Hillary L Ditmars1, Mark W Logue2,3,4, Rosemary Toomey1, Ruth E McKenzie1,5, Carol E Franz6,7, Matthew S Panizzon6,7, Chandra A Reynolds8, Kristy N Cuthbert1, Richard Vandiver1, Daniel E Gustavson9, Graham M L Eglit6,7,10, Jeremy A Elman6,7, Mark Sanderson-Cimino6,11, McKenna E Williams6,11, Ole A Andreassen12,13, Anders M Dale14,15, Lisa T Eyler6, Christine Fennema-Notestine6,14, Nathan A Gillespie16, Richard L Hauger6,7,17, Amy J Jak6,17, Michael C Neale16,18, Xin M Tu19, Nathan Whitsel6, Hong Xian20, William S Kremen6,7,17, Michael J Lyons1. 1. Department of Psychological and Brain Sciences, Boston University, Boston, MA, USA. 2. Research Service, VA Boston Healthcare System, Boston, MA, USA. 3. Biomedical Genetics Program, Boston University School of Medicine, Boston, MA, USA. 4. Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA. 5. School of Education and Social Policy, Merrimack College, North Andover, MA, USA. 6. Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla, CA, USA. 7. Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla, CA, USA. 8. Department of Psychology, University of California, Riverside, Riverside, CA, USA. 9. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. 10. VA San Diego Healthcare System, San Diego, CA, USA. 11. San Diego State University/UC San Diego Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA. 12. NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine University of Oslo, Oslo, Norway. 13. Division of Mental Health and Addiction, Oslo University Hospital Oslo, Oslo, Norway. 14. Department of Radiology, School of Medicine, University of California, San Diego, La Jolla, CA, USA. 15. Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA. 16. Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. 17. Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System, San Diego, CA, USA. 18. Department of Human and Molecular Genetics, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. 19. Department of Family Medicine and Public Health, VA San Diego Healthcare System, San Diego, CA, USA. 20. Department of Epidemiology & Biostatistics, Saint Louis University College for Public Health & Social Justice, Saint Louis, MO, USA.
Abstract
BACKGROUND: Clarifying the relationship between depression symptoms and cardiometabolic and related health could clarify risk factors and treatment targets. The objective of this study was to assess whether depression symptoms in midlife are associated with the subsequent onset of cardiometabolic health problems. METHODS: The study sample comprised 787 male twin veterans with polygenic risk score data who participated in the Harvard Twin Study of Substance Abuse ('baseline') and the longitudinal Vietnam Era Twin Study of Aging ('follow-up'). Depression symptoms were assessed at baseline [mean age 41.42 years (s.d. = 2.34)] using the Diagnostic Interview Schedule, Version III, Revised. The onset of eight cardiometabolic conditions (atrial fibrillation, diabetes, erectile dysfunction, hypercholesterolemia, hypertension, myocardial infarction, sleep apnea, and stroke) was assessed via self-reported doctor diagnosis at follow-up [mean age 67.59 years (s.d. = 2.41)]. RESULTS: Total depression symptoms were longitudinally associated with incident diabetes (OR 1.29, 95% CI 1.07-1.57), erectile dysfunction (OR 1.32, 95% CI 1.10-1.59), hypercholesterolemia (OR 1.26, 95% CI 1.04-1.53), and sleep apnea (OR 1.40, 95% CI 1.13-1.74) over 27 years after controlling for age, alcohol consumption, smoking, body mass index, C-reactive protein, and polygenic risk for specific health conditions. In sensitivity analyses that excluded somatic depression symptoms, only the association with sleep apnea remained significant (OR 1.32, 95% CI 1.09-1.60). CONCLUSIONS: A history of depression symptoms by early midlife is associated with an elevated risk for subsequent development of several self-reported health conditions. When isolated, non-somatic depression symptoms are associated with incident self-reported sleep apnea. Depression symptom history may be a predictor or marker of cardiometabolic risk over decades.
BACKGROUND: Clarifying the relationship between depression symptoms and cardiometabolic and related health could clarify risk factors and treatment targets. The objective of this study was to assess whether depression symptoms in midlife are associated with the subsequent onset of cardiometabolic health problems. METHODS: The study sample comprised 787 male twin veterans with polygenic risk score data who participated in the Harvard Twin Study of Substance Abuse ('baseline') and the longitudinal Vietnam Era Twin Study of Aging ('follow-up'). Depression symptoms were assessed at baseline [mean age 41.42 years (s.d. = 2.34)] using the Diagnostic Interview Schedule, Version III, Revised. The onset of eight cardiometabolic conditions (atrial fibrillation, diabetes, erectile dysfunction, hypercholesterolemia, hypertension, myocardial infarction, sleep apnea, and stroke) was assessed via self-reported doctor diagnosis at follow-up [mean age 67.59 years (s.d. = 2.41)]. RESULTS: Total depression symptoms were longitudinally associated with incident diabetes (OR 1.29, 95% CI 1.07-1.57), erectile dysfunction (OR 1.32, 95% CI 1.10-1.59), hypercholesterolemia (OR 1.26, 95% CI 1.04-1.53), and sleep apnea (OR 1.40, 95% CI 1.13-1.74) over 27 years after controlling for age, alcohol consumption, smoking, body mass index, C-reactive protein, and polygenic risk for specific health conditions. In sensitivity analyses that excluded somatic depression symptoms, only the association with sleep apnea remained significant (OR 1.32, 95% CI 1.09-1.60). CONCLUSIONS: A history of depression symptoms by early midlife is associated with an elevated risk for subsequent development of several self-reported health conditions. When isolated, non-somatic depression symptoms are associated with incident self-reported sleep apnea. Depression symptom history may be a predictor or marker of cardiometabolic risk over decades.
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