AT IPA 2016

SAN FRANCISCO – Metabolic dysregulation and particularly abdominal obesity lead to failure to remit in late-life depression, according to a multicenter, prospective cohort study.

The finding highlights the need for comprehensive interventions for comorbid late-life depression and metabolic syndrome, Radboud M. Marijnissen, MD, said during an oral presentation at the 2016 congress of the International Psychogeriatric Association..

Late-life depression is notoriously refractory to antidepressant monotherapy, he said. Metabolic syndrome becomes more common with age and is reciprocally related to depression, but few studies have examined links between these two conditions, said Dr. Marijnissen of the department of old age psychiatry at the Pro Persona Medical Center in Wolfheze, the Netherlands. Therefore, he and his associates examined Inventory of Depressive Symptomatology ( IDS ) scores and metabolic data from 285 patients aged 60 years and older who met DSM-IV criteria for depressive disorders. The patients were participants in the observational, prospective multicenter Netherlands study of depression in older persons ( NESDO ), which assessed patients every 6 months for 2 years. The researchers defined metabolic syndrome based on National Cholesterol Education Program ( NCEP-ATP III ) criteria, which include measures for central obesity, hypertension, and elevated blood levels of glucose, triglycerides, and high-density lipoprotein cholesterol, Dr. Marijnissen said. In his study, most patients were receiving regular mental health care, including antidepressants and psychotherapy.

At 2 years, patients were significantly less likely to have achieved complete remission from depression when they had components of metabolic syndrome than otherwise (42% vs. 58%; P = .01). Furthermore, each additional component of metabolic syndrome increased the odds of failure to remit by 27% (odds ratio, 1.27; 95% confidence interval, 1.03-1.58; P = .028), even after the investigators controlled for multiple potential confounders, including age, sex, marital status, tobacco and alcohol use, level of education, physical activity, comorbidities, the presence of cognitive impairment, and the use of psychotropic and anti-inflammatory drugs.

Interestingly, specific components of metabolic syndrome seemed to exert different effects on the likelihood of remission, Dr. Marijnissen said. Increased waist circumference and HDL cholesterol each independently predicted failure to achieve remission, with odds ratios of 1.96 (95% CI, 1.15-3.32; P = .013) and 2.35 (1.21-4.53; P = .011), respectively. In contrast, elevated triglycerides predicted remission failure, but the link did not reach statistical significance, and hypertension and elevated fasting blood glucose levels showed no trend in either direction.

Further analyses of scores on the three subscales of the IDS again linked abdominal obesity, as well as elevated fasting blood glucose, with persistent somatic features of depression (P = .046 and .02, respectively). In contrast, neither the total number of metabolic syndrome components nor the presence or absence of any individual component predicted persistently elevated scores on the mood or motivation subscales of the IDS (P greater than .4 for each association). In addition, neither metabolic syndrome nor its individual components predicted depression severity.

These findings suggest that metabolic dysregulation leads to remission failure with persistent somatic symptoms in late-life depression, and that central obesity drives this relationship, Dr. Marijnissen concluded. “Metabolic depression calls for specific interventions,” he added. “People who are suffering from this subtype of depression may benefit from vascular disease management, healthy nutrition, and programs that emphasize exercise, including resistance training to help turn white fat into brown fat , which lowers metabolic risk as well as depressive symptoms.”

Dr. Marijnissen reported no funding sources or conflicts of interest.

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