Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study.

Exposure to stress is a risk factor for poor health and accelerated aging. Immune aging, including declines in naïve and increases in terminally differentiated T cells, plays a role in immune health and tissue specific aging, and may contribute to elevated risk for poor health among those who experience high psychosocial stress. Past data have been limited in estimating the contribution of life stress to the development of accelerated immune aging and investigating mediators such as lifestyle and cytomegalovirus (CMV) infection. This study utilizes a national sample of 5,744 US adults over age 50 to assess the relationship of social stress (viz., everyday discrimination, stressful life events, lifetime discrimination, life trauma, and chronic stress) with flow cytometric estimates of immune aging, including naïve and terminally differentiated T cell percentages and the ratio of CD4+ to CD8+ cells. Experiencing life trauma and chronic stress was related to a lower percentage of CD4+ naïve cells. Discrimination and chronic stress were each associated with a greater percentage of terminally differentiated CD4+ cells. Stressful life events, high lifetime discrimination, and life trauma were related to a lower percentage of CD8+ naïve cells. Stressful life events, high lifetime discrimination, and chronic stress were associated with a higher percentage of terminally differentiated CD8+ cells. High lifetime discrimination and chronic stress were related to a lower CD4+:CD8+ ratio. Lifestyle factors and CMV seropositivity partially reduced these effects. Results identify psychosocial stress as a contributor to accelerating immune aging by decreasing naïve and increasing terminally differentiated T cells.

Heterogeneity in the Association Between the Presence of Coronary Artery Calcium and Cardiovascular Events: A Machine-Learning Approach in the MESA Study.

BACKGROUND: Coronary artery calcium (CAC) has been widely recognized as an important predictor of cardiovascular disease (CVD). Given the finite resources, it is important to identify individuals who would receive the most benefit from detecting positive CAC by screening. However, the evidence is limited as to whether the burden of positive CAC on CVD differs by multidimensional individual characteristics. We sought to investigate the heterogeneity in the association between positive CAC and incident CVD. METHODS: This cohort study included adults from MESA (Multi-Ethnic Study of Atherosclerosis) ages ≥45 years and free of cardiovascular disease. After propensity score matching in a 1:1 ratio, we applied a machine learning causal forest model to (1) evaluate the heterogeneity in the association between positive CAC and incident CVD, and (2) predict the increase in CVD risk at 10-years when CAC>0 (versus CAC=0) at the individual level. We then compared the estimated increase in CVD risk when CAC>0 to the absolute 10-year atherosclerotic CVD (ASCVD) risk calculated by the 2013 American College of Cardiology/American Heart Association pooled cohort equations. RESULTS: Across 3328 adults in our propensity score-matched analysis, our causal forest model showed the heterogeneity in the association between CAC>0 and incident CVD. We found a dose-response relationship of the estimated increase in CVD risk when CAC>0 with higher 10-year ASCVD risk. Almost all individuals (2293 of 2428 [94.4%]) with borderline risk of ASCVD or higher showed ≥2.5% increase in CVD risk when CAC>0. Even among 900 adults with low ASCVD risk, 689 (69.2%) showed ≥2.5% increase in CVD risk when CAC>0; these individuals were more likely to be male, Hispanic, and have unfavorable CVD risk factors than others. CONCLUSIONS: The expected increases in CVD risk when CAC>0 were heterogeneous across individuals. Moreover, nearly 70% of people with low ASCVD risk showed a large increase in CVD risk when CAC>0, highlighting the need for CAC screening among such low-risk individuals. Future studies are needed to assess whether targeting individuals for CAC measurements based on not only the absolute ASCVD risk but also the expected increase in CVD risk when CAC>0 improves cardiovascular outcomes.

Short sleep and insomnia are associated with accelerated epigenetic age.

