Psychosomatic Medicine最新文献

Objective: Social stress-loneliness, isolation, and low relationship quality-increase risks of aging-related diseases. However, the ways in which they intersect to undermine healthy aging remain poorly understood. We used latent class analysis to identify groups of older adults based on their social stress in both the United States and Mexico. Thereafter, we examined their cross-sectional associations with markers of functional and biological aging.

Method: Participants in the Health and Retirement Study (HRS; N = 8316) and Mexican Health and Aging Study (MHAS; N = 15,001) reported their loneliness, isolation (i.e., living alone), and relationship quality with spouse, children, and friends. Outcomes included C-reactive protein, functional limitations, self-rated health, comorbidities, gait speed, and grip strength. Models controlled for demographics, health behaviors, and body mass index.

Results: In both countries, five classes emerged, a supported group and four with elevated social stress: a) strained, b) isolated, c) spousal ambivalence, and d) unhappily married. Compared with the others, strained participants in both samples had greater functional limitations, poorer self-rated health, and more comorbidities, as well as slower gait in HRS and weaker grip in MHAS. Generally, supported participants fared better than the other groups. In HRS, C-reactive protein levels differed between the strained group and others, but these associations were explained by health behaviors and body mass index.

Conclusions: Older adults in both countries with strained relationships fared worst in their aging-related outcomes, revealing new insights about the links between toxic social stress and unhealthy aging.

Abstract: The "geroscience hypothesis" posits that slowing the physiological processes of aging would lead to delayed disease onset and longer healthspan and lifespan. This shift from a focus on solely treating existing disease to slowing the aging process is a shift toward prevention, including a focus on risk factors found in the social environment. Although geroscience traditionally has focused on the molecular and cellular drivers of biological aging, more fundamental causes of aging may be found in the social exposome-the complex array of human social environmental exposures that shape health and disease. The social exposome may interact with physiological processes to accelerate aging biology. In this commentary, we review the potential of these insights to shape the emerging field of translational geroscience. The articles in this special issue highlight how social stress and social determinants of health are associated with biomarkers of aging such as inflammation, epigenetic clocks, and telomeres, and spotlight promising interventions to mitigate stress-related inflammation. For geroscience to incorporate the social exposome into its translational agenda, studies are needed that elucidate and quantify the effects of social exposures on aging and that consider social exposures as intervention targets. The life course perspective allows us to measure both exposures and aging biology over time including sensitive periods of development and major social transitions. In addition, given rapid changes in the measurement of aging biology, which include machine learning techniques, multisystem phenotypes of aging are being developed to better reflect whole body aging, replacing reliance on single system biomarkers. In this expanded and more integrated field of translational geroscience, strategies targeting factors in the social exposome hold promise for achieving aging health equity and extending healthy longevity.

Objective: In long-term relationships, conflict is inevitable, but physical and psychological aggression is not. Intimate partner violence is a known risk factor for age-related disease onset, and inflammation likely links the two. This study explores relationships between frequency of constructive (i.e., negotiation) and destructive (i.e., aggression) conflict tactics with inflammation in both younger and older adulthood. Based on the theory of inflammaging, the study investigates whether these associations were stronger in mid-to-late adulthood.

Methods: At one visit, 214 participants in long-term romantic relationships had their blood drawn to assess six inflammatory markers (interleukin-6 [IL-6], tumor necrosis factor α [TNF-α], C-reactive protein, serum amyloid A (SAA), soluble intercellular adhesion molecule (sICAM), soluble vascular cell adhesion molecule) and reported frequency of destructive and constructive conflict tactics with their partner in the past year on the Revised Conflict Tactics Scale short form.

Results: Age interacted with number of destructive conflicts per year to predict serum IL-6 ( F (1,200) = 5.3, p = .022), TNF-α ( F (1,180) = 4.2, p = .043), sICAM ( F (1,193) = 7.0, p = .008), and marginally SAA ( F (1,199) = 3.7, p = .055), such that middle-aged and older adults who reported more destructive tactics had higher inflammation. Also, the relationship between constructive conflict frequency and TNF-α also depended on age ( F (1,177) = 4.9, p = .029), in that older adults who reported a greater number of constructive tactics had lower TNF-α.

Conclusion: Couples' conflict tactics may influence levels of inflammation and therefore aging rate in mid-to-late life. Middle-aged and older adults may disproportionately benefit from a healthy partnership and suffer from an unhealthy partnership.

Objective: Lower socioeconomic status (SES) can accelerate immune aging; however, it is unknown whether and how lifespan socioeconomic context (SEC)-the relative wealth and quality of the communities an individual lives in across their lifespan-impacts immune aging. We examined the effects of childhood and adulthood SEC on late-differentiated immune cells and investigated the mediating and moderating role of cytomegalovirus (CMV), a key driver of immune aging.

Methods: Adults 60 years and older ( N = 109) reported their addresses from birth to age 60 years, which were coded for county-level employment, education, and income to construct a latent SEC variable, averaged across ages 0 to 18 years (childhood SEC) and 19 to 60 years (adulthood SEC). Blood was drawn semiannually for 5 years for CMV serostatus and flow cytometry estimates of late-differentiated CD8 + T and natural killer cells. Models were adjusted for chronological age, time, sex, and individual SES (current income and education).

Results: Lower childhood SEC was associated with higher percentages of late-differentiated CD8 + T and natural killer cells via CMV seropositivity (indirect effects, p values = .015-.028). In addition, an interaction between CMV serostatus and SEC on CD8 + T-cell aging ( p = .049) demonstrated that adulthood SEC was negatively associated with immune aging among CMV- but not CMV+ adults.

