Psychosomatic Medicine最新文献

Objective: Childhood maltreatment is associated with shorter leukocyte telomere length (LTL). However, the influence of cardiac vagal control on this relation is unknown. We examined whether cardiac vagal control at rest and in response to stress moderates or cross-sectionally mediates the relationship between childhood maltreatment and LTL.

Methods: Participants were 1179 men and women (aged 65 [7.2] years) suffering from coronary artery disease or non-cardiovascular chronic disease. They completed a childhood maltreatment questionnaire and underwent a stress protocol while electrocardiogram was monitored. High-frequency heart rate variability (HF-HRV) measures were obtained at rest, during stress, and after stress in absolute and normalized units (nu). LTL was measured using quantitative polymerase chain reaction. Mediation and moderation analyses were performed.

Result: HF-HRV and HF-HRV in normalized units (HFnu) measures did not mediate the childhood maltreatment-LTL relation. However, baseline HFnu ( p = .027) and HFnu reactivity ( p = .051) moderated the relation. Specifically, maltreatment was associated with significantly lower LTL among those with baseline HFnu at ( b = -0.059, p = .003) or below the mean ( b = -0.103, p < .001), but not among those with higher baseline HFnu. It was also associated with significantly lower LTL among participants who showed either blunted ( b = -0.058, p = .004) or increased HFnu ( b = -0.099, p = .001) responses to stress but not in those with large decreases in HFnu.

Conclusions: Childhood maltreatment was associated with lower LTL in those who showed a distinct cardiac vagal profile at baseline and in response to stress. The mechanisms and implications remain to be determined.

Objective: This study aimed to investigate the frequency of long COVID diagnosis among patients infected with severe acute respiratory syndrome coronavirus 2 with preexisting psychiatric conditions versus those without preexisting psychiatric conditions.

Methods: The TriNetX Analytics platform, an aggregated electronic health record research network containing the deidentified electronic health record data of more than 90 million patients, was queried for patients who were diagnosed with COVID-19 infection based on International Classifications of Disease, Tenth Revision codes. Patients were stratified based on their preexisting psychiatric conditions, and new diagnoses of long COVID were recorded and reported as the primary outcome.

Results: Among 1,180,948 patients previously diagnosed with COVID-19, 17,990 patients (1.52%) were diagnosed with long COVID based on the newly implemented International Classifications of Disease, Tenth Revision code "U09: post-COVID-19 condition." After propensity score matching, patients with any preexisting psychiatric diagnosis had a 1.52 (95% confidence interval [CI] = 1.47-1.58) times greater prevalence of diagnosed long COVID within 180 days of infection than patients without preexisting psychiatric diagnoses. Patients with diagnosed anxiety disorders (relative risk [RR] = 1.64; 95% CI = 1.57-1.71), mood disorders (RR = 1.65; 95% CI = 1.57-1.72), bipolar disorder (RR = 1.37; 95% CI = 1.21-1.54), major depressive disorder (RR = 1.69; 95% CI = 1.56-1.83), psychotic disorders (RR = 1.23; 95% CI = 1.06-1.44), and substance use disorders (RR = 1.28; 95% CI = 1.22-1.36) had higher risks for long COVID diagnoses when compared with patients without preexisting psychiatric illness at the time of diagnosis.

Conclusions: Multiple preexisting psychiatric diagnoses are associated with an increased risk of being diagnosed with long COVID after COVID-19 infection.

Objective: Psychosocial stressors have been linked with accelerated biological aging in adults; however, few studies have examined stressors across the life course in relation to biological aging.

Methods: In 359 individuals (57% White, 34% Black) from the Child Health and Development Studies Disparities study, economic (income, education, financial strain), social (parent-child relations, caretaker responsibilities) and traumatic (death of a sibling or child, violence exposure) stressors were assessed at multiple time points (birth and ages 9, 15, and 50 years). Experiences of major discrimination were assessed at age 50. Life period stress scores were then assessed as childhood (birth-age 15 years) and adulthood (age 50 years). At age 50 years, participants provided blood samples, and DNA methylation was assessed with the EPIC BeadChip. Epigenetic age was estimated using six epigenetic clocks (Horvath, Hannum, Skin and Blood age, PhenoAge, GrimAge, Dunedin Pace of Aging). Age acceleration was determined using residuals from regressing chronologic age on each of the epigenetic age metrics. Telomere length was assessed using the quantitative polymerase chain reaction-based methods.

Results: In linear regression models adjusted for race and gender, total life stress, and childhood and adult stress independently predicted accelerated aging based on GrimAge and faster pace of aging based on the DunedinPace. Associations were attenuated after adjusting for smoking status. In sex-stratified analyses, greater childhood stress was associated with accelerated epigenetic aging among women but not men. No associations were noted with telomere length.