OBJECTIVE: Short sleep and insomnia are each associated with greater risk for age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relate to epigenetic age among older adults. METHODS: A total of 3,795 men (46.3%) and women aged 56-100 years from the Health and Retirement Study were included. Insomnia was defined as reporting at least one insomnia symptom (difficulty falling asleep, waking up at night, or waking up too early in the morning) and feeling unrested when waking up most of the time. Those reporting <6 hours of bedtime were categorized as short sleepers. Three second- or third-generation epigenetic age acceleration clocks were derived from the 2016 HRS Venous Blood Study. The linear regression analysis was adjusted for age, sex, race/ethnicity, education, and obesity status. RESULTS: Insomnia and short sleep were associated with an 0.49 (95%CI:0.03-0.94; P:0.04) and 1.29 (95%CI:0.52-2.07; P:0.002) years acceleration of GrimAge, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 (95%CI:0.004-0.033; P:0.02); 0.022(95%CI:-0.004-0.048; P:0.11)). Compared to healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95%CI:0.07-1.87; P:0.04) and a greater DunedinPACE (0.032; 95%CI:0.003-0.060; P:0.04). CONCLUSION: Our findings indicate short sleep, insomnia, and the combination of the two, are linked to epigenetic age acceleration, suggesting that these individuals have an older biological age that may contribute to risk for comorbidity and mortality.

Social relationships and epigenetic aging in older adulthood: Results from the Health and Retirement Study.

Growing evidence suggests that social relationship quality can influence age-related health outcomes, although how the quality of one's relationships directly relates to the underlying aging process is less clear. We hypothesized that the absence of close relationships as well as lower support and higher strain within existing relationships would be associated with an accelerated epigenetic aging profile among older adults in the Health and Retirement Study. Adults (N = 3,647) aged 50-100 years completed ratings of support and strain in relationships with their spouse, children, other family members, and friends. They also provided a blood sample that was used for DNA methylation profiling to calculate a priori-specified epigenetic aging measures: Horvath, Hannum, PhenoAge, GrimAge, and Dunedin Pace of Aging methylation (DunedinPoAm38). Generalized linear models that adjusted for chronological age, sex, and race/ethnicity and applied a false discovery rate correction revealed that the absence of marital and friend relationships related to an older GrimAge and faster DunedinPoAm38. Among those with existing relationships, lower support from a spouse, child, other family, and friends and higher strain with friends related to an older PhenoAge and GrimAge and faster DunedinPoAm38. In secondary analyses that further adjusted for socioeconomic and lifestyle factors, lower support from other family members and friends was associated with greater epigenetic aging. Findings suggest that the absence of close relationships and lower support within existing relationships-particularly with family members and friends-relate to accelerated epigenetic aging in older adulthood, offering one mechanism through which social relationships might influence risk for age-related declines and disease.

Effects of stress-induced inflammation on reward processing in healthy young women.

BACKGROUND: Anhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing. METHODS: Healthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor. RESULTS: Stress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6. CONCLUSIONS: Contrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting. CLINICAL TRIAL REGISTRATION: NCT03828604.

Feeling needed: Effects of a randomized generativity intervention on well-being and inflammation in older women.

Generativity, or concern for and contribution to the well-being of younger generations, plays an important role in successful aging. The purpose of this study was to develop a novel, writing-based intervention to increase feelings of generativity and test the effect of this intervention on well-being and inflammation in a sample of older women. Participants in this study (n = 73; mean age = 70.9 years, range 60-86 years) were randomly assigned to a 6-week generativity writing condition (writing about life experiences and sharing advice with others) or a control writing condition (neutral, descriptive writing). Self-reported measures of social well-being, mental health, and physical health, as well as objective measures of systemic and cellular levels of inflammation (plasma pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-α; genome-wide RNA transcriptional profiling), were assessed pre- and post-intervention. The generativity intervention led to significant improvements across multiple domains, including increases in participation in social activities, decreases in psychological distress, more positive expectations regarding aging in the physical health domain, and decreases in pro-inflammatory gene expression. Thus, this study provides preliminary evidence for the ability of a novel, low-cost, low-effort intervention to favorably impact inflammation and well-being in older women.

Sleep problems in adolescence are prospectively linked to later depressive symptoms via the cortisol awakening response.

