Optimizing approaches to addressing depression in cardiac patients: a comment on O'Neil et al

Comment on: Efficacy and feasibility of a tele-health intervention for acute coronary syndrome patients with depression: results of the "MoodCare" randomized controlled trial

Number of Recent Stressful Life Events and Incident Cardiovascular Disease: Moderation by Lifetime Depressive Disorder

Objective We investigated whether number of recent stressful life events is associated with incident cardiovascular disease (CVD) and whether this relationship is stronger in adults with a history of clinical depression. Methods Prospective data from 28,583 U.S. adults (mean age = 45 years) initially free of CVD who participated in Waves 1 (2001–2002) and 2 (2004–2005) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were examined. Number of past-year stressful life events (Wave 1), lifetime depressive disorder (Wave 1), and incident CVD (Wave 2) were determined by structured interviews. Results There were 1069 cases of incident CVD. Each additional stressful life event was associated with a 15% increased odds of incident CVD [Odds Ratio (OR) = 1.15, 95% Confidence Interval (CI): 1.11, 1.19]. As hypothesized, a stressful life events by lifetime depressive disorder interaction was detected (P = 0.003). Stratified analyses indicated that stressful life events had a stronger association with incident CVD among adults with (OR = 1.18, 95% CI: 1.10, 1.27, n = 4908) versus without (OR = 1.10, 95% CI: 1.07, 1.14, n = 23,675) a lifetime depressive disorder. Conclusion Our findings suggest that a greater number of recent stressful life events elevate the risk of new-onset CVD and that this risk is potentiated in adults with a history of clinical depression

Atypical depression and double depression predict new-onset cardiovascular disease in U.S. adults

BACKGROUND: Although depression is a risk factor for cardiovascular disease (CVD), it is unknown whether this risk varies across depressive disorder subtypes. Thus, we investigated atypical major depressive disorder (MDD) and double depression as predictors of new-onset CVD in a nationally representative sample of U.S. adults. METHODS: Prospective data from 28,726 adults initially free of CVD who participated in Wave 1 (2001-2002) and Wave 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were examined. Lifetime depressive disorder subtypes (Wave 1) and incident CVD (Wave 2) were determined by structured interviews. RESULTS: We identified 1,116 incident CVD cases. In demographics adjusted models, the atypical MDD group had a higher odds of incident CVD than the no depression history (OR = 2.19, 95% CI: 1.71-2.81, P < .001), dysthymic disorder only (OR = 1.61, 95% CI: 1.08-2.39, P = .019), and nonatypical MDD (OR = 1.46, 95% CI: 1.11-1.91, P = .006) groups. Likewise, the double depression group had a higher odds of incident CVD than the no depression history (OR = 2.17, 95% CI: 1.92-2.45, P < .001), dysthymic disorder only (OR = 1.59, 95% CI: 1.16-2.19, P = .004), and MDD only (OR = 1.46, 95% CI: 1.20-1.77, P < .001) groups. Relationships were similar but attenuated after adjustment for CVD risk factors and anxiety disorders. CONCLUSIONS: Adults with atypical MDD or double depression may be subgroups of the depressed population at particularly high risk of new-onset CVD. Thus, these subgroups may (a) be driving the overall depression-CVD relationship and (b) be in need of earlier and/or more intense CVD primary prevention efforts to reduce their excess CVD burden

Double Depression is Associated with Greater Risk of Incident Cardiovascular Disease than Major Depression: Data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC)

