a1 Biostatistics Unit, Orygen Youth Health Research Centre & Centre for Youth Mental Health, The University of Melbourne, Australia. email@example.com
a2 Statistical and Computational Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom & Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, The University of Melbourne, Australia.
a3 Department of Psychiatry, Washington University School of Medicine, United States of America.
a4 Department of Psychiatry, Washington University School of Medicine, United States of America.
a5 Genetic and Molecular Epidemiology Laboratories, Queensland Institute of Medical Research, Brisbane, Australia.
a6 Genetic and Molecular Epidemiology Laboratories, Queensland Institute of Medical Research, Brisbane, Australia.
The aim of this study is to characterize the relationship between major depression and the metabolic syndrome in a large community based sample of Australian men and women aged 26–90 years. A lifetime history of major depression was assessed by telephone interview following the DSM–III-R. A current history of metabolic syndrome was assessed following the United States National Cholesterol Education Program Adult Treatment Panel III (NCEP AP-III) guidelines 1 to 3 years later. Logistic regression was used to estimate the association between depression and the metabolic syndrome, and its component criteria, controlling for age, sex and alcohol dependence. There was no association between a lifetime history of major depression and the presence of the metabolic syndrome. There was a weak association between depression and low high-density lipoprotein cholesterol but not with other component criteria of the metabolic syndrome. Despite calls for interventions directed at depression to reduce the onset of the metabolic syndrome there are important failures to replicate in large samples such as this, no consensus regarding the threshold at which depression may pose a significant risk even allowing for heterogeneity across populations, and no consensus regarding confounders that may explain inter-study differences. The absence of any dosage effect of depression on the associated risk for the metabolic syndrome in other unselected samples does not support a direct causal relationship. The call for intervention studies on the basis of the currently published evidence base is unwarranted.
(Received April 09 2010)
(Accepted April 24 2010)
c1 Address for correspondence: Debra Foley, Orygen Youth Health Research Centre, 35 Poplar Road, Parkville VIC 3052, Australia.