Sleep disturbance is a symptom of and a well-known risk factor for depression. Further, atypical functioning of the HPA axis has been linked to the pathogenesis of depression. The purpose of this study was to examine the role of adolescent HPA axis functioning in the link between adolescent sleep problems and later depressive symptoms. Methods: A sample of 157 17-18 year old adolescents (61.8% female) completed the Pittsburgh Sleep Quality Inventory (PSQI) and provided salivary cortisol samples throughout the day for three consecutive days. Two years later, adolescents reported their depressive symptoms via the Center for Epidemiological Studies Depression Scale (CES-D). Results: Individuals (age 17-18) with greater sleep disturbance reported greater depressive symptoms two years later (age 19-20). This association occurred through the indirect effect of sleep disturbance on the cortisol awakening response (CAR) (indirect effect = 0.14, 95%CI [.02 -.39]). Conclusions: One pathway through which sleep problems may lead to depressive symptoms is by up-regulating components of the body's physiological stress response system that can be measured through the cortisol awakening response. Behavioral interventions that target sleep disturbance in adolescents may mitigate this neurobiological pathway to depression during this high-risk developmental phase.

Psychological resilience and the gene regulatory impact of posttraumatic stress in Nepali child soldiers.

Adverse social conditions in early life have been linked to increased expression of proinflammatory genes and reduced expression of antiviral genes in circulating immune cells-the conserved transcriptional response to adversity (CTRA). However, it remains unclear whether such effects are specific to the Western, educated, industrialized, rich, and democratic (WEIRD) cultural environments in which previous research has been conducted. To assess the roles of early adversity and individual psychological resilience in immune system gene regulation within a non-WEIRD population, we evaluated CTRA gene-expression profiles in 254 former child soldiers and matched noncombatant civilians 5 y after the People's War in Nepal. CTRA gene expression was up-regulated in former child soldiers. These effects were linked to the degree of experienced trauma and associated distress-that is, posttraumatic stress disorder (PTSD) severity-more than to child soldier status per se. Self-perceived psychological resilience was associated with marked buffering of CTRA activation such that PTSD-affected former child soldiers with high levels of personal resilience showed molecular profiles comparable to those of PTSD-free civilians. These results suggest that CTRA responses to early life adversity are not restricted to WEIRD cultural contexts and they underscore the key role of resilience in determining the molecular impact of adverse environments.

Associations of objective versus subjective social isolation with sleep disturbance, depression, and fatigue in community-dwelling older adults.

Objective: Older adults are at higher risk of experiencing social isolation, which has been linked to impaired physical and mental health. The link between social isolation and health might be due to objective deprivation of social network and/or subjective experience of loneliness. This community-based cross-sectional study examined whether the associations between social isolation and behavioral symptoms including sleep disturbance, depression, and fatigue are mostly explained by its subjective component. Methods: Randomly selected 2541 community-dwelling individuals in Los Angeles aged ≥60 years were telephone-interviewed regarding their objective and subjective social isolation (respectively social network size and loneliness), sleep disturbance, depression, and fatigue. Results: When objective and subjective social isolation were separately included in multivariate regression models, both were significantly associated with behavioral symptoms. However, once they were simultaneously included in the same multivariate models, while subjective social isolation remained strongly associated (adjusted beta 0.24 for sleep disturbance [P < 0.001], 0.44 for depression [P < 0.001], 0.17 for fatigue [P < 0.001]), objective social isolation was weakly or non-significantly associated (-0.04 for sleep disturbance [P = 0.03], -0.01 for depression [P = 0.48], -0.003 for fatigue [P = 0.89]). Additionally, those with objective social isolation were found to have worse symptoms mostly when they also experienced subjective social isolation. Conclusions: Older adults with objective social isolation may experience sleep disturbance, depression, and fatigue because they feel socially isolated, not just because they are deprived of social networks. Interventions that target social isolation might serve as potential treatments for improving behavioral health of older adults, especially by targeting its subjective component.

Cardiovascular and Metabolic Risk in Women in the First Year Postpartum: Allostatic Load as a Function of Race, Ethnicity, and Poverty Status.