poster abstractEvidence suggests depressive disorders are risk factors for cardiovascular disease (CVD), however, little attention has been given to double depression (major depressive disorder (MDD) superimposed on dysthymia). The current study sought to determine if double depression is a stronger predictor of incident CVD due to greater duration of exposure and severity of depression in adults initially free of CVD. We analyzed data from 29,581 adults (mean age = 45 years, 58% female, 42% non-white) from Waves 1 (2001-2002) and 2 (2004-2005) of the NESARC study. At Wave 1, the Alcohol Use Disorder and Associated Disabilities Interview Schedule was administered to assess lifetime history of DSM-IV MDD and/or dysthymia. A 4-level variable was created for depression: no depression history (n=24,339), lifetime MDD only (n=4,028), lifetime dysthymia only (n=246), lifetime MDD and dysthymia (double depression; n=968). At Wave 2, participants who reported being diagnosed with myocardial infarction, stroke, angina, or arteriosclerosis in the past year were coded as having incident CVD; those diagnosed with myocardial infarction or stroke were coded as having had a hard CVD event. There were 1,380 CVD events and 365 hard CVD events. Logistic regression models adjusted for demographics (age, sex, race-ethnicity, education) and CVD risk factors (hypertension, hypercholesterolemia, diabetes, smoking, BMI) revealed that lifetime double depression (OR=1.72, 95% CI: 1.31-2.25, p.43). Our findings partially support our hypothesis and suggest that persons with double depression may have a stronger connection to an elevated CVD risk in which prevention efforts should be intensified

Depressive Symptoms are Associated with Poor Adherence to Some Lifestyle but not Medication Recommendations to Prevent Cardiovascular Disease: National Health and Nutrition Examination Survey (NHANES) 2005-2010

poster abstractDepression has been linked to poor medical adherence; however, most studies have involved persons with preexisting conditions, such as cardiovascular disease (CVD). Our aim was to examine relationships between depressive symptoms and adherence to medication and lifestyle recommendations intended to prevent CVD in a community sample. We selected adults ≥18 years (53%-56% female, 47%-52% non-white) with a history of hypertension and/or hypercholesterolemia, but free of CVD, who participated in 2005-2010 waves of NHANES – a survey of a large probability sample representative of the U.S. population. The Patient Health Questionnaire-9 (PHQ-9) was used to assess depressive symptoms (converted to z-scores). The NHANES Blood Pressure and Cholesterol questionnaire was used to assess self-reported adherence to five medication and lifestyle recommendations: take antihypertensive medication (N=3313), take lipid-lowering medication (N=2266), control/lose weight (N=2177), eat fewer high fat/cholesterol foods (N=2924), and increase physical activity (N=2540). Logistic regression models (adjusting for age, sex, race-ethnicity, education, body mass, diabetes, smoking status, daily alcohol intake and NHANES sample design) revealed that a 1-SD increase in PHQ-9 total score was associated with a 14% lower likelihood of adherence to the control/lose weight recommendation (OR=0.86, 95% CI: 0.75-0.98, p=.02) and a 25% lower likelihood of adherence to the increase physical activity recommendation (OR=0.75, 95% CI: 0.65-0.86, p<.001). PHQ-9 total score was not associated with the likelihood of adherence to antihypertensive medication (OR, 0.93, 95% CI: 0.82-1.05, p=0.21), lipid-lowering medication (OR=0.99, 95% CI: 0.86-1.14, p=0.90), or eat fewer high fat/cholesterol foods recommendations (OR=0.94, 95% CI: 0.82-1.08, p=0.40). Adherence rates for depressed verses nondepressed adults to the control/lose weight recommendation were 75% and 85% and the increase physical activity recommendation were 63% and 79%, respectively. Our findings suggest that poor adherence to weight and activity recommendations, but not medication and diet recommendations, may partially explain the excess CVD risk of depressed persons

Effect of collaborative depression treatment on risk for diabetes: A 9-year follow-up of the IMPACT randomized controlled trial

