Genetic, environmental factors drive metabolic disorder-related depression

The risk of depression is higher in individuals with endocrine-metabolic disorders, which can be explained by genetic and environmental influences, reveals a study.

“Depression is common in individuals with endocrine-metabolic disorders and vice versa, and a better understanding of the underlying factors contributing to the comorbidity of these disorders is needed,” the authors said.

A population-based cohort study was conducted involving 2.2 million individuals in Sweden between 1973 and 1996, with follow-up through 2013. The authors linked participants to their biological parents, which allowed the identification of full siblings, maternal half siblings, and paternal half siblings.

The authors then assessed diagnoses of depression and endocrine-metabolic conditions, grouping the latter into autoimmune disorders (autoimmune hypothyroidism, Graves’ disease, and type 1 diabetes) and nonautoimmune disorders (type 2 diabetes, obesity, and polycystic ovary syndrome).

Associations between endocrine-metabolic disorders and depression within the same individual and across siblings were estimated using logistic regression and Cox regression. The relative contribution of genetic and environmental factors was also examined using quantitative genetic modeling.

Individuals with endocrine-metabolic disorders showed a significantly higher risk of depression, with odds ratios ranging from 1.43 (95 percent confidence interval [CI], 1.30‒1.57) for Graves’ disease to 3.48 (95 percent CI, 3.25‒3.72) for type 2 diabetes. Such increased risk extended to full and half siblings.

The associations between depression risk and endocrine-metabolic disorders were driven by shared genetic influences for nonautoimmune conditions and by nonshared environmental factors for autoimmune disorders, particularly for type 1 diabetes.

“These findings provide phenotypic and aetiological insights into the co-occurrence of depression and various endocrine-metabolic conditions, which could guide future research aiming at identifying pathophysiological mechanisms and intervention targets,” the authors said.