OBJECTIVE: Allostatic load (AL) represents multisystem physiological "wear-and-tear" reflecting emerging chronic disease risk. We assessed AL during the first year postpartum in a diverse community sample with known health disparities. STUDY DESIGN: The Eunice Kennedy Shriver National Institute for Child Health and Human Development Community Child Health Network enrolled 2,448 predominantly low-income African-American, Latina, and White women immediately after delivery of liveborn infants at ≥20 weeks' gestation, following them over time with interviews, clinical measures, and biomarkers. AL at 6 and 12 months postpartum was measured by body mass index, waist:hip ratio, blood pressure, pulse, hemoglobin A1c, high-sensitive C-reactive protein, total cholesterol and high-density lipoprotein, and diurnal cortisol slope. RESULTS: Adverse AL health-risk profiles were significantly more prevalent among African-American women compared with non-Hispanic Whites, with Latinas intermediate. Breastfeeding was protective, particularly for White women. Complications of pregnancy were associated with higher AL, and disparities persisted or worsened through the first year postpartum. CONCLUSION: Adverse AL profiles occurred in a substantial proportion of postpartum women, and disparities did not improve from birth to 1 year. Breastfeeding was protective for the mother.

Social stratification and allostatic load: shapes of health differences in the MIDUS study in the United States.

Social stratification is an important mechanism of human organization that helps to explain health differences between demographic groups commonly associated with socioeconomic gradients. Individuals, or group of individuals, with similar health profiles may have had different stratification experiences. This is particularly true as social stratification is a significant non-measurable source of systematic unobservable differences in both SES indicators and health statuses of disadvantage. The goal of the present study was to expand the bulk of research that has traditionally treated socioeconomic and demographic characteristics as independent, additive influences on health by examining data from the United States. It is hypothesized that variation in an index of multi-system physiological dysregulation - allostatic load - is associated with social differentiation factors, sorting individuals with similar demographic and socioeconomic characteristics into mutually exclusive econo-demographic classes. The data were from the Longitudinal and Biomarker samples of the national Study of Midlife Development in the US (MIDUS) conducted in 1995 and 2004/2006. Latent class analyses and regression analyses revealed that physiological dysregulation linked to socioeconomic variation among black people, females and older adults are associated with forces of stratification that confound socioeconomic and demographic indicators. In the United States, racial stratification of health is intrinsically related to the degree to which black people in general, and black females in particular, as a group, share an isolated status in society. Findings present evidence that disparities in health emerge from group-differentiation processes to the degree that individuals are distinctly exposed to the ecological, political, social, economic and historical contexts in which social stratification is ingrained. Given that health policies and programmes emanate from said legal and political environments, interventions should target the structural conditions that expose different subgroups to different stress risks in the first place.

Impact of Experience Corps® Participation on Children's Academic Achievement and School Behavior.

This article reports on the impact of the Experience Corps® (EC) Baltimore program, an intergenerational, school-based program aimed at improving academic achievement and reducing disruptive school behavior in urban, elementary school students in Kindergarten through third grade (K-3). Teams of adult volunteers aged 60 and older were placed in public schools, serving 15 h or more per week, to perform meaningful and important roles to improve the educational outcomes of children and the health and well-being of volunteers. Findings indicate no significant impact of the EC program on standardized reading or mathematical achievement test scores among children in grades 1-3 exposed to the program. K-1st grade students in EC schools had fewer principal office referrals compared to K-1st grade students in matched control schools during their second year in the EC program; second graders in EC schools had fewer suspensions and expulsions than second graders in non-EC schools during their first year in the EC program. In general, both boys and girls appeared to benefit from the EC program in school behavior. The results suggest that a volunteer engagement program for older adults can be modestly effective for improving selective aspects of classroom behavior among elementary school students in under-resourced, urban schools, but there were no significant improvements in academic achievement. More work is needed to identify individual- and school-level factors that may help account for these results.

Chronic Physiologic Effects of Stress Among Lesbian, Gay, and Bisexual Adults: Results From the National Health and Nutrition Examination Survey.