Considerable epidemiologic evidence and plausible biobehavioral mechanisms suggest that depression is an independent risk factor for diabetes. Moreover, reducing the elevated diabetes risk of depressed individuals is imperative given that both conditions are leading causes of death and disability. However, because no prior study has examined clinical diabetes outcomes among depressed patients at risk for diabetes, the question of whether depression treatment prevents or delays diabetes onset remains unanswered. Accordingly, we examined the effect of a 12-month collaborative care program for late-life depression on 9-year diabetes incidence among depressed, older adults initially free of diabetes. Participants were 119 primary care patients [M (SD) age: 67.2 (6.9) years, 41% African American] with a depressive disorder but without diabetes enrolled at the Indiana sites of the Improving Mood-Promoting Access to Collaborative Treatment (IMPACT) trial. Incident diabetes cases were defined as diabetes diagnoses, positive laboratory values, or diabetes medication prescription, and were identified using electronic medical record and Medicare/Medicaid data. Surprisingly, the rate of incident diabetes in the collaborative care group was 37% (22/59) versus 28% (17/60) in the usual care group. Even though the collaborative care group exhibited greater reductions in depressive symptom severity (p = .024), unadjusted (HR = 1.29, 95% CI: 0.69-2.43, p = .428) and adjusted (HR = 1.18, 95% CI: 0.61-2.29, p = .616) Cox proportional hazards models indicated that the risk of incident diabetes did not differ between the treatment groups. Our novel preliminary findings raise the possibility that depression treatment alone may be insufficient to reduce the excess diabetes risk of depressed, older adults

Effect of collaborative care for depression on risk of cardiovascular events: data from the IMPACT randomized controlled trial

OBJECTIVE: Although depression is a risk and prognostic factor for cardiovascular disease (CVD), depression trials involving cardiac patients have not observed the anticipated cardiovascular benefits. To test our hypothesis that depression treatment delivered before clinical CVD onset reduces risk of CVD events, we conducted an 8-year follow-up study of the Indiana sites of the Improving Mood-Promoting Access to Collaborative Treatment (IMPACT) randomized controlled trial. METHODS: Participants were 235 primary care patients 60 years or older with major depression or dysthymia who were randomized to a 12-month collaborative care program involving antidepressants and psychotherapy (85 without and 35 with baseline CVD) or usual care (83 without and 32 with baseline CVD). Hard CVD events (fatal/nonfatal) were identified using electronic medical record and Medicare/Medicaid data. RESULTS: A total of 119 patients (51%) had a hard CVD event. As hypothesized, the treatment × baseline CVD interaction was significant (p = .021). IMPACT patients without baseline CVD had a 48% lower risk of an event than did usual care patients (28% versus 47%, hazard ratio = 0.52, 95% confidence interval = 0.31-0.86). The number needed to treat to prevent one event for 5 years was 6.1. The likelihood of an event did not differ between IMPACT and usual care patients with baseline CVD (86% versus 81%, hazard ratio = 1.19, 95% confidence interval, 0.70-2.03). CONCLUSIONS: Collaborative depression care delivered before CVD onset halved the excess risk of hard CVD events among older, depressed patients. Our findings raise the possibility that the IMPACT intervention could be used as a CVD primary prevention strategy. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01561105

POSITIVE AFFECT PREDICTS FUTURE BODY MASS INDEX: A 2-YEAR PROSPECTIVE ANALYSIS OF THE AFRICAN AMERICAN HEALTH STUDY

poster abstractAlthough prospective studies indicate that negative affective factors (e.g., depression) predict increases in body mass index (BMI), few studies have examined whether positive affect is prospectively related to BMI in African Americans. Thus, it is unknown whether positive affect is related to BMI, independently of negative affect, for this ethnic group. This deficit in the literature is unfortunate, given that positive affect may protect against increases in BMI, and African Americans have among the highest rates of obesity (BMI ≥ 30 m/kg2). Accordingly, our objective was to determine whether positive affect predicts 2-year changes in BMI, independently of negative affective factors, in middle-aged African Americans. Participants were 674 African Americans aged 57-72 years who were enrolled in the African American Health study. For our study, all variables were measured in 2008 (baseline) and at 2-year follow-up. Positive affect was assessed using the 4-item positive affect subscale of the Center for Epidemiologic Studies-Depression Scale (CES-D), whereas depressive symptoms were assessed using the remaining CES-D items. Anxiety was measured using the GAD-7, and low vitality was assessed with the SF-36. Self-reported BMIs were used. Multiple linear regressions revealed that greater baseline positive affect predicted 2-year decreases in BMI (β = -.048, p = .026) after adjusting for age, sex, baseline BMI, depressive symptoms, anxiety, and low vitality. Depressive symptoms, anxiety, and low vitality did not predict BMI (ps > .10). Baseline BMI did not predict 2-year changes in positive affect (p = 55). Our findings suggest that positive affect may exert a protective effect against obesity in African Americans, whereas negative affective factors (i.e., depressive symptoms, anxiety, and low vitality) were unrelated to BMI in our sample. A key implication is that interventions for increasing positive affect in African Americans may be helpful in obesity prevention efforts for this at-risk population

