Objective: Anxiety and depression predict poor physical health longitudinally, but are neglected in primary care settings compared to other risk factors such as obesity and smoking. Further, anxiety ...has been less commonly studied than depression, and whether anxiety has unique predictive effects for physical health is unknown. We compared anxiety and depression to obesity and smoking as predictors of physical health indices and examined unique predictive effects of anxiety and depression. Method: Using data from the Health and Retirement study, a US population-based cohort study of older adults, we tested longitudinal associations of anxiety and depression symptoms with onset of self-reported physical health indices (N = 15,418; M age = 68). Medical illnesses (heart disease, stroke, arthritis, high blood pressure, diabetes, and cancer) and somatic symptoms (stomach problems, shortness of breath, dizziness, back pain, headache, pain, and eyesight difficulties) were assessed on two occasions over four years. Anxiety and depression were measured at the initial time point and tested as predictors of medical illness and somatic symptom onset. Results: Anxiety and depression symptoms predicted greater incidence of nearly all medical illnesses and somatic symptoms. Effects were as strong as or stronger than those of obesity and smoking, and anxiety and depression independently increased risk for most physical health indices assessed. Conclusions: Findings suggest that anxiety and depression are as strongly predictive of poor future physical health as obesity and smoking and that anxiety is independently linked to poor physical health. Greater attention should be paid towards these conditions in primary care.
•We tested longitudinal associations of depression and anxiety with inflammation.•Inflammation had a bidirectional relationship with depression in older adults.•Higher inflammation predicted ...worsening depressive symptoms in women, but not men.•More depressive symptoms predicted increasing inflammation in men, but not women.•Associations between anxiety and inflammation were not significant.
Depression and anxiety have been linked to elevated inflammation in cross-sectional and longitudinal studies. Yet, in terms of longitudinal studies, findings are inconsistent regarding whether depression predicts worsening inflammation or vice versa, and anxiety has been infrequently examined. Further, we know little about longitudinal relationships between inflammation and specific symptom profiles of depression and anxiety. The current study examined longitudinal associations between depression and anxiety symptoms and inflammation in 13,775 people (59% women, average age = 67) participating in the Health and Retirement Study - a population-based study focused on older adults. High sensitivity C-reactive protein and depression and anxiety symptoms were measured at two time-points separated by four years. We used cross-lagged panel models to examine bidirectional relationships, and tested interactions with gender. We found that depressive symptoms predicted increasing inflammation for men, but not for women, and inflammation predicted worsening depression for women, but not for men. These gender differences were driven by somatic symptoms. Specifically, somatic symptoms predicted increasing inflammation for men only and were predicted by inflammation for women only. Regardless of gender, inflammation predicted worsening dysphoric symptoms of depression, and lack of positive affect predicted increasing inflammation over time. Anxiety was not associated with inflammation longitudinally. These findings indicate bidirectional relationships between depressive symptoms and inflammation, but not between anxiety symptoms and inflammation, and that the direction of these effects may differ by gender and type of depressive symptom.
Summary Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological ...stress promotes oxidative damage are poorly understood. This study investigates the theory that cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F2α (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-oxoG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary cortisol responses were measured. The increase from 0 to 30 min was defined as “peak” cortisol reactivity, while the increase from 0 to 15 min was defined as “anticipatory” cortisol reactivity, representing a cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA ( p < .01). A moderated mediation model was tested, in which it was hypothesized that heightened anticipatory cortisol reactivity would mediate the relationship between perceived stress and elevated oxidative stress damage, but only among women under chronic stress. Consistent with this model, bootstrapped path analysis found significant indirect paths from perceived stress to 8-oxoG and IsoP (but not 8-OHdG) via anticipatory cortisol reactivity, showing the expected relations among chronically stressed participants ( p ≤ .01) Intriguingly, among those with low chronic stress exposure, moderate (compared to low) levels of perceived stress were associated with reduced levels of oxidative damage. Hence, this study supports the emerging model that chronic stress exposure promotes oxidative damage through frequent and sustained activation of the hypothalamic-pituitary-adrenal axis. It also supports the less studied model of ‘eustress’ – that manageable levels of life stress may enhance psychobiological resilience to oxidative damage.
Abstract Objective Experiencing potentially traumatic events across one’s lifecourse increases risk for poor physical health outcomes. Existing models emphasize the effects of any lifetime trauma ...exposure, risk accumulation (multiple traumas over time), and sensitive periods of exposure (specific exposure timepoints leading to lasting consequences). We examined how different indices of trauma exposure across the lifecourse were associated with later life arthritis, a common and debilitating health condition. Methods Data include 5,717 Health and Retirement Study participants (age mean = 65.3, SD = 12.9) who reported on lifetime adversity and trauma in 2006-2008. Lifetime trauma exposure was modeled as any trauma, accumulation of traumas, and lifecourse profiles (no exposure, childhood only, adulthood only, childhood and adulthood exposure). Outcomes included prevalent arthritis at baseline and incident arthritis across 12 years of follow-up. Covariate-adjusted generalized linear models for prevalence ratios (PR) and Cox proportional hazards models for hazard ratios (HR) were conducted. Results Any lifetime trauma was associated with both prevalent arthritis at baseline (PR = 1.13, 95%CI 1.05-1.22) and incident arthritis over 12 years (HR = 1.25, 95%CI 1.17-1.47). Greater trauma accumulation was significantly associated with both prevalent and incident arthritis. Childhood exposure was particularly strongly associated with prevalent and incident cases, with adulthood exposure being unassociated with incident arthritis. Across models, trauma exposure was associated with prevalent cases of both immune-related and osteoarthritis types. Conclusions Higher lifetime trauma burden, especially during childhood, may predispose individuals to arthritis later in life. Early intervention or prevention efforts should identify trauma as an important risk factor for musculoskeletal health across the lifecourse.
Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors ...elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic–pituitary–adrenal axis, sympathetic–adrenal–medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called
sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.
Gut microbiota composition as influenced by long-term diet may be associated with the risk of adult chronic diseases. Thus, establishing the relation of long-term diet, particularly starting from ...early life, with adult microbiota composition would be an important research advance.
We aimed to investigate the association of long-term intake of energy, carbohydrate, fiber, protein, and fat from infancy to late adolescence with microbiota composition in adulthood.
Within the prospective DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study, we sampled stool 1 or 2 times within 1 y from 128 adults (median age: 29 y). Microbiota composition was profiled by 16S ribosomal RNA sequencing. Annual dietary records from age 1 to 18 y were retrieved. We estimated trajectories of energy, energy-adjusted carbohydrate, fiber, protein, and fat intake with multilevel models, producing predicted intake at age 1 y and rates of change in intake. A multivariate, zero-inflated, logistic-normal model was used to model the association between intake trajectories and the composition of 158 genera in single-sampled individuals. Associations found in this model were confirmed in double-sampled individuals using a zero-inflated Beta regression model.
Adjusting for covariates and temporal differences in microbiota composition, long-term carbohydrate intake was associated with 3 genera. Specifically, carbohydrate intake at age 1 y was negatively associated with Phascolarctobacterium coefficient = −4.31; false discovery rate (FDR)–adjusted P = 0.006 and positively associated with Dialister (coefficient = 3.06; FDR-adjusted P = 0.003), and the rate of change in carbohydrate intake was positively associated with Desulfovibrio (coefficient = 13.16; FDR-adjusted P = 0.00039). Energy and other macronutrients were not associated with any genus.
This work links long-term carbohydrate intake to microbiota composition. Considering the associations of high carbohydrate intake and microbiota composition with some diseases, these findings could inform the development of gut microbiota–targeted dietary recommendations for disease prevention.
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Chronic psychological stress is associated with detrimental effects on physical health, and may operate in part through accelerated cell aging, as indexed by shorter telomeres at the ends of ...chromosomes. However, not all people under stress have distinctly short telomeres, and we examined whether exercise can serve a stress-buffering function. We predicted that chronic stress would be related to short telomere length (TL) in sedentary individuals, whereas in those who exercise, stress would not have measurable effects on telomere shortening.
63 healthy post-menopausal women underwent a fasting morning blood draw for whole blood TL analysis by a quantitative polymerase chain reaction method. Participants completed the Perceived Stress Scale (Cohen et al., 1983), and for three successive days reported daily minutes of vigorous activity. Participants were categorized into two groups-sedentary and active (those getting Centers for Disease Control-recommended daily amount of activity). The likelihood of having short versus long telomeres was calculated as a function of stress and exercise group, covarying age, BMI and education. Logistic regression analyses revealed a significant moderating effect of exercise. As predicted, among non-exercisers a one unit increase in the Perceived Stress Scale was related to a 15-fold increase in the odds of having short telomeres (p<.05), whereas in exercisers, perceived stress appears to be unrelated to TL (B = -.59, SE = .78, p = .45).
Vigorous physical activity appears to protect those experiencing high stress by buffering its relationship with TL. We propose pathways through which physical activity acts to buffer stress effects.
Abstract Background Posttraumatic stress disorder (PTSD) is associated with endocrine and immune abnormalities that could increase risk for autoimmune disorders. However, little is known about the ...risk for autoimmune disorders among individuals with PTSD. Methods We conducted a retrospective cohort study of 666,269 Iraq and Afghanistan veterans under age 55 who were enrolled in the Department of Veterans Affairs health care system between October 7, 2001, and March 31, 2011. Generalized linear models were used to examine if PTSD, other psychiatric disorders, and military sexual trauma exposure increased risk for autoimmune disorders, including thyroiditis, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and lupus erythematosus, adjusting for age, gender, race, and primary care visits. Results PTSD was diagnosed in 203,766 veterans (30.6%), and psychiatric disorders other than PTSD were diagnosed in an additional 129,704 veterans (19.5%). Veterans diagnosed with PTSD had significantly higher adjusted relative risk (ARR) for diagnosis with any of the autoimmune disorders alone or in combination compared with veterans with no psychiatric diagnoses (ARR = 2.00; 95% confidence interval, 1.91–2.09) and compared with veterans diagnosed with psychiatric disorders other than PTSD (ARR = 1.51; 95% confidence interval, 1.43–1.59; p < .001). The magnitude of the PTSD-related increase in risk for autoimmune disorders was similar in women and men, and military sexual trauma exposure was independently associated with increased risk in both women and men. Conclusions Trauma exposure and PTSD may increase risk for autoimmune disorders. Altered immune function, lifestyle factors, or shared etiology may underlie this association.
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