Browsing by Author "Berntson, Jessica"
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Item Are Cardiovascular Risk Factors Stronger Predictors of Incident Cardiovascular Disease in U.S. Adults With Versus Without a History of Clinical Depression?(Oxford University Press, 2018-12) Polanka, Brittanny M.; Berntson, Jessica; Vrany, Elizabeth A.; Stewart, Jesse C.; Psychology, School of ScienceBackground Several mechanisms underlying the depression-to-cardiovascular disease (CVD) relationship have been proposed; however, few studies have examined whether depression promotes CVD through potentiating traditional cardiovascular risk factors. Purpose To test the combined influence of three cardiovascular risk factors and lifetime depressive disorder on incident CVD in a large, diverse, and nationally representative sample of U.S. adults. Methods Respondents were 26,840 adults without baseline CVD who participated in Waves 1 (2001–2002) and 2 (2004–2005) of the National Epidemiologic Survey on Alcohol and Related Conditions. Lifetime depressive disorder, tobacco use, hypertension, and incident CVD were determined from structured interviews, and body mass index (BMI) was computed from self-reported height and weight. Results Logistic regression models predicting incident CVD (1,046 cases) revealed evidence of moderation, as the interactions between lifetime depressive disorder and current tobacco use (p = .002), hypertension (p < .001), and BMI (p = .031) were significant. The Former Tobacco Use × Lifetime Depressive Disorder interaction was not significant (p = .85). In models stratified by lifetime depressive disorder, current tobacco use (OR = 1.78, 95% CI = 1.36–2.32, p < .001 vs. OR = 1.41, 95% CI = 1.24–1.60, p < .001), hypertension (OR = 2.46, 95% CI = 1.98–3.07, p < .001 vs. OR = 1.39, 95% CI = 1.28–1.51, p < .001), and BMI (OR = 1.10, 95% CI = 1.01–1.20, p = .031 vs. OR = 1.03, 95% CI = 0.99–1.07, p = .16) were stronger predictors of incident CVD in adults with versus without a lifetime depressive disorder. Conclusions Our findings suggest that amplifying the atherogenic effects of traditional cardiovascular risk factors may be yet another candidate mechanism that helps to explain the excess CVD risk of people with depression.Item Associations between affective traits and endothelial function in depressed adults(2018) Berntson, Jessica; Stewart, Jesse C.; Cyders, Melissa A.; Rand, Kevin L.; Gupta, Samir K.Depressed adults are at increased risk of developing atherosclerotic cardiovascular disease (CVD). However, heterogeneity in the depressed population engenders a key question: Are there subgroups of depressed adults at greater risk of developing CVD? Because other affective traits – i.e., anxiety, hostility/anger, and low trait positive affect – have also been associated with increased CVD risk, depressed adults with higher levels of these co-occurring affective traits may have an elevated risk of developing CVD. Consequently, the present study’s first aim was to examine, in depressed adults, which affective traits (depression, anxiety, hostility/anger, or low positive affect) are associated with endothelial function, a marker of cumulative CVD risk. In addition, because the other affective traits overlap with depressive symptom severity, this study’s second aim was to investigate which components of pairs of affective traits (shared versus unique) are related to endothelial function. Finally, given that the mechanisms underlying affective trait-endothelial function relationships in depressed adults are unknown, this study’s third aim was to explore traditional CVD risk status as a candidate mediator of observed relationships. To achieve these aims, I combined pre-treatment, cross-sectional data from three randomized controlled trials involving 138 depressed primary care patients with no history of clinical CVD. Assessments included validated self-report questionnaires for affective traits, brachial artery flow-mediated dilation (FMD) for endothelial function, and 10-year Framingham risk score for traditional CVD risk status. I conducted structural equation modeling (SEM) with confirmatory factor analysis to examine the relationships of interest after adjusting for age, sex, race/ethnicity, education, and baseline arterial diameter. Although the shared variance between each affective trait pair could not be modeled due to poor fit, adequate fitting models revealed that hostility/anger and the unique components of hostility/anger were associated with poorer endothelial function (standardized coefficients = -.18 and -.22, respectively). All of the other affective traits and their components (depression, anxiety, positive affect, unique depression, unique anxiety, and unique positive affect) were not related to endothelial function (all ps > .08). Traditional CVD risk status did not partially explain the relationship between the unique components of hostility/anger and endothelial function (standardized coefficient for the indirect effect = .00; p = .89). If my results are supported by future findings, it would suggest that depressed adults with hostility/anger (a) may be a subgroup of the depressed population at greater risk of developing CVD and (b) may be in need of earlier, more intense, and/or different CVD primary prevention efforts. Future studies are needed to confirm this relationship and identify underlying mechanisms.Item Depressive Symptom Severity, Stressful Life Events, and Subclinical Atherosclerosis in African American Adults(2015) Berntson, Jessica; Stewart, Jesse; Cyders, Melissa Anne; Rand, Kevin L.; Grahame, Nicholas J.Prospective epidemiologic evidence indicates that both stressful life events (SLEs) and depression are associated with an increased risk of subclinical atherosclerosis and cardiovascular disease (CVD) events. Even though stressful life events (SLEs) and depression co-occur and may act together to influence cardiovascular disease (CVD) risk, these psychosocial factors have been mainly examined in isolation. For instance, depression may moderate the relationship between SLEs and CVD outcomes. I hypothesized that depressive symptoms would potentiate the deleterious effect of SLEs on subclinical