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Browsing by Subject "Depressive Disorder, Major"
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Item Effect of collaborative care for depression on risk of cardiovascular events: data from the IMPACT randomized controlled trial(Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2014-01) Stewart, Jesse C.; Perkins, Anthony J.; Callahan, Christopher M.; Department of Psychology, School of ScienceOBJECTIVE: 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.Item Polygenic Scores for Major Depressive Disorder and Risk of Alcohol Dependence(American Medical Association, 2017-11-01) Andersen, Allan M.; Pietrzak, Robert H.; Kranzler, Henry R.; Ma, Li; Zhou, Hang; Liu, Xiaoming; Kramer, John; Kuperman, Samuel; Edenberg, Howard J.; Nurnberger, John I., Jr.; Rice, John P.; Tischfield, Jay A.; Goate, Alison; Foroud, Tatiana M.; Meyers, Jacquelyn L.; Porjesz, Bernice; Dick, Danielle M.; Hesselbrock, Victor; Boerwinkle, Eric; Southwick, Steven M.; Krystal, John H.; Weissman, Myrna M.; Levinson, Douglas F.; Potash, James B.; Gelernter, Joel; Han, Shizhong; Biochemistry and Molecular Biology, School of MedicineImportance: Major depressive disorder (MDD) and alcohol dependence (AD) are heritable disorders with significant public health burdens, and they are frequently comorbid. Common genetic factors that influence the co-occurrence of MDD and AD have been sought in family, twin, and adoption studies, and results to date have been promising but inconclusive. Objective: To examine whether AD and MDD overlap genetically, using a polygenic score approach. Design, Settings, and Participants: Association analyses were conducted between MDD polygenic risk score (PRS) and AD case-control status in European ancestry samples from 4 independent genome-wide association study (GWAS) data sets: the Collaborative Study on the Genetics of Alcoholism (COGA); the Study of Addiction, Genetics, and Environment (SAGE); the Yale-Penn genetic study of substance dependence; and the National Health and Resilience in Veterans Study (NHRVS). Results from a meta-analysis of MDD (9240 patients with MDD and 9519 controls) from the Psychiatric Genomics Consortium were applied to calculate PRS at thresholds from P < .05 to P ≤ .99 in each AD GWAS data set. Main Outcomes and Measures: Association between MDD PRS and AD. Results: Participants analyzed included 788 cases (548 [69.5%] men; mean [SD] age, 38.2 [10.8] years) and 522 controls (151 [28.9.%] men; age [SD], 43.9 [11.6] years) from COGA; 631 cases (333 [52.8%] men; age [SD], 35.0 [7.7] years) and 756 controls (260 [34.4%] male; age [SD] 36.1 [7.7] years) from SAGE; 2135 cases (1375 [64.4%] men; age [SD], 39.4 [11.5] years) and 350 controls (126 [36.0%] men; age [SD], 43.5 [13.9] years) from Yale-Penn; and 317 cases (295 [93.1%] men; age [SD], 59.1 [13.1] years) and 1719 controls (1545 [89.9%] men; age [SD], 64.5 [13.3] years) from NHRVS. Higher MDD PRS was associated with a significantly increased risk of AD in all samples (COGA: best P = 1.7 × 10-6, R2 = 0.026; SAGE: best P = .001, R2 = 0.01; Yale-Penn: best P = .035, R2 = 0.0018; and NHRVS: best P = .004, R2 = 0.0074), with stronger evidence for association after meta-analysis of the 4 samples (best P = 3.3 × 10-9). In analyses adjusted for MDD status in 3 AD GWAS data sets, similar patterns of association were observed (COGA: best P = 7.6 × 10-6, R2 = 0.023; Yale-Penn: best P = .08, R2 = 0.0013; and NHRVS: best P = .006, R2 = 0.0072). After recalculating MDD PRS using MDD GWAS data sets without comorbid MDD-AD cases, significant evidence was observed for an association between the MDD PRS and AD in the meta-analysis of 3 GWAS AD samples without MDD cases (best P = .007). Conclusions and Relevance: These results suggest that shared genetic susceptibility contributes modestly to MDD and AD comorbidity. Individuals with elevated polygenic risk for MDD may also be at risk for AD.