Conclusions: We found that cumulative stressors across the life course were associated with accelerated epigenetic age, with differences by sex (e.g., accelerated among women). Further research of this association in large and diverse samples is needed.

Objective: Structural forms of stigma and discrimination are associated with adverse health outcomes across numerous stigmatized groups, including lesbian, gay, and bisexual (LGB) individuals. However, the biological consequences of structural stigma among LGB populations are understudied. To begin to address this gap, we assessed associations between indicators of structural stigma (i.e., state-level policies) targeting LGB individuals and allostatic load (AL) indices representing physiological dysregulations.

Methods: Pooled data from the continuous 2001-2014 National Health and Nutritional Examination Survey were analyzed (LGB: n = 864; heterosexual: n = 20,310). Ten state-level LGB-related policies (e.g., employment nondiscrimination protections, same-sex marriage) were used to operationalize structural stigma. A sex-specific AL index representing 11 immune, metabolic, and cardiovascular biomarkers was estimated. Multilevel models were used to examine associations between structural stigma and AL, net of nine individual-level characteristics (e.g., education, race/ethnicity, age, and health behaviors).

Results: Sexual minority men living in states with low levels of structural stigma experienced significantly lower AL ( β = -0.45, p = .02) compared with sexual minority men living in states with high structural stigma (i.e., fewer protective policies). There was no significant association between structural stigma and AL among sexual minority women.

Conclusions: By demonstrating direct associations between structural stigma and indices of physiological dysregulation, our findings provide a mechanistic understanding of how the social environment can "get under the skin and skull" for sexual minority men in the United States. Future research should explore whether these mechanisms generalize to other marginalized groups exposed to structural stigma.

Objective: The effects of trauma exposure on depression risk and severity are well established, but psychosocial and biological factors that impact or explain those relationships remain poorly understood. This study examined the moderating and mediating effects of perceived control and inflammation in the relationship between trauma and depression.

Methods: Moderation analyses and longitudinal mediation analyses were conducted on data from 945 adults who completed all three waves (spanning around 19 years) of the Midlife Development in the United States (MIDUS) study and the MIDUS Biomarker Study. Data were collected during a phone interview, self-report surveys distributed in the mail, and an in-person blood draw. Two dimensions of perceived control-mastery and constraints-were examined separately in all analyses.

Results: Perceived control did not significantly moderate the relationship between trauma and depression severity at MIDUS 2 ( b = 0.03, SE = .02, p = .091). Constraints significantly mediated the relationship between trauma and MIDUS 3 depression (indirect effect = 0.03, SE = 0.01, p = .016) but not after accounting for MIDUS 2 depression. Perceived control did not have a significant moderating effect in the relationships between trauma and inflammation or inflammation and depression.

Conclusions: Findings from this study revealed that perceived control may be better characterized as an explanatory factor rather than a buffer in trauma-associated depression. Perceived constraints in particular may be a useful treatment target for trauma-associated depression. Further research is needed to examine whether these results generalize to populations other than among mostly non-Hispanic White adults in the United States.

Objective: Inflammation may be an integral physiological mechanism through which discrimination impacts cardiovascular health and contributes to racial health disparities. Limited research has examined psychosocial factors that protect against the negative effects of discrimination on inflammation. Perceived control is a promising possible protective factor, given that it has been shown to moderate the relationship between other psychosocial stressors and physiological outcomes. This study thus tested whether systemic inflammation mediated the link between discrimination and cardiovascular health and whether perceived control moderated this relationship.

Methods: Data for this project included 347 non-Hispanic/Latinx Black adults (mean [standard deviation] age = 51.64 [11.24] years; 33% female) taken from the Midlife in the United States study. Perceived control and daily discrimination were assessed via self-report, and inflammation was measured via circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, and tumor necrosis factor α. Cardiovascular health was measured by morbidity of cardiovascular conditions: heart disease, hypertension, and/or stroke.

Results: CRP (indirect effect: b = 0.004, 95% confidence interval [CI] = 0.001-0.007) and fibrinogen (indirect effect: b = 0.002, 95% CI = 0.0003-0.005) mediated the link between discrimination and cardiovascular conditions. Perceived control moderated the relationship between discrimination and CRP ( F (1, 293) = 4.58, Δ R2 = 0.013, b = -0.02, SE = 0.01, p = .033). CRP mediated the link between discrimination and cardiovascular conditions only for those who reported low levels of perceived control (Index = -0.003, 95% CI = -0.007 to -0.0001).

Conclusion: Findings provide empirical evidence of inflammation as a mechanism linking discrimination to cardiovascular conditions among Black Americans. Additionally, perceived control may be protective. Findings could suggest beliefs about control as a potential intervention target to help reduce the negative effects of discrimination on cardiovascular health among Black Americans.