atherosclerosis. This hypothesis is plausible, given that depressed adults exhibit exaggerated and prolonged sympathetic nervous system, hypothalamic-pituitary-adrenal (HPA) axis, and inflammatory responses to stress, which in turn could promote atherosclerosis. As compared to their nondepressed counterparts, depressed individuals may also be more likely to engage in maladaptive methods to cope with SLEs (e.g., increased tobacco use, alcohol use, and consumption of low-nutrient, energy dense foods), which could also promote atherosclerosis. I examined cross-sectional data from 274 to 279 (depending on the outcome measure) older, African American adults (mean age = 66 years, 67% female) with no evidence of clinical CVD or dementia who participated in the St. Louis African American Health-Heart study (2009–2011). Number of SLEs was assessed using the Life Events Calendar, a structured interview. From this interview, a continuous SLEs variable was computed (number of adult SLEs: 0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11+). Severity of depression symptoms was measured using the 17-item Hamilton Rating Scale for Depression (HAM-D). Two measures of subclinical atherosclerosis were obtained: carotid intima-media thickness (CIMT; assessed by ultrasonography) and coronary artery calcification (CAC; assessed by multi-detector computerized tomography). I conducted linear (CIMT) and logistic (CAC) regression models, first adjusted for demographics (age, sex, education) and then fully-adjusted (demographics; mean arterial pressure; low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C); hemoglobin A1c; BMI; tobacco use; diabetes diagnosis; and use of antihypertensitve, lipid lowering, antidiabetic, and antidepressant medications). No main effects of SLEs or HAM-D were found for CIMT or CAC. There were also no SLEs by HAM-D interactions for CIMT or CAC. Because the current results are largely inconsistent with prior literature and there is a paucity of studies utilizing African American samples, future research is needed to examine the independent and interactive associations of SLEs and depressive symptoms with measures of subclinical atherosclerosis. If the present results are replicated, it may suggest that SLEs, depressive symptoms, and their interactive effect are not cardiotoxic among African American adults.Item 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(Office of the Vice Chancellor for Research, 2013-04-05) Berntson, Jessica; Stewart, Kendra Ray; Vrany, Elizabeth; Khambaty, Tasneem; Stewart, Jesse CDepression 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.Item Effect of Modernized Collaborative Care for Depression on Depressive Symptoms and Cardiovascular Disease Risk Biomarkers: eIMPACT Randomized Controlled Trial(Elsevier, 2023) Stewart, Jesse C.; Patel, Jay S.; Polanka, Brittanny M.; Gao, Sujuan; Nurnberger, John I., Jr.; MacDonald, Krysha L.; Gupta, Samir K.; Considine, Robert V.; Kovacs, Richard J.; Vrany, Elizabeth A.; Berntson, Jessica; Hsueh, Loretta; Shell, Aubrey L.; Rollman, Bruce L.; Callahan, Christopher M.; Psychology, School of ScienceAlthough depression is a risk and prognostic factor for cardiovascular disease (CVD), clinical trials treating depression in patients with CVD have not demonstrated cardiovascular benefits. We proposed a novel explanation for the null results for CVD-related outcomes: the late timing of depression treatment in the natural history of CVD. Our objective was to determine whether successful depression treatment before, versus after, clinical CVD onset reduces CVD risk in depression. We conducted a single-center, parallel-group, assessor-blinded randomized controlled trial. Primary care patients with depression and elevated CVD risk from a safety net healthcare system (N = 216, Mage = 59 years, 78% female, 50% Black, 46% with income <$10,000/year) were randomized to 12 months of the eIMPACT intervention (modernized collaborative care involving internet cognitive-behavioral therapy [CBT], telephonic CBT, and/or select antidepressants) or usual primary care for depression (primary care providers supported by embedded behavioral health clinicians and psychiatrists). Outcomes were depressive symptoms and CVD risk biomarkers at 12 months. Intervention participants, versus usual care participants, exhibited moderate-to-large (Hedges' g = -0.65, p < 0.01) improvements in depressive symptoms. Clinical response data yielded similar results - 43% of intervention participants, versus 17% of usual care participants, had a ≥ 50% reduction in depressive symptoms (OR = 3.73, 95% CI: 1.93-7.21, p < 0.01). However, no treatment group differences were observed for the CVD risk biomarkers - i.e., brachial flow-mediated dilation, high-frequency heart rate variability, interleukin-6, high-sensitivity C-reactive protein, β-thromboglobulin, and platelet factor 4 (Hedges' gs = -0.23 to 0.02, ps ≥ 0.09). Our modernized collaborative care intervention - which harnessed technology to maximize access and minimize resources - produced clinically meaningful improvements in depressive symptoms. However, successful depression treatment did not lower CVD risk biomarkers. Our findings indicate that depression treatment alone may not be sufficient to reduce the excess CVD risk of people with depression and that alternative approaches are needed. In addition, our effective intervention highlights the utility of eHealth interventions and centralized, remote treatment delivery in safety net clinical settings and could inform contemporary integrated care approaches.Item Number of Recent Stressful Life Events and Incident Cardiovascular Disease: Moderation by Lifetime Depressive Disorder(Elsevier, 2017) Berntson, Jessica; Patel, Jay S.; Stewart, Jesse C.; Department of Psychology, School of ScienceObjective 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.Item Somatic Symptoms, but Not Nonsomatic Symptoms, of Depression are Associated with Insulin Resistance: National Health and Nutrition Examination Survey (NHANES) 2005-2010(Office of the Vice Chancellor for Research, 2013-04-05) Vrany, Elizabeth; Berntson, Jessica; Khambaty, Tasneem; Stewart, Jesse CWhile 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.