experience poor health. Identifying pediatric health conditions associated with accelerated aging could help develop treatment approaches to slow midlife aging and prevent poor health in later life. OBJECTIVE: To examine the association between 4 treatable health conditions in adolescence and accelerated aging at midlife. DESIGN, SETTING, AND PARTICIPANTS: This cohort study analyzed data from participants in the Dunedin Study, a longitudinal investigation of health and behavior among a birth cohort born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand, and followed up until age 45 years. Participants underwent an assessment at age 45 years and had data for at least 1 adolescent health condition (asthma, smoking, obesity, and psychological disorders) and outcome measure (pace of aging, gait speed, brain age, and facial age). Data analysis was performed from February 11 to September 27, 2021. EXPOSURES: Asthma, cigarette smoking, obesity, and psychological disorders were assessed at age 11, 13, and 15 years. MAIN OUTCOMES AND MEASURES: The outcome was a midlife aging factor composite score comprising 4 measures of biological aging: pace of aging, gait speed, brain age (specifically, BrainAGE score), and facial age. RESULTS: A total of 910 participants (459 men [50.4%]) met the inclusion criteria, including an assessment at age 45 years. Participants who had smoked daily (0.61 [95% CI, 0.43-0.79] SD units), had obesity (0.82 [95% CI, 0.59-1.06] SD units), or had a psychological disorder diagnosis (0.43 [95% CI, 0.29-0.56] SD units) during adolescence were biologically older at midlife compared with participants without these conditions. Participants with asthma were not biologically older at midlife (0.02 [95% CI, -0.14 to 0.19] SD units) compared with those without asthma. These results remained unchanged after adjusting for childhood risk factors such as poor health, socioeconomic disadvantage, and adverse experiences. CONCLUSIONS AND RELEVANCE: This study found that adolescent smoking, obesity, and psychological disorder diagnoses were associated with older biological age at midlife. These health conditions could be treated during adolescence to reduce the risk of accelerated biological aging later in life.

Lower Cardiovascular Reactivity is Associated with More Childhood Adversity and Poorer Midlife Health: Replicated Findings from the Dunedin and MIDUS Cohorts.

Cardiovascular reactivity has been proposed as a biomarker linking childhood adversity and poorer health. The current study examined the association of childhood adversity, cardiovascular reactivity, and health in the Dunedin (n=922) and MIDUS studies (n=1,015). In both studies, participants who experienced more childhood adversity had lower cardiovascular reactivity. In addition, people with lower cardiovascular reactivity had poorer self-reported health and greater inflammation. Dunedin participants with lower cardiovascular reactivity were aging biologically faster, and MIDUS participants with lower heart rate reactivity had increased risk of early mortality. Cardiovascular reactivity was not associated with hypertension in either study. Results were partially accounted for by greater reactivity among more conscientious, less depressed, and higher-functioning participants. These results suggest that people who experienced childhood adversity have a blunted physiological response, which is associated with poorer health. The findings highlight the importance of accounting for individual differences when assessing cardiovascular reactivity using cognitive stressor tasks.

Vital personality scores and healthy aging: Life-course associations and familial transmission.

OBJECTIVES: Personality traits are linked with healthy aging, but it is not clear how these associations come to manifest across the life-course and across generations. To study this question, we tested a series of hypotheses about (a) personality-trait prediction of markers of healthy aging across the life-course, (b) developmental origins, stability and change of links between personality and healthy aging across time, and (c) intergenerational transmission of links between personality and healthy aging. For our analyses we used a measure that aggregates the contributions of Big 5 personality traits to healthy aging: a "vital personality" score. METHODS: Data came from two population-based longitudinal cohort studies, one based in New Zealand and the other in the UK, comprising over 6000 study members across two generations, and spanning an age range from birth to late life. RESULTS: Our analyses revealed three main findings: first, individuals with higher vital personality scores engaged in fewer health-risk behaviors, aged slower, and lived longer. Second, individuals' vital personality scores were preceded by differences in early-life temperament and were relatively stable across adulthood, but also increased from young adulthood to midlife. Third, individuals with higher vital personality scores had children with similarly vital partners, promoted healthier behaviors in their children, and had children who grew up to have more vital personality scores themselves, for genetic and environmental reasons. CONCLUSION: Our study shows how the health benefits associated with personality accrue throughout the life-course and across generations.