Conclusions: Beyond current SES, SEC related to immune aging in distinct patterns by lifespan phase. Lower childhood SEC importantly may influence who acquires CMV, which in turn predicts higher levels of immune aging, whereas higher adulthood SEC was protective against immune aging among CMV- older adults. These initial results need to be explored in larger samples.

Objective: Despite advances toward understanding the etiology of Alzheimer's disease (AD), it remains unclear which aspects of this disease are affected by environmental factors. Chronic life stress increases the risk of aging-related diseases including AD. The impact of stress on tauopathies remains understudied. We examined the effects of stress elicited by social (chronic subordination stress [CSS]) or psychological/physical (chronic restraint stress [CRS]) factors on the PS19 mouse model of tauopathy.

Methods: Male PS19 mice (average age, 6.3 months) were randomized to receive CSS or CRS, or to remain as singly housed controls. Behavioral tests were used to assess anxiety-like behaviors and cognitive functions. Immunofluorescence staining and Western blotting analysis were used to measure levels of astrogliosis, microgliosis, and tau burden. Immunohistochemistry was used to assess glucocorticoid receptor expression.

Results: PS19 mice exhibit neuroinflammation (glial fibrillary acidic protein, t tests: p = .0297; allograft inflammatory factor 1, t tests: p = .006) and tau hyperphosphorylation ( t test, p = .0446) in the hippocampus, reduced anxiety (post hoc, p = .046), and cognitive deficits, when compared with wild-type mice. Surprisingly, CRS reduced hippocampal levels of both total tau and phospho-tau S404 ( t test, p = .0116), and attenuated some aspects of both astrogliosis and microgliosis in PS19 mice ( t tests, p = .068-.0003); however, this was not associated with significant changes in neurodegeneration or cognitive function. Anxiety-like behaviors were increased by CRS (post hoc, p = .046). Conversely, CSS impaired spatial learning in Barnes maze without impacting tau phosphorylation or neurodegeneration and having a minimal impact on gliosis.

Conclusions: Our results demonstrate that social or psychological stress can differentially impact anxiety-like behavior, select cognitive functions, and some aspects of tau-dependent pathology in PS19 male mice, providing entry points for the development of experimental approaches designed to slow AD progression.

Objective: Parental trauma exposure and trauma-related distress can increase the risk of adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines the associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism.

Methods: Mothers ( n = 127) and a subset of the fathers ( n = 84) reported on PTSD symptoms before conception. Mothers provided blood spots in the second and third trimesters that were assayed for CRP. At age 4 years, children provided buccal cells for measurement of telomere length. Models adjusted for parental age, socioeconomic status, maternal prepregnancy body mass index, child biological sex, and child age.

Results: Mothers' PTSD symptoms were significantly associated with shorter child telomere length ( β = -0.22, SE = 0.10, p = .023). Fathers' PTSD symptoms were also inversely associated with child telomere length ( β = -0.21, SE = 0.11), although nonsignificant ( p = .065). There was no significant indirect effect of mothers' PTSD symptoms on child telomere length through CRP in pregnancy, but higher second-trimester CRP was significantly associated with shorter child telomere length ( β = -0.35, SE = 0.18, p = .048).

Conclusions: Maternal symptoms of PTSD before conception and second-trimester inflammation were associated with shorter telomere length in offspring in early childhood, independent of covariates. Findings indicate that intergenerational transmission of parental trauma may occur in part through accelerated biological aging processes and provide further evidence that prenatal proinflammatory processes program child telomere length.Open Science Framework Preregistration:https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97 .

Objective: This analysis examined if financial hardship was associated with age-related decrements in kidney function using a material-psychosocial-behavioral framework. We also tested if this association was mediated by comorbidity of cardiometabolic risk factors (obesity, elevated blood pressure, and insulin resistance).

Methods: Data from 1361 non-Hispanic Black and White adults (ages 26-94 years; non-Hispanic Black = 258) were obtained from the Wave 3 and Refresher phases of the Midlife in the United States project. Kidney function was based on serum creatinine-based estimated glomerular filtration rate (eGFR; Chronic Kidney Disease Epidemiology Collaboration formula without race adjustment). Financial hardship was evaluated in three domains: material (income to poverty line ratio, health insurance coverage, and public/government financial assistance), psychological (perceived financial status, control over financial status, and perceived financial strains), and behavioral responses (financial adjustment/coping such as sold possessions and cutting back on spending).

Results: More severe financial hardship (overall score and in each domain) was associated with age-related decrements in eGFR, even after adjusting for sociodemographic, education, and health-related covariates. The association between financial hardship and age-related decrements in eGFR was conditional on sex but not race. Finally, cardiometabolic risk factors mediated the association between financial hardship and age-related decrements in eGFR.

Conclusions: These findings affirm the negative effects of financial hardship on age-related decrements in renal clearance. In addition to incorporating traditionally used indicators of SES, such as education and income, future research on social hallmarks of aging should also consider the role of financial hardship on the aging process and age-related diseases.

Objective: Short sleep and insomnia are each associated with a greater risk of age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relates to epigenetic age among older adults.

Methods: A total of 3795 men (46.3%) and women aged 56 to 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 Health and Retirement Study 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 acceleration of GrimAge of 0.49 (95% confidence interval [CI] = 0.03-0.94 years; p = .04) and 1.29 (95% CI = 0.52-2.07 years; p = .002) years, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 [95% CI = 0.004-0.033; p = .02] and 0.022 [95% CI = -0.004 to 0.048; p = .11]). Compared with healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95% CI = 0.07-1.87 years, p = .04) and a greater DunedinPACE (0.032; 95% CI = 0.003-0.060, p = .04).

Conclusions: Our findings indicate that 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 of comorbidity and mortality.