OBJECTIVE: Social disadvantage is associated with markers of physiological dysregulation, which is linked to disease trajectories. Chronic experiences with discrimination are thought to result in the accumulation of physiological "wear and tear" known as allostatic load (AL) among socially marginalized populations such as sexual minorities. Using a nationally representative US sample, we examined whether (1) people who self-identified as homosexual or bisexual display higher levels of AL than heterosexual individuals and (2) subgroups of sexual identity would further differ from each other as a consequence of distinct experiences of marginalization. METHODS: We use data from the 2001-2010 National Health and Nutrition Examination Survey. Employing multivariate regression methods with sex-specific analyses, we examined AL score differences among lesbian/gay (n = 211), bisexual (n = 307), homosexually experienced (n = 424), and exclusively heterosexual (n = 12,969) individuals, adjusting for possible confounding due to demographics, health indicators, and, among men, HIV infection status. RESULTS: Results indicate that elevated AL was more common in bisexual men compared with exclusively heterosexual men (adjusted ß = 0.25, 95% confidence interval [CI] = 0.05 to 0.44), with significantly higher levels of glycosylated hemoglobin A1c (adjusted odd ratio = 3.51, 95% CI = 1.46-7.92) and systolic blood pressure (adjusted odd ratio = 2.07, 95% CI = 1.02 to 4.18). Gay-identified men evidenced significantly lower AL (adjusted ß = -0.22, 95% CI = -0.41 to -0.04). No significant differences in AL were observed among women. CONCLUSIONS: These findings indicate that physiological dysregulation is more common in bisexual males compared with all other men. The results are discussed with regard to differences in health outcomes between individuals with different sexual orientations.

Social Support and Strain Across Close Relationships: A Twin Study.

Social relationships play a critical role in health and well-being throughout life. We analyzed the genetic and environmental variance co-variance structure for social support and strain across four sets of relationships including with one's co-twin, spouse/partner, family and friends. The sample included 5288 Norwegian twins aged 40-80. Older people reported less support from their co-twin and friends and less strain from their family and friends. Genetic influences contribute importantly to variation across all the measures, with estimates ranging from 0 to 58%; variance due to shared environmental influences was most important for the twin-relationship, ranging from 0.11 to 0.42%. Social support was negatively correlated with social strain across all sets of relationships. With the exception of the co-twin relationship, these associations were primarily mediated by genetic and non-shared environmental effects.

The Roles of Parental Support and Family Stress in Adolescent Sleep.

The current study examines the association between parental support and adolescent sleep under varying levels of family stress. Participants included 316 adolescents (Mage  = 16.40 years, 43% male) and their parents (Mage  = 45.67 years, 91% mothers) from diverse ethnic backgrounds. Both adolescents and parents completed questionnaires and adolescents wore wrist actigraphs and completed self-reports on their sleep for 7 consecutive days. Results indicated that under contexts of family stress, more parental support was linked to longer sleep duration, less sleep variability, and less time spent awake during the night. Findings suggest that under contexts of family stress, cohesive family relationships may provide a sense of stability and security that is necessary for healthful sleep.

Modeling Multisystem Physiological Dysregulation.

OBJECTIVES: The purposes of this study were to compare the relative fit of two alternative factor models of allostatic load (AL) and physiological systems, and to test factor invariance across age and sex. METHODS: Data were from the Midlife in the United States II Biomarker Project, a large (n = 1255) multisite study of adults aged 34 to 84 years (56.8% women). Specifically, 23 biomarkers were included, representing seven physiological systems: metabolic lipids, metabolic glucose, blood pressure, parasympathetic nervous system, sympathetic nervous system, hypothalamic-pituitary-adrenal axis, and inflammation. For factor invariance tests, age was categorized into three groups (≤45, 45-60, and >60 years). RESULTS: A bifactor model where biomarkers simultaneously load onto a common AL factor and seven unique system-specific factors provided the best fit to the biomarker data (comparative fit index = 0.967, root mean square error of approximation = 0.043, standardized root mean square residual = 0.028). Results from the bifactor model were consistent with invariance across age groups and sex. CONCLUSIONS: These results support the theory that represents and operationalizes AL as multisystem physiological dysregulation and operationalizing AL as the shared variance across biomarkers. Results also demonstrate that in addition to the variance in biomarkers accounted for by AL, individual physiological systems account for unique variance in system-specific biomarkers. A bifactor model allows researchers greater precision to examine both AL and the unique effects of specific systems.

