Background-The purpose of this study was to assess the relation of adverse childhood experiences (ACEs), including abuse, neglect, and household dysfunction, to the risk of ischemic heart disease (IHD) and to examine the mediating impact on this relation of both traditional IHD risk factors and psychological factors that are associated with ACEs. Methods and Results-Retrospective cohort survey data were collected from 17 337 adult health plan members from 1995 to 1997. Logistic regression adjusted for age, sex, race, and education was used to estimate the strength of the ACE-IHD relation and the mediating impact of IHD risk factors in this relation. Nine of 10 categories of ACEs significantly increased the risk of IHD by 1.3-to 1.7-fold versus persons with no ACEs. The adjusted odds ratios for IHD among persons with Ն7 ACEs was 3.6 (95% CI, 2.4 to 5.3). The ACE-IHD relation was mediated more strongly by individual psychological risk factors commonly associated with ACEs than by traditional IHD risk factors. We observed significant association between increased likelihood of reported IHD (adjusted ORs) and depressed affect (2.1, 1.9 to 2.4) and anger (2.5, 2.1 to 3.0) as well as traditional risk factors (smoking, physical inactivity, obesity, diabetes and hypertension), with ORs ranging from 1.2 to 2.7. Conclusions-We found a dose-response relation of ACEs to IHD and a relation between almost all individual ACEs and IHD. Psychological factors appear to be more important than traditional risk factors in mediating the relation of ACEs to the risk of IHD. These findings provide further insights into the potential pathways by which stressful childhood experiences may increase the risk of IHD in adulthood.
OBJECTIVE -The goal of this study was to determine whether depressive symptoms predict type 2 diabetes. RESEARCH DESIGN AND METHODS-We analyzed data on depressive symptoms (including recent fatigue, sleep disturbance, feelings of hopelessness, loss of libido, and increased irritability) in a longitudinal, biracial cohort study of 11,615 initially nondiabetic adults aged 48 -67 years, who were subsequently followed for 6 years for the development of type 2 diabetes.RESULTS -At baseline, depressive symptoms were positively associated with BMI, fasting insulin, systolic blood pressure, caloric intake, physical inactivity, and current smoking (all P Ͻ 0.05). In prospective analyses, after adjusting for age, race, sex, and education, individuals in the highest quartile of depressive symptoms had a 63% increased risk of developing diabetes compared with those in the lowest quartile (relative hazard [RH] 1.63, 95% CI 1.31-2.02). This relation persisted after adjustment for stress-associated lifestyle factors (smoking, physical activity, caloric intake, and adiposity) (1.28, 1.02-1.60) and metabolic covariates (fasting insulin and glucose, lipids, blood pressure, and adiposity) (1.38, 1.10 -1.73).CONCLUSIONS -In this cohort, depressive symptoms predicted incident type 2 diabetes. This relation is only partially explained by demographic, metabolic, and lifestyle factors. Possible neuroendocrine mediators of the stress-obesity-diabetes relationship require further evaluation in prospective cohort studies that use an established tool to assess depression and incorporate neurohormonal measurements. Diabetes Care 27:429 -435, 2004T here has been a growing interest in depression as a novel risk factor for the development of type 2 diabetes as several studies have demonstrated that the presence of depressive symptoms is predictive of incident type 2 diabetes (1,2). Possible mechanisms include the influence of depressive symptoms on behaviors, such as physical activity, diet, and adherence to treatment recommendations (3-7), or their influence on the activity of the hypothalamic-pituitaryadrenal (HPA) axis and sympathetic nervous system (8 -13). Similar mechanisms have been proposed for parallel observations regarding depressive symptoms as predictors of coronary heart disease (14). Previous epidemiological studies of psychological risk factors as predictors of diabetes, however, have been limited by small sample sizes, limited physiological data, and reliance on self-report of diabetes measures (1,2).The Atherosclerosis Risk in Communities (ARIC) study is an attractive study in which to evaluate this relationship because data from standardized measurements are available on clinical outcomes, such as type 2 diabetes, and on depressive symptoms (as captured by a Vital Exhaustion Questionnaire) in a large, biracial, community-based cohort of middle-aged adults who were followed over a 6-year period. Therefore, we conducted a prospective analysis of depressive symptoms as predictors of type 2 diabetes in middleaged adults in ARIC....
