Paola Gilsanz

Psychological Distress Across the Life Course and Cardiometabolic Risk: Findings From the 1958 British Birth Cohort Study.

BACKGROUND Research suggests cardiovascular and metabolic diseases are influenced by psychological distress in adulthood; however, this research is often limited to adult populations and/or a snapshot measure of distress. Given emerging recognition that cardiometabolic diseases have childhood origins, an important question is whether psychological distress earlier in life influences disease development. OBJECTIVES This study sought to assess whether life course patterns of psychological distress assessed from childhood through adulthood predict biomarkers of cardiometabolic risk in adulthood and whether effects of sustained distress differ from more limited exposure. METHODS The sample (n = 6,714) consists of members of the 1958 British Birth Cohort Study who completed repeated measures of psychological distress and a biomedical survey at age 45 years. Psychological distress profiles over the life course (no distress, childhood only, adulthood only, or persistent distress) were identified from 6 assessments between ages 7 and 42 years. Cardiometabolic risk was assessed by combining information on 9 biomarkers of immune, cardiovascular, and metabolic system function. Covariate adjusted linear regression models were used to assess associations between distress profiles and cardiometabolic risk. RESULTS Compared with those with no distress, cardiometabolic risk was higher among people with psychological distress in childhood only (β = 0.11, SE = 0.03, p = 0.0002), in adulthood only (β = 0.09, SE = 0.03, p = 0.007), and persistent across the life course (β = 0.26, SE = 0.04, p < 0.0001). CONCLUSIONS Psychological distress at any point in the life course is associated with higher cardiometabolic risk. This is the first study to suggest that even if distress appears to remit by adulthood, heightened risk of cardiometabolic disease remains. Findings suggest early emotional development may be a target for primordial prevention and for promoting lifelong cardiovascular health.

Body mass index and cognitive function: the potential for reverse causation

Objective:Higher late life body mass index (BMI) is unrelated to or even predicts lower risk of dementia in late life, a phenomenon that may be explained by reverse causation due to weight loss during preclinical phases of dementia. We aim to investigate the association of baseline BMI and changes in BMI with dementia in a large prospective cohort, and to examine whether weight loss predicts cognitive function.Methods:Using a national cohort of adults average age 58 years at baseline in 1994 (n=7029), we investigated the associations between baseline BMI in 1994 and memory scores from 2000 to 2010. We also examined the association of BMI change from 1994 to 1998 with memory scores from 2000 to 2010. Last, to investigate reverse causation, we examined whether memory scores in 1996 predicted BMI trajectories from 2000 to 2010.Results:Baseline overweight predicted better memory scores 6 to 16 years later (β=0.012, 95% confidence interval (CI)=0.001; 0.023). Decline in BMI predicted lower memory scores over the subsequent 12 years (β=−0.026, 95% CI= −0.041; −0.011). Lower memory scores at mean age 60 years in 1996 predicted faster annual rate of BMI decline during follow-up (β=−0.158 kg m−2 per year, 95% CI= −0.223; −0.094).Conclusion:Consistent with reverse causation, greater decline in BMI over the first 4 years of the study was associated with lower memory scores over the next decade and lower memory scores was associated with a decline in BMI. These findings suggest that preclinical dementia predicts weight loss for people as early as their late 50s.

Changes in Depressive Symptoms and Incidence of First Stroke Among Middle-Aged and Older US Adults

Background Although research has demonstrated that depressive symptoms predict stroke incidence, depressive symptoms are dynamic. It is unclear whether stroke risk persists if depressive symptoms remit. Methods and Results Health and Retirement Study participants (n=16 178, stroke free and noninstitutionalized at baseline) were interviewed biennially from 1998 to 2010. Stroke and depressive symptoms were assessed through self-report of doctors’ diagnoses and a modified Center for Epidemiologic Studies - Depression scale (high was ≥3 symptoms), respectively. We examined whether depressive symptom patterns, characterized across 2 successive interviews (stable low/no, onset, remitted, or stable high depressive symptoms) predicted incident stroke (1192 events) during the subsequent 2 years. We used marginal structural Cox proportional hazards models adjusted for demographics, health behaviors, chronic conditions, and attrition. We also estimated effects stratified by age (≥65 years), race or ethnicity (non-Hispanic white, non-Hispanic black, Hispanic), and sex. Stroke hazard was elevated among participants with stable high (adjusted hazard ratio 2.14, 95% CI 1.69 to 2.71) or remitted (adjusted hazard ratio 1.66, 95% CI 1.22 to 2.26) depressive symptoms compared with participants with stable low/no depressive symptoms. Stable high depressive symptom predicted stroke among all subgroups. Remitted depressive symptoms predicted increased stroke hazard among women (adjusted hazard ratio 1.86, 95% CI 1.30 to 2.66) and non-Hispanic white participants (adjusted hazard ratio 1.66, 95% CI 1.18 to 2.33) and was marginally associated among Hispanics (adjusted hazard ratio 2.36, 95% CI 0.98 to 5.67). Conclusions In this cohort, persistently high depressive symptoms were associated with increased stroke risk. Risk remained elevated even if depressive symptoms remitted over a 2-year period, suggesting cumulative etiologic mechanisms linking depression and stroke.

