Association of treatment response with obesity and other metabolic risk factors in adults with depressive disorders: Results from a National Depression Cohort study in Korea (the CRESCEND study).
Available studies indicate that obesity may exert a moderational effect on antidepressant treatment response. The aim of this study was to investigate the relationship between treatment response and metabolic abnormalities amongst patients with depressive disorders in a large naturalistic clinical setting.



A nationwide prospective study was conducted in 18 hospitals in South Korea; 541 depressive patients meeting DSM-IV criteria were recruited. After baseline evaluation, subjects received naturalistic clinician-determined antidepressant interventions. Assessment was performed at baseline and weeks 1, 2, 4, 8, 12, 24 and 52. Treatment response was defined as a ≥50% reduction from baseline on at least one evaluation point.



In univariate comparison, the patients who showed insufficient response to antidepressant therapy were more likely to be male, unmarried, unemployed, and obese. After adjusting for baseline variables, male sex (OR=1.82) and obesity (OR=1.55) remained as were significant variables. Stratification of the subjects into one of three groups, i.e. male, pre-menopausal female and post-menopausal female, revealed that males with concurrent metabolic problems, (i.e. the presence of one or more of hypertension, hyperglycemia, or hypercholesterolemia) had significantly higher risk for insufficient response (OR=2.32) and, after adjusting for baseline variables, obesity predicted insufficient response in post-menopausal female (OR=2.41).



The presence of metabolic abnormalities in patients with depressive disorders was associated with decreased treatment response to antidepressants. These results underscore the neurobiological relationship between obesity and the central nervous system, and provide empiric evidence supporting stratification of treatment response in depression.
Department of Psychiatry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea; Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, Ontario, Canada.
Young Sup
YS
Woo
Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
Roger S
RS
McIntyre
Department of Psychiatry, Keimyung University, School of Medicine, Daegu, Republic of Korea.
Jung-Bum
JB
Kim
Department of Psychiatry, College of Medicine, Korea University, Seoul, Republic of Korea.
Min-Soo
MS
Lee
Department of Psychiatry, Chonnam National University Medical School, Kwangju, Republic of Korea.
Jae-Min
JM
Kim
Department of Preventive Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Hyeon Woo
HW
Yim
Department of Psychiatry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea. Electronic address: tyjun@catholic.ac.kr.
Tae-Youn
TY
Jun
D000328:Adult; D000928:Antidepressive Agents / Q000627:therapeutic use*; D015331:Cohort Studies; D003863:Depression / Q000150:complications* / Q000188:drug therapy*; D039721:Diagnostic and Statistical Manual of Mental Disorders; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000378:metabolism*; D011446:Prospective Studies; D056910:Republic of Korea; D012307:Risk Factors; D016896:Treatment Outcome
D000928:Antidepressive Agents
Antidepressant; Depression; Gender difference; Menopause; Metabolic abnormalities; Treatment outcome