Background-Increased research attention is being paid to the negative impact of anger on coronary heart disease (CHD). Methods and Results-This study examined prospectively the association between trait anger and the risk of combined CHD (acute myocardial infarction [MI]/fatal CHD, silent MI, or cardiac revascularization procedures) and of "hard" events (acute MI/fatal CHD). Participants were 12 986 black and white men and women enrolled in the Atherosclerosis Risk In Communities study. In the entire cohort, individuals with high trait anger, compared with their low anger counterparts, were at increased risk of CHD in both event categories. The multivariate-adjusted hazard ratio (HR) (95% CI) was 1.54 (95% CI 1.10 to 2.16) for combined CHD and 1.75 (95% CI 1.17 to 2.64) for "hard" events. Heterogeneity of effect was observed by hypertensive status. Among normotensive individuals, the risk of combined CHD and of "hard" events increased monotonically with increasing levels of trait anger. The multivariate-adjusted HR of CHD for high versus low anger was 2.20 (95% CI 1.36 to 3.55) and for moderate versus low anger was 1.32 (95% CI 0.94 to 1.84). For "hard" events, the multivariate-adjusted HRs were 2.69 (95% CI 1.48 to 4.90) and 1.35 (95% CI 0.87 to 2.10), respectively. No statistically significant association between trait anger and incident CHD risk was observed among hypertensive individuals. Conclusions-Proneness to anger places normotensive middle-aged men and women at significant risk for CHD morbidity and death independent of the established biological risk factors.
The objective of the study was to determine which component of an anger-prone personality more strongly predicts coronary heart disease (CHD) risk. Proneness to anger, as assessed by the Spielberger Trait Anger Scale, is composed of two distinct subcomponents-anger-temperament and anger-reaction. Participants were 12,990 middle-aged Black men and women and White men and women from the Atherosclerosis Risk in Communities Study who were followed for the occurrence of acute myocardial infarction (MI)/fatal CHD, silent MI, or cardiac revascularization procedures (average = 53 months; maximum = 72 months) through December 31, 1995. Among normotensive persons, a strong, angry temperament (tendency toward quick, minimally provoked, or unprovoked anger) was associated with combined CHD (acute MI/fatal CHD, silent MI, or cardiac revascularization procedures) (multivariate-adjusted hazard ratio = 2.10, 95% confidence interval: 1.34, 3.29) and with 'hard" events (acute MI/fatal CHD) (multivariate adjusted hazard ratio = 2.28, 95% confidence interval: 1.29, 4.02). CHD event-free survival among normotensives who had a strong, angry temperament was not significantly different from that of hypertensives at either level of anger. These data suggest that a strong, angry temperament rather than anger in reaction to criticism, frustration, or unfair treatment places normotensive, middle-aged persons at increased risk for cardiac events and may confer a CHD risk similar to that of hypertension.
There has been mounting evidence suggesting that psychosocial factors, including anger proneness, depression and social isolation, are risk factors for coronary heart disease (CHD). 1,2 Studies have shown a positive relationship between anger proneness and CHD risk factors. The Atherosclerosis Risk in Communities (ARIC) Study found that anger proneness was an independent risk factor for CHD among normotensive, middle-aged men and women. 3 A meta-analysis reviewing several major epidemiological studies concluded that depression is an independent risk factor in the development of CHD in initially healthy people, with an overall relative risk of 1.64. 4 Other studies have also shown that depression increases short and long term mortality risk in patients with known CHD. 5,6 Lack of social support also portends a poor prognosis in patients after myocardial infarction (MI). 7,8 For example, among MI survivors, those with low to moderate levels of perceived social support had a 1-year post-CHD mortality rate about twofold higher than those with high levels of social support. 9 Furthermore, there is an interaction between depression and social support in relation to MI survival. 9 Although epidemiologic evidence is indicative, the results of psychosocial interventions after MI have
Vital exhaustion, defined as excessive fatigue, feelings of demoralization, and increased irritability, has been identified as a risk factor for incident and recurrent cardiac events, but there are no prospective studies of this association in United States samples. We examined the predictive value of vital exhaustion for incident myocardial infarction or fatal coronary heart disease (CHD) among middle-aged men and women in four US communities. Participants were 12,895 black or white men and women enrolled in the Atherosclerosis Risk In Communities (ARIC) Study cohort and followed for the occurrence of cardiac morbidity and mortality from 1990 through 2002 (maximum follow-up = 13.0 years). Vital exhaustion was assessed using the 21-item Maastricht Questionnaire, and partitioned into approximate quartiles for statistical analyses. High vital exhaustion (the fourth quartile) predicted adverse cardiac events in age-, gender-, and race-center-adjusted analyses (1.69 [95% C.I: 1.40 to 2.05]) and in analyses further adjusted for educational level, body mass index, plasma low density lipoprotein-and high density lipoprotein-cholesterol, systolic and diastolic blood pressure levels, diabetes mellitus, cigarette smoking status, and pack-years of cigarette smoking (1.46 [95% C.I: 1.20 to 1.79]). The risk for adverse cardiac events increased monotonically from the first through the fourth quartile of vital exhaustion. The probabilities of adverse cardiac events over time were significantly higher in people with high vital exhaustion compared to those with low exhaustion (p = 0.002). In conclusion, vital exhaustion predicts the long-term risk for adverse cardiac events in men and women, independent of the established biomedical risk factors.
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