Somatic Symptoms, but Not Nonsomatic Symptoms, of Depression are Associated with Insulin Resistance: National Health and Nutrition Examination Survey (NHANES) 2005-2010

poster abstractWhile there is a well-established link between depression and type 2 diabetes, depressive symptoms have received little attention in this literature. To begin to address this gap, we examined relationships among the somatic and nonsomatic symptoms of depression and insulin resistance, which is involved in the development of type 2 diabetes. Participants were 4,834 adults (mean age = 44.3 years, 50% female, 19% African American, 20% Mexican American) who participated in the 2005-2010 waves of NHANES – a survey of a large representative sample of the U.S. population. Participants with the following conditions were excluded: diabetes, cardiovascular disease, liver disease, kidney disease, or pregnancy. Depressive symptoms were measured using the Patient Health Questionnaire (PHQ-9), and somatic and nonsomatic subscales were derived based on confirmatory factor analysis. Our index of insulin resistance was the homeostatic model assessment (HOMA) score, which we computed from fasting plasma glucose and insulin levels. Separate regression analyses (adjusted for age, sex, race-ethnicity, education, BMI, and NHANES sample design) demonstrated positive relationships between PHQ-9 total (B=0.04, SEB=0.01, p<0.0001), somatic (B=0.07, SEB=0.02, p=0.0004), and nonsomatic (B=0.06, SEB=0.02, p=0.0004) scores and HOMA score. When the subscales were entered simultaneously into a regression model, the somatic score (B=0.05, SEB=0.02, p=0.03), but not the nonsomatic score (B=0.03, SEB=0.02, p=0.06), remained associated with HOMA score. A significant interaction was found for race-ethnicity, and further analyses demonstrate that the somatic symptoms of depression are only significantly associated with HOMA among Caucasians (B=0.07, SEB=0.02, p=0.02). Our cross-sectional findings suggest that the relationship between depression and insulin resistance may be driven by the somatic symptoms of depression and that this relationship may only be present only occur in Caucasians. The findings suggest that Caucasian adults with the somatic symptoms of depression may be at an elevated risk of type 2 diabetes

Association between depressive symptom clusters and food attentional bias

Background The mechanisms underlying the depression-obesity relationship are unclear. Food attentional bias (FAB) represents one candidate mechanism that has not been examined. We evaluated the hypothesis that greater depressive symptoms are associated with increased FAB. Method Participants were 89 normal weight or overweight adults (mean age = 21.2 ± 4.0 years, 53% female, 33% non-white, mean body mass index in kg/m2 = 21.9 ± 1.8 for normal weight; 27.2 ± 1.5 for overweight). Total, somatic, and cognitive-affective depressive symptom scores were computed from the Patient Health Questionnaire-8 (PHQ-8). FAB scores were calculated using reaction times (RT) and eye-tracking (ET) direction and duration measures for a food visual probe task. Age, gender, race/ethnicity, and body fat percent were covariates. Results Only PHQ-8 somatic symptoms were positively associated with RT-measured FAB (β = 0.23, p = .04). The relationship between somatic symptoms and ET direction (β = 0.18, p = .17) and duration (β = 0.23, p = .08) FAB indices were of similar magnitude but were not significant. Somatic symptoms accounted for 5% of the variance in RT-measured FAB. PHQ-8 total and cognitive-affective symptoms were unrelated to all FAB indices (ps ≥ 0.09). Conclusions Only greater somatic symptoms of depression were linked to food attentional bias as measured using reaction time. Well-powered prospective studies should examine whether this bias replicates, particularly for eye-tracking measures, and whether it partially mediates the depression-to-obesity relationship