Childhood Psychological Distress as a Mediator in the Relationship Between Early-Life Social Disadvantage and Adult Cardiometabolic Risk: Evidence From the 1958 British Birth Cohort.

Objectives Prior research on the relationship between early adversity and adult chronic disease has often relied on retrospective reports of a limited range of exposures and has not considered childhood psychological distress as a mediator. We investigate whether distress in childhood is one pathway by which early social disadvantage leads to greater cardiometabolic risk in middle adulthood. Methods Data are from the 1958 British Birth Cohort study (sample n = 6027). We created an early social disadvantage index based on 16 exposures related to family and socioeconomic hardship from birth to age 7. Childhood psychological distress was ascertained from internalizing and externalizing symptoms at ages 7, 11, and 16 years. Cardiometabolic risk was assessed with a Z-standardized score derived from 9 immune, cardiovascular, and metabolic biomarkers measured at age 45. We used linear regression models and formal tests of mediation to assess relationships between disadvantage, distress, and subsequent cardiometabolic risk. Results Higher social disadvantage predicted increased adult cardiometabolic risk (&bgr; = 0.05; 95% CI = 0.03–0.07). Mediation analyses revealed a significant direct (path c′; &bgr; = 0.03; 95% CI = 0.01–0.05) and indirect (path ab; &bgr; = 0.02; 95% CI = 0.01–0.02) effect of social disadvantage on cardiometabolic risk, adjusting for potential confounders. Child psychological distress accounted for 37% (95% CI = 34–46%) of the observed association. Conclusions Results suggest childhood distress may be one factor on the pathway linking early disadvantage to higher risk of developing cardiometabolic diseases. Such results may point to the importance of blocking the translation of psychosocial to biological risk during a potentially sensitive developmental window.

Associations of Trauma Exposure and Posttraumatic Stress Symptoms With Venous Thromboembolism Over 22 Years in Women

Background Trauma exposure and posttraumatic stress disorder (PTSD) have been linked to myocardial infarction and stroke in women, with biological and behavioral mechanisms implicated in underlying risk. The third most common cardiovascular illness, venous thromboembolism (VTE), is a specific health risk for women. Given previous associations with other cardiovascular diseases, we hypothesized that high levels of trauma and PTSD symptoms would be associated with higher risk of incident VTE in younger and middle‐aged women. Methods and Results We used proportional hazards models to estimate hazard ratios (HRs) and 95% CIs for new‐onset VTE (960 events) over 22 years in 49 296 women in the Nurses’ Health Study II. Compared to no trauma exposure, both trauma exposure and PTSD symptoms were significantly associated with increased risk of developing VTE, adjusting for demographics, family history, and childhood adiposity. Women with the most PTSD symptoms exhibited the greatest risk elevation: trauma/6 to 7 symptoms: HR=2.42 (95% CI, 1.83–3.20); trauma/4 to 5 symptoms: HR=2.00 (95% CI, 1.55–2.59); trauma/1 to 3 symptoms: HR=1.44 (95% CI, 1.12–1.84); trauma/no symptoms: HR=1.72 (95% CI, 1.43–2.08). Results were similar, although attenuated, when adjusting for VTE‐relevant medications, medical conditions, and health behaviors. Conclusions Women with the highest PTSD symptom levels had nearly a 2‐fold increased risk of VTE compared to women without trauma exposure in fully adjusted models. Trauma exposure alone was also associated with elevated VTE risk. Trauma and PTSD symptoms may be associated with a hypercoagulable state. Treatment providers should be aware that women with trauma exposure and PTSD symptoms may be vulnerable to VTE.

Posttraumatic stress disorder and accelerated aging: PTSD and leukocyte telomere length in a sample of civilian women

Studies in male combat veterans have suggested posttraumatic stress disorder (PTSD) is associated with shorter telomere length (TL). We examined the cross‐sectional association of PTSD with TL in women exposed to traumas common in civilian life.

Early life predictors of Atrial Fibrillation-related mortality: Evidence from the Health and Retirement Study

Prior research found that Americans born in 6 southeastern states (the AF-risk zone) had elevated risk of AF-related mortality, but no mechanisms were identified. We hypothesized the association between AF-related mortality and AF-risk zone birth is explained by indicators of childhood social disadvantage or adult risk factors. In 24,323 participants in the US Health and Retirement Study, we found that birth in the AF-risk zone was significantly associated with hazard of AF-related mortality. Among whites, the relationship was specific to place of birth, rather than place of adult residence. Neither paternal education nor subjectively assessed childhood SES predicted AF-related mortality. Conventional childhood and adult cardiovascular risk factors did not explain the association between place of birth and AF-related mortality.