Linking stressful life events and chronic inflammation using suPAR (soluble urokinase plasminogen activator receptor).

Stressful life events have been linked to declining health, and inflammation has been proposed as a physiological mechanism that might explain this association. Using 828 participants from the Dunedin Longitudinal Study, we tested whether people who experienced more stressful life events during adulthood would show elevated systemic inflammation when followed up in midlife, at age 45. We studied three inflammatory biomarkers: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer biomarker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to index systemic chronic inflammation. Stressful life events were not associated with CRP or IL-6. However, people who experienced more stressful life events from age 38 to 44 had elevated suPAR at age 45, and had significantly greater increases in suPAR from baseline to follow-up across the same period. When examining stressful life events across the lifespan, both adverse childhood experiences (ACEs) and adult stressful life events were independently associated with suPAR at age 45. ACEs moderated the association of adult stressful life events and suPAR at age 45-children with more ACEs showed higher suPAR levels after experiencing stressful life events as adults. The results suggest systemic chronic inflammation is one physiological mechanism that could link stressful life events and health, and support the use of suPAR as a useful biomarker for such research.

Long-term Neural Embedding of Childhood Adversity in a Population-Representative Birth Cohort Followed for 5 Decades.

BACKGROUND: Childhood adversity has been previously associated with alterations in brain structure, but heterogeneous designs, methods, and measures have contributed to mixed results and have impeded progress in mapping the biological embedding of childhood adversity. We sought to identify long-term differences in structural brain integrity associated with childhood adversity. METHODS: Multiple regression was used to test associations between prospectively ascertained adversity during childhood and adversity retrospectively reported in adulthood with structural magnetic resonance imaging measures of midlife global and regional cortical thickness, cortical surface area, and subcortical gray matter volume in 861 (425 female) members of the Dunedin Study, a longitudinal investigation of a population-representative birth cohort. RESULTS: Both prospectively ascertained childhood adversity and retrospectively reported adversity were associated with alterations in midlife structural brain integrity, but associations with prospectively ascertained childhood adversity were consistently stronger and more widely distributed than associations with retrospectively reported childhood adversity. Sensitivity analyses revealed that these associations were not driven by any particular adversity or category of adversity (i.e., threat or deprivation) or by childhood socioeconomic disadvantage. Network enrichment analyses revealed that these associations were not localized but were broadly distributed along a hierarchical cortical gradient of information processing. CONCLUSIONS: Exposure to childhood adversity broadly is associated with widespread differences in midlife gray matter across cortical and subcortical structures, suggesting that biological embedding of childhood adversity in the brain is long lasting, but not localized. Research using retrospectively reported adversity likely underestimates the magnitude of these associations. These findings may inform future research investigating mechanisms through which adversity becomes embedded in the brain and influences mental health and cognition.

Financial Stressors During the Great Recession and Subsequent Risk of Early Mortality.

OBJECTIVE: The Great Recession in 2008 was a period of severe economic upheaval and myriad financial stressors. Financial stress is associated with poorer health, but for whom is this stress the most health-relevant? The current study examined the association between financial stressors and mortality, as well as whether this association varied based on people's financial status. METHODS: Participants from the Midlife in the United States study (n = 2760) were assessed before (2004-2005) and after (2013-2014) the Great Recession (2008). Mortality status was then tracked from 2013 to 2017. RESULTS: People who experienced more financial stressors during the Great Recession were at greater risk of early mortality over the 4-year follow-up (hazard ratio [HR] = 1.14 [1.00-1.29], p = .046). This association was moderated by the importance of financial security (B = 0.34 [0.08-0.59], p = .009). Financial stressors were more strongly associated with mortality among people who reported that financial security was important to their well-being (HR = 1.29 [1.08-1.54], p = .006) compared with people who reported it was not (HR = 1.02 [0.82-1.26], p = .89). Household income and subjective financial status did not moderate the association between financial stressors and mortality. CONCLUSIONS: Experiencing financial stressors during the Great Recession was associated with increased mortality over the 4-year follow-up period, particularly for people who reported financial security was important to their well-being. Interventions designed to reduce financial stress to improve health may benefit from targeting people for whom such stressors are particularly important.

State-Level Stay-at-Home Orders and Objectively Measured Movement in the United States During the COVID-19 Pandemic.

