Psychosomatic Medicine最新文献

Objective: Evidence shows that higher depressive symptoms are associated with mortality among people living with and beyond cancer (LWBC). However, prior studies have not accounted for a wider range of potential confounders, and no study has explored whether socioeconomic position (SEP) moderates the association. This study aimed to examine the association between depressive symptoms and mortality among people LWBC, and moderation by SEP.

Methods: Participants from the English Longitudinal Study of Aging, diagnosed with cancer and with a measure of depressive symptoms within 4 years after their diagnosis, were included. Elevated depressive symptoms were indicated by a score of ≥3 on the eight-item Center for Epidemiologic Studies Depression Scale. Cox regression models examined associations with all-cause mortality. Competing risk regression examined associations with cancer mortality.

Results: In 1352 people LWBC (mean age = 69.6 years), elevated depressive symptoms were associated with a 93% increased risk of all-cause mortality (95% confidence interval = 1.52-2.45) within the first 4 years of follow-up and a 48% increased risk within a 4- to 8-year follow-up (95% confidence interval = 1.02-2.13) after multivariable adjustment. Elevated depressive symptoms were associated with a 38% increased risk of cancer mortality, but not after excluding people who died within 1 year after baseline assessments. There were no interactions between depressive symptoms and SEP.

Conclusions: Elevated depressive symptoms are associated with a greater risk of all-cause mortality among people LWBC within an 8-year follow-up period. Associations between depressive symptoms and cancer mortality might be due to reverse causality.

Objective: Depression can promote inflammation and accelerate aging. Metformin, a widely prescribed antidiabetic, has shown promising preclinical evidence of aging-related health benefits, including decreased inflammation. The current study examined whether metformin usage buffers the association between depressive symptoms and inflammatory markers in two large samples of middle-aged and older, primarily White adults, and older Latino adults.

Methods: Data from the Midlife in the United States Study ( N = 1255) and the Sacramento Area Latino Study on Aging ( N = 1786) included information on medication use, depressive symptoms, and inflammatory markers, namely, interleukin 6 (IL-6), tumor necrosis factor α, and C-reactive protein (CRP). These data were merged into a harmonized sample, and the sample group variable was included in a three-way interaction for analysis.

Results: Specifically, in the Midlife in the United States Study sample, metformin buffered the association between depressive symptoms and CRP ( b = -0.029, standard error [SE] = 0.013, p = .007) and IL-6 ( b = 0.21, SE = 0.010, p = .046), whereas no significant association was found with tumor necrosis factor α. Metformin nonusers displayed higher depressive symptoms associated with elevated CRP ( b = 0.01, SE = 0.003, p < .001) and IL-6 ( b = 0.011, SE = 0.003, p < .001), whereas this association was not present among metformin users ( p values > .068). Conversely, in the Sacramento Area Latino Study on Aging sample, metformin use did not show a significant protective link.

Conclusions: Results from mostly White, highly educated adults supported a mitigating role of metformin in ties between depression, a well-known behavioral risk factor, and inflammation, a key source of biological aging. However, the benefits did not extend to a large sample of older Mexican Americans. The findings reveal a hidden potential benefit of this therapeutic agent and raise important questions around its health equity.

Trial registration: The study was preregistered on OSF ( https://osf.io/c92vw/ ).

Objective: Eudaimonic facets of psychological well-being (PWB), like purpose in life and sense of mastery, are associated with healthy aging. Variation in the gut microbiome may be one pathway by which mental health influences age-related health outcomes. However, associations between eudaimonic PWB and the gut microbiome are understudied. We examined whether purpose in life and sense of mastery, separately, were associated with features of the gut microbiome in older women.

Methods: Participants were from the Mind-Body Study ( N = 206, mean age = 61 years), a substudy of the Nurses' Health Study II cohort. In 2013, participants completed the Life Engagement Test and the Pearlin Mastery Scale. Three months later, up to two pairs of stool samples were collected, 6 months apart. Covariates included sociodemographics, depression, health status, and health behaviors. Analyses examined associations of PWB with gut microbiome taxonomic diversity, overall community structure, and specific species/pathways. To account for multiple testing, statistical significance was established using Benjamini-Hochberg adjusted p values (i.e., q values ≤0.25).

Results: We found no evidence of an association between PWB and gut microbiome alpha diversity. In multivariate analysis, higher purpose levels were significantly associated with lower abundance of species previously linked with poorer health outcomes, notably Blautia hydrogenotrophica and Eubacterium ventriosum ( q values ≤0.25). No significant associations were found between PWB and metabolic pathways.

Conclusions: These findings offer early evidence suggesting that eudaimonic PWB is linked with variation in the gut microbiome, and this might be one pathway by which PWB promotes healthy aging.

Objective: Aging is associated with increased proinflammatory gene expression and systemic inflammation, and psychosocial stress may accelerate these changes. Mindfulness interventions show promise for reducing psychosocial stress and extending healthspan. Inflammatory pathways may play a role. In a sample of lonely older adults, we tested whether mindfulness training reduces proinflammatory gene expression and protein markers of systemic inflammation.

Methods: Lonely older adults (65-85 years; N = 190) were randomly assigned to an 8-week Mindfulness-Based Stress Reduction (MBSR) or matched Health Enhancement Program (HEP). Blood was drawn before and after the intervention and at 3-month follow-up. In peripheral blood mononuclear cells, RNA profiling was used to assess transcriptional regulation by proinflammatory nuclear factor κB (NF-κB) as well as β-adrenergic cAMP response element-binding protein (CREB), antiviral interferon regulatory factor (IRF), and glucocorticoid receptor (GR) transcription factors. Plasma was assayed for proinflammatory markers interleukin 6 (IL-6) and C-reactive protein (CRP). Analyses tested time (pre, post, follow-up) by condition (MBSR versus HEP) effects.

Results: MBSR reduced NF-κB ( d = 0.17, p = .028) but did not alter CREB ( d = 0.10, p = .20), IRF ( d = 0.13, p = .086), or GR activity ( d = 0.14, p = .063) relative to HEP over time. Contrary to predictions, there were no time by condition effects of MBSR compared with HEP on reducing circulating IL-6 or CRP.

Conclusions: In lonely older adults, MBSR reduced cellular proinflammatory gene regulation in ways that would predict reduced disease risk. However, no similar effect was observed for circulating protein markers of inflammation. These results provide specificity about how mindfulness interventions may impact distinct inflammatory markers among aging adults in ways that may have important implications for healthspan.

Trial registration: Clinical Trials identifier NCT02888600.

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.