Changes in depressive symptoms and subsequent risk of stroke in the cardiovascular health study

Background and Purpose— Depression is associated with stroke, but the effects of changes in depressive symptoms on stroke risk are not well understood. This study examined whether depressive symptom changes across 2 successive annual assessments were associated with incident stroke the following year. Methods— We used visit data from 4319 participants of the Cardiovascular Health Study who were stroke free at baseline to examine whether changes in depressive symptoms classified across 2 consecutive annual assessments predicted incident first stroke during the subsequent year. Depressive symptoms were assessed using the 10-item Center for Epidemiologic Studies Depression scale (high versus low at ≥10). Survival models were inverse probability weighted to adjust for demographics, health behaviors, medical conditions, past depressive symptoms, censoring, and survival. Results— During follow-up, 334 strokes occurred. Relative to stable low scores of depressive symptoms, improved depression symptoms were associated with almost no excess risk of stroke (adjusted hazards ratio, 1.02; 95% confidence interval, 0.66–1.58). New-onset symptoms were nonsignificantly associated with elevated stroke risk (adjusted hazards ratio, 1.44; 95% confidence interval, 0.97–2.14), whereas persistently high depressive symptoms were associated with elevated adjusted hazard of all-cause stroke (adjusted hazards ratio, 1.65; 95% confidence interval, 1.06–2.56). No evidence for effect modification by race, age, or sex was found. Conclusions— Persistently high symptoms of depression predicted elevated hazard of stroke. Participants with improved depressive symptoms had no elevation in stroke risk. Such findings suggest that strategies to reduce depressive symptoms may ameliorate stroke risk.

Validation of a theoretically motivated approach to measuring childhood socioeconomic circumstances in the Health and Retirement Study

Childhood socioeconomic status (cSES) is a powerful predictor of adult health, but its operationalization and measurement varies across studies. Using Health and Retirement Study data (HRS, which is nationally representative of community-residing United States adults aged 50+ years), we specified theoretically-motivated cSES measures, evaluated their reliability and validity, and compared their performance to other cSES indices. HRS respondent data (N = 31,169, interviewed 1992–2010) were used to construct a cSES index reflecting childhood social capital (cSC), childhood financial capital (cFC), and childhood human capital (cHC), using retrospective reports from when the respondent was <16 years (at least 34 years prior). We assessed internal consistency reliability (Cronbach’s alpha) for the scales (cSC and cFC), and construct validity, and predictive validity for all measures. Validity was assessed with hypothesized correlates of cSES (educational attainment, measured adult height, self-reported childhood health, childhood learning problems, childhood drug and alcohol problems). We then compared the performance of our validated measures with other indices used in HRS in predicting self-rated health and number of depressive symptoms, measured in 2010. Internal consistency reliability was acceptable (cSC = 0.63, cFC = 0.61). Most measures were associated with hypothesized correlates (for example, the association between educational attainment and cSC was 0.01, p < 0.0001), with the exception that measured height was not associated with cFC (p = 0.19) and childhood drug and alcohol problems (p = 0.41), and childhood learning problems (p = 0.12) were not associated with cHC. Our measures explained slightly more variability in self-rated health (adjusted R2 = 0.07 vs. <0.06) and number of depressive symptoms (adjusted R2 > 0.05 vs. < 0.04) than alternative indices. Our cSES measures use latent variable models to handle item-missingness, thereby increasing the sample size available for analysis compared to complete case approaches (N = 15,345 vs. 8,248). Adopting this type of theoretically motivated operationalization of cSES may strengthen the quality of research on the effects of cSES on health outcomes.

Childhood Psychological Distress and Healthy Cardiovascular Lifestyle 17–35 Years Later: The Potential Role of Mental Health in Primordial Prevention

Background Maintaining a healthy lifestyle in adulthood has been shown to significantly reduce cardiovascular disease risk. Increasing evidence suggests that behavioral risk factors for cardiovascular disease are established in childhood; however, limited research has evaluated whether childhood psychological factors play a role. Purpose To evaluate the association between childhood psychological distress and young to mid adulthood healthy lifestyle. Methods Using prospective data from the 1958 British Birth Cohort, we assessed whether psychological distress in childhood (captured by internalizing and externalizing symptoms at ages 7, 11, and 16 years) predicted healthy lifestyle at ages 33 (N = 10,748) and 42 (N = 9,581) years. Healthy lifestyle was measured using an index previously demonstrated to predict cardiovascular disease, consisting of five components: absence of smoking, moderate alcohol consumption, regular physical activity, healthy diet, and ideal body weight. Results Few participants (3.8% at age 33 years and 2.8% at age 42 years) endorsed all five healthy lifestyle components. Linear regression models, adjusting for potential child- and family-level confounders, revealed that higher distress levels in childhood were negatively associated with healthy lifestyle at age 33 years (β = -0.11, SE = 0.01, p < .001) and 42 years (β = -0.13, SE = 0.01, p < .001). Higher distress was also associated with significantly lower odds of endorsing each lifestyle component, except physical activity, at both ages. Additional analyses indicated that childhood distress levels were highest among those whose lifestyle scores were low at age 33 and further declined between ages 33 and 42. Conclusions Psychological distress in childhood may indicate children at risk of less healthy lifestyle practices later in life. Although our findings are preliminary, psychological distress may also provide an important target for public health interventions aimed at preventing cardiovascular disease.