OBJECTIVE: Social distancing has been one of the primary interventions used to slow the spread of COVID-19 during the ongoing pandemic. Although statewide stay-at-home orders in the United States received a large degree of media and political attention, relatively little peer-reviewed research has examined the impacts of such orders on social distancing behaviors. METHOD: This study used daily GPS-derived movement from 2858 counties in the United States from March 1 to May 7, 2020, to test the degree to which changes in state-level stay-at-home orders were associated with movement outside the home. RESULTS: From early March to early April, people in counties with state-level stay-at-home orders decreased their movement significantly more than counties without state-level stay-at-home orders; 3.1% more people stayed within 1 mile of home, and 1.6% fewer vehicle miles were driven per day. From early April to early May, people in counties within states that ended their stay-at-home orders increased their movement significantly more than counties in states whose stay-at-home orders remained in place; 1.2% fewer people remained within 1 mile of home, and 6.2% more vehicle miles were driven per day. The magnitude of changes associated with state-level stay-at-home orders was many times smaller than the total changes in movement across all counties over the same periods. CONCLUSIONS: Stay-at-home orders were associated with greater social distancing but accounted for only part of this behavioral change. Research on behavior change would be useful to determine additional interventions that could support social distancing during the COVID-19 pandemic.

Posttraumatic Stress Disorder Treatment Effects on Cardiovascular Physiology: A Systematic Review and Agenda for Future Research.

Posttraumatic stress disorder (PTSD) is linked to both altered physiological functioning and poorer cardiovascular health outcomes, including an increased risk for cardiovascular disease and cardiovascular-related mortality. An important question is whether interventions for PTSD might ameliorate the risk for poorer health by improving cardiovascular physiological intermediaries. To begin to characterize the literature addressing this question, we conducted a systematic review of empirical studies examining the impact of PTSD interventions on cardiovascular physiological intermediaries, including blood pressure (BP), heart rate (HR), cardiac impedance, and subclinical atherosclerosis. Outcomes included both tonic (i.e., resting) cardiovascular functioning and cardiovascular reactivity (CVR). A total of 44 studies met the inclusion criteria. There was mixed evidence regarding whether PTSD treatment improved tonic cardiovascular functioning. There was stronger evidence that PTSD treatments reduced CVR to trauma-related stressors, particularly for higher-quality studies of cognitive behavioral interventions. No studies examined cardiac impedance or subclinical atherosclerosis. The studies had a high degree of heterogeneity in the populations sampled and interventions tested. Moreover, they generally included small sample sizes and lacked control conditions. Interventions for PTSD may improve cardiovascular physiological outcomes, particularly CVR to trauma cues, although additional methodologically rigorous studies are needed. We outline changes to future research that would improve the literature regarding this important question, including the more frequent use of control groups and larger sample sizes.

Posttraumatic Stress Disorder Symptom Cluster Structure in Prolonged Exposure Therapy and Virtual Reality Exposure.

The emotional processing theory of posttraumatic stress disorder (PTSD) posits that avoidance is central to PTSD development and maintenance. Prolonged exposure (PE) therapy, which clinically focuses on avoidance reduction, has strong empirical support as a PTSD treatment. Virtual reality exposure (VRE) has been utilized to accelerate avoidance reduction by increasing multisensory engagement. Although some exposure therapy studies have found associations between avoidance and PTSD symptoms, others have indicated that reexperiencing or hyperarousal symptoms drive symptom trajectories. Using a cross-lagged panel design, the present secondary data analysis examined temporal associations between clinician-assessed PTSD symptom clusters during treatment with PE, VRE, or a waitlist control condition. There were no significant differences between PE and VRE regarding symptom clusters at any assessment. Compared to the waitlist condition, individuals who received VRE or PE exhibited earlier reductions in avoidance/numbing symptoms, ß = -.19, 95% CI [-.33, -.05], followed by reductions in hyperarousal symptoms, ß = -.21, 95% CI [-.33, -.09]. Hyperarousal symptoms predicted changes in later avoidance/numbing and reexperiencing outcomes across treatment: pretreatment to midtreatment, ß = .29, 95% CI [.17, .42]; midtreatment to posttreatment, ß = .23, 95% CI [.07, .39]. Reexperiencing symptoms predicted changes in hyperarousal outcomes earlier in treatment, ß = .22, 95% CI [.02, .37], whereas avoidance/numbing symptoms predicted changes in hyperarousal outcomes later in treatment, ß = .18, 95% CI [.04, .32]. These findings support the efficacy of exposure therapy in addressing avoidance/numbing symptoms and highlight the potential importance of hyperarousal symptoms in relation to other symptom clusters.