Sleep and Inflammation During Adolescence.

OBJECTIVE: To investigate the associations between objective and subjective dimensions of adolescent sleep and C-reactive protein (CRP), a key biomarker of inflammation that predicts chronic health problems in adulthood, and whether the associations vary as a function of adolescents' age. METHODS: A total of 315 adolescents (14.5-18.4 years) wore wrist actigraphs at night to objectively estimate their sleep duration and variability across nights, and completed the Pittsburgh Sleep Quality Index to assess their subjective sleep quality. CRP levels were assayed from dried blood spots obtained from finger pricks. To control for adiposity, age- and sex-specific body mass index percentiles were obtained from height and weight measurements. RESULTS: Nightly variability in sleep duration was associated with higher levels of CRP (b = 0.13, p = .045). Shorter average sleep duration was associated with higher CRP, but only among younger adolescents (b = -0.11, p = .041). Subjective sleep quality was not associated with CRP. CONCLUSIONS: The association of sleep with inflammation during adolescence seems more evident in objective dimensions of sleep duration and variability than in the subjective dimensions of sleep quality. Insufficient sleep may be particularly consequential for younger adolescents.

Parental support buffers the association of depressive symptoms with cortisol and C-reactive protein during adolescence.

Social experiences can affect the relationship between depression and physical health. The current study examined how social support from parents and friends may moderate the association of depressive symptoms with hypothalamic-pituitary-adrenal (HPA) axis activity and C-reactive protein among adolescents (N=316, Mage=16.40, SD=.74; 57% female) from diverse ethnic backgrounds (23.1% Asian, 29.1% European, 41.8% Latino, and 6.0% other backgrounds). Results indicated that parent support, but not friend support, moderated the link between depressive symptoms and both total daily cortisol output (a measure HPA activity) and C-reactive protein (a marker of inflammation). These patterns did not differ by ethnicity. Overall, the study highlights the continued, and perhaps accumulated, importance of parents during adolescence despite increasing needs for autonomy from and exploration outside of the family unit.

Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans.

Age-related disease risk has been linked to short sleep duration and sleep disturbances; however, the specific molecular pathways linking sleep loss with diseases of aging are poorly defined. Key cellular events seen with aging, which are thought to contribute to disease, may be particularly sensitive to sleep loss. We tested whether one night of partial sleep deprivation (PSD) would increase leukocyte gene expression indicative of DNA damage responses (DDR), the senescence-associated secretory phenotype (SASP), and senescence indicator p16(INK4a) in older adult humans, who are at increased risk for cellular senescence. Community-dwelling older adults aged 61-86years (n=29; 48% male) underwent an experimental partial sleep deprivation (PSD) protocol over 4 nights, including adaptation, an uninterrupted night of sleep, partial sleep deprivation (sleep restricted 3-7AM), and a subsequent full night of sleep. Blood samples were obtained each morning to assess peripheral blood mononuclear cell (PBMC) gene expression using Illumina HT-12 arrays. Analyses of microarray results revealed that SASP (p<.05) and DDR (p=.08) gene expression were elevated from baseline to PSD nights. Gene expression changes were also observed from baseline to PSD in NFKB2, NBS1 and CHK2 (all p's<.05). The senescence marker p16(INK4a) (CDKN2A) was increased 1day after PSD compared to baseline (p<.01), however confirmatory RT-PCR did not replicate this finding. One night of partial sleep deprivation activates PBMC gene expression patterns consistent with biological aging in this older adult sample. PSD enhanced the SASP and increased the accumulation of damage that initiates cell cycle arrest and promotes cellular senescence. These findings causally link sleep deprivation to the molecular processes associated with biological aging.