SHERITA HILL GOLDEN, MD, MHS 3,4OBJECTIVE -It has been argued that the relationship between depression and diabetes is bi-directional, but this hypothesis has not been explicitly tested. This systematic review examines the bi-directional prospective relationships between depression and type 2 diabetes.RESEARCH DESIGN AND METHODS -A search was conducted using Medline for publications from 1950 through 2007. Reviewers assessed the eligibility of each report by exposure/outcome measurement and study design. Only comparative prospective studies of depression and type 2 diabetes that excluded prevalent cases of depression (for diabetes predicting depression) or diabetes (for depression predicting diabetes) were included. Two sets of pooled risk estimates were calculated using random effects: depression predicting type 2 diabetes and type 2 diabetes predicting depression.RESULTS -Of 42 full-text publications reviewed, 13 met eligibility for depression predicting onset of diabetes, representing 6,916 incident cases. Seven met criteria for diabetes predicting onset of depression, representing 6,414 incident cases. The pooled relative risk (RR) for incident depression associated with baseline diabetes was 1.15 (95% CI 1.02-1.30). The RR for incident diabetes associated with baseline depression was 1.60 (1.37-1.88).CONCLUSIONS -Depression is associated with a 60% increased risk of type 2 diabetes. Type 2 diabetes is associated with only modest increased risk of depression. Future research should focus on identifying mechanisms linking these conditions.

Crucial advances have been made in our knowledge of the social determinants of health and health behaviors. Existing research on health disparities, however, generally fails to address a known paradox in the literature: While blacks have higher risk of medical morbidity relative to non-Hispanic whites, blacks have lower rates of common stress-related forms of psychopathology such as major depression and anxiety disorders. In this article we propose a new theoretical approach, the Environmental Affordances Model, as an integrative framework for the origins of both physical and mental health disparities. We highlight early empirical support and a growing body of experimental animal and human research on self-regulatory health behaviors and stress coping that is consistent with the proposed framework. We conclude that transdisciplinary approaches, such as the Environmental Affordances Model, are needed to understand the origins of group-based disparities to implement effective solutions to racial and ethnic group inequalities in physical and mental health.

Prevalence of depression is associated inversely with some indicators of socioeconomic position, and the stress of social disadvantage is hypothesized to mediate this relation. Relative to whites, blacks have a higher burden of most physical health conditions but, unexpectedly, a lower burden of depression. This study evaluated an etiologic model that integrates mental and physical health to account for this counterintuitive patterning. The Baltimore Epidemiologic Catchment Area Study (Maryland, 1993-2004) was used to evaluate the interaction between stress and poor health behaviors (smoking, alcohol use, poor diet, and obesity) and risk of depression 12 years later for 341 blacks and 601 whites. At baseline, blacks engaged in more poor health behaviors and had a lower prevalence of depression compared with whites (5.9% vs. 9.2%). The interaction between health behaviors and stress was nonsignificant for whites (odds ratio (OR = 1.04, 95% confidence interval: 0.98, 1.11); for blacks, the interaction term was significant and negative (β: -0.18, P < 0.014). For blacks, the association between median stress and depression was stronger for those who engaged in zero (OR = 1.34) relative to 1 (OR = 1.12) and ≥2 (OR = 0.94) poor health behaviors. Findings are consistent with the proposed model of mental and physical health disparities.

Background Many of the symptoms, consequences, and risk factors for frailty are shared with late-life depression. However, thus far, few studies have addressed the conceptual and empirical interrelationships between these conditions. This review synthesizes existing studies that examined depression and frailty among older adults and provides suggestions for future research. Methods A search was conducted using PubMed for publications through 2010. Reviewers assessed the eligibility of each report and abstracted information on study design, sample characteristics, and key findings, including how depression and frailty were conceptualized and treated in the analysis. Results Of 133 abstracted articles, 39 full-text publications met inclusion criteria. Overall, both cross-sectional (n = 16) and cohort studies (n = 23) indicate that frailty, its components, and functional impairment are risk factors for depression. Although cross-sectional studies indicate a positive association between depression and frailty, findings from cohort studies are less consistent. The majority of studies included only women and non-Hispanic Whites. None used diagnostic measures of depression or considered antidepressant use in the design or analysis of the studies. Conclusions A number of empirical studies support for a bidirectional association between depression and frailty in later life. Extant studies have not adequately examined this relationship among men or racial/ethnic minorities, nor has the potential role of antidepressant medications been explored. An interdisciplinary approach to the study of geriatric syndromes such as late-life depression and frailty may promote cross-fertilization of ideas leading to novel conceptualization of intervention strategies to promote health and functioning in later life.

Social integration is negatively affected by driving cessation even among elders who feel competent in using alternative forms of transportation, at least concerning networks of friends.

Results indicate that the correlation of frailty and depression in late life is substantial. The association between the two constructs cannot be fully explained by symptom overlap, suggesting that psychological vulnerability may be an important component of frailty.

Objective-To describe trends in prevalence and incidence of depressive disorder in a cohort from Eastern Baltimore. Results-Older age, lower education, non-White race, and cognitive impairment are independent predictors of attrition due to death and loss of contact, but depressive disorder is not related to attrition. Prevalence rates rise for females between 1981, 1993, and 2004. Incidence rates in the period 1993-2004 are lower than the period 1981-1993, suggesting the rise in prevalence is due to increasing chronicity. MethodConclusion-There has been a rise in the prevalence of depression in the prior quarter century among middle-aged females.

Telomere length has been hypothesized to be a marker of cumulative exposure to stress, and stress is an established cause of depression and anxiety disorders. The goal of this study was to examine the relationship between depression, anxiety and telomere length, and to assess whether this relationship is moderated by race/ethnicity, gender, and/or antidepressant use. Data were from the National Health and Nutrition Examination Survey, 1999–2002. Telomere length was assessed using the quantitative polymerase chain reaction method of telomere length relative to standard reference DNA. Past year major depression (MD), generalized anxiety disorder (GAD) and panic disorder (PD), as well as depressed affect and anxious affect, were assessed using the Composite International Diagnostic Inventory (N=1,290). Multiple linear regression was used to assess the relationship between depression and anxiety disorders and telomere length. Among women, those with GAD or PD had shorter telomeres than those with no anxious affect (β: −0.07, p<0.01), but there was no relationship among men (β: 0.08, p>0.05). Among respondents currently taking an antidepressant, those with MD had shorter telomeres than those without (β: −.26, p<.05), but there was no association between MD and telomere length among those not using antidepressants (β: −.00, p>.05). Neither depressive nor anxiety disorders were directly associated with telomere length in young adults. There was suggestive evidence that pharmacologically-treated MD is associated with shorter telomere length, likely reflecting the more severe nature of MD that has come to clinical attention.