Intimate partner violence and lower relationship quality are associated with faster biological aging.

The characteristics of people's relationships have relevance to health-high quality romantic relationships are associated with improved health whereas intimate partner violence is associated with poorer health. Recently, increased attention has been focused on the biological processes underpinning these associations. A geroscience approach-examining whether close relationship characteristics are associated with biological aging-would complement previous research focused on individual disease pathways. This study used participants from the Dunedin Study (N = 974) to investigate relationship characteristics and biological aging across almost 20 years, from age 26 to 45. Being involved in romantic relationships was associated with slower biological aging, ß = -0.12, p < .001. This difference represented 2.9 years of aging over the two decades. Greater relationship quality was also associated with slower biological aging, ß = -0.19, p < .001, whereas higher levels of partner violence were associated with faster biological aging, ß = 0.25, p < .001. A 1 SD difference in these characteristics was associated with a difference of 1.0 and 1.3 years of aging over the two decades, respectively. Secondary analyses suggested that experiencing violence from a partner was more strongly associated with biological aging than perpetrating violence, and that the experience of physical violence was more strongly associated with aging than psychological violence. These findings suggest that the characteristics of romantic relationships have relevance for biological aging in midlife. Interventions designed to increase relationship quality and decrease partner violence could reduce future morbidity and early mortality by slowing people's biological aging. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Social Distancing as a Health Behavior: County-Level Movement in the United States During the COVID-19 Pandemic Is Associated with Conventional Health Behaviors.

BACKGROUND: Social distancing-when people limit close contact with others outside their household-is a primary intervention available to combat the COVID-19 pandemic. The importance of social distancing is unlikely to change until effective treatments or vaccines become widely available. However, relatively little is known about how best to promote social distancing. Applying knowledge from social and behavioral research on conventional health behaviors (e.g., smoking, physical activity) to support public health efforts and research on social distancing is promising, but empirical evidence supporting this approach is needed. PURPOSE: We examined whether one type of social distancing behavior-reduced movement outside the home-was associated with conventional health behaviors. METHOD: We examined the association between GPS-derived movement behavior in 2,858 counties in USA from March 1 to April 7, 2020 and the prevalence of county-level indicators influenced by residents' conventional health behaviors. RESULTS: Changes in movement were associated with conventional health behaviors, and the magnitude of these associations were similar to the associations among the conventional health behaviors. Counties with healthier behaviors-particularly less obesity and greater physical activity-evidenced greater reduction in movement outside the home during the initial phases of the pandemic in the USA. CONCLUSIONS: Social distancing, in the form of reduced movement outside the home, is associated with conventional health behaviors. Existing scientific literature on health behavior and health behavior change can be more confidently used to promote social distancing behaviors during the COVID-19 pandemic.

Bereavement is associated with reduced systemic inflammation: C-reactive protein before and after widowhood.

BACKGROUND: Bereavement is associated with poorer health and early mortality. Increased systemic inflammation is one pathophysiological pathway thought to explain this health risk. However, few studies have examined systemic inflammation before and after widowhood. PURPOSE: The current study examined the associations between inflammation and widowhood status before and after bereavement in a sample of married adults who became widowed between assessments in the English Longitudinal Study of Ageing. METHODS: We examined levels and change over time in systemic inflammation, as assessed by C-reactive protein (CRP), among participants who became bereaved (n = 199). We then compared these results to a sample of participants whose spouse remained living, selected using a propensity score matching algorithm (n = 199). RESULTS: Contrary to expectations, widowed participants' CRP decreased following bereavement, d = -0.29, p < 0.001. Change in CRP was not associated with pre-loss depression levels, caregiving status, marital quality, number of chronic diseases, prescribed medications, body mass index, age, or sex. Compared to continuously married participants, widowed participants' evidenced a significantly greater decrease in CRP after their spouse's death, ß = -0.14, p < 0.001. CONCLUSIONS: Widowed adults' systemic inflammation decreased significantly following bereavement, both as a group and compared to people who remained married. We discuss possible explanations for this counterintuitive finding, including the measure of inflammation used in the study and the timing of the study measurements.