Psychosomatic Medicine最新文献

Objective: The objectives of this study were to a) evaluate associations between social isolation and change in cognition over a 3-year period, and b) evaluate whether physical activity mediates the association between social isolation and cognition change.

Methods: Using baseline and follow-up 1 data from the Canadian Longitudinal Study on Aging, latent change score models, incorporating direct and indirect pathways, were constructed to estimate the indirect effect of social isolation on cognitive change through physical activity. Multigroup models were constructed based on age group (45-65 versus 65+ years) and sex to allow for varying estimates across age and sex. The final analytic sample included 51,338 participants.

Results: Indirect effects of social isolation on cognition through physical activity were evident in men and women 65+ years old for memory change ( = -0.005 [99.9% confidence interval = -0.007 to -0.002], p < .001 in both groups) and in male adults 65+ years old for executive function change ( = -0.01 [99.9% confidence interval = -0.02 to -0.006], p < .001). Statistically significant indirect effects were not observed for adults between 45 and 65 years old.

Conclusions: Social isolation is associated with diminished physical activity, and in turn, diminished physical activity is associated with decline in memory in older women and men, with larger declines in executive function in older men. Public health initiatives to promote physical activity-perhaps incorporating social interaction-among older adults experiencing social isolation could be one way to mitigate the negative impact of social isolation on cognitive health.

Objective: Loneliness is linked to interleukin 6 (IL-6), a marker of systemic inflammation, which chronically has deleterious effects on physical and mental health across the adult life span. This study investigated cross-sectional relationships among loneliness, IL-6, demographics, multimorbidity, depression, obesity, friendship quantity, and slowed gait.

Methods: Data from the Midlife Development in the United States Biomarker Project, a national adult sample ( N = 822; age range, 26-78 years) was used for this study. The PROCESS macro tested the hypothesis that IL-6 would mediate the relationship between loneliness and gait, after adjusting for demographic and health risk factors.

Results: Age ( β = 0.292, p < .001), sex ( β = 0.197, p < .001), body mass index (BMI, β = 0.374, p < .001), waist-hip ratio ( β = 0.242, p < .001), and loneliness ( β = 0.089, p = .025) but not multimorbidity ( β = 0.043, p = .20), depression history ( β = 0.022, p = .47), depression symptoms ( β = 0.036, p = .28), and number of friends ( β = 0.022, p = .46) contributed to the variance in IL-6. Serial mediation analyses supported the chained effect of loneliness on walking time through BMI and IL-6. Results also showed specific indirect effects of BMI and IL-6 on walking time, suggesting more than one pathway by which loneliness influences health.

Conclusions: These results suggest that loneliness may increase the risk of systemic inflammation, leading to slowed gait and adverse health outcomes. Psychosocial interventions that address loneliness may provide an optimal treatment target for reducing inflammation and preventing declines in health.

Objective: Psychosocial stress is transduced into disease risk through energy-dependent release of hormones from the hypothalamic-pituitary-adrenal and sympathetic-adrenal-medullary axes. The levels of glucocorticoid and adrenergic hormones, together with the sensitivity of tissues to their signaling, define stress responses. To understand existing pathways responsible for the psychobiological transduction of stressful experiences, we provide a quantitative whole-body map of glucocorticoid and adrenergic receptor (AR) expression.

Methods: We systematically examined gene expression levels for the glucocorticoid receptor (GR), α- and β-ARs (AR-α1B, AR-α2B AR-β2, and AR-β3), across 55 different organs using the Human Protein Atlas and Human Proteome Map datasets. Given that mitochondria produce the energy required to respond to stress, we leveraged the Human Protein Atlas and MitoCarta3.0 data to examine the link between stress hormone receptor density and mitochondrial gene expression. Finally, we tested the functional interplay between GR activation and AR expression in human fibroblast cells.

Results: The GR was expressed ubiquitously across all investigated organ systems, whereas AR subtypes showed lower and more localized expression patterns. Receptor co-regulation, meaning the correlated gene expression of multiple stress hormone receptors, was found between GR and AR-α1B, as well as between AR-α1B and AR-α2B. In cultured human fibroblasts, activating the GR selectively increased AR-β2 and AR-α1B expression. Consistent with the known energetic cost of stress responses, GR and AR expressions were positively associated with the expression of specific mitochondrial pathways.

Conclusions: Our results provide a cartography of GR and AR expression across the human body. Because stress-induced GR and AR signaling triggers energetically expensive cellular pathways involving energy-transforming mitochondria, the tissue-specific expression and co-expression patterns of hormone receptor subtypes may in part determine the resilience or vulnerability of different organ systems.