Associations between thyroid hormones and biochemical metabolism in major depressive disorder patients with and without comorbid eating disorders.
TL;DR
Findings reveal concurrent thyroid hormone irregularities and neurometabolic changes in the thalamic-cerebellum circuitry in MDD with ED, providing preliminary insights into the neurobiology of abnormal eating behaviors in depression.
Abstract
Objectives
The underlying mechanism of major depressive disorder (MDD) with eating disorder (ED) remains unclear. We aim to clarify the characteristic changes of THs and brain neurometabolic alterations in ED, and to explore their relationships.
Methods
The study included 28 individuals with MDD and ED, 81 individuals with MDD without ED, and 37 age-matched healthy controls (HCs). Serum TH levels were assessed, and 1H proton magnetic spectroscopy was utilized to determine the N-acetylaspartic acid to creatine (NAA/Cr) and choline-containing compounds to creatine ratios in the prefrontal cortex, anterior cingulate cortex, and thalamus. Subsequently, differential analysis, receiver operating characteristic (ROC) analysis, and correlation analysis were performed to explore their characteristics and interrelationships.
Results
In both MDD with ED and MDD without ED cohorts, free tri-iodothyronine (FT3) levels were significantly lower compared to HCs, whereas free thyroxine (FT4) and total thyroxine (TT4) levels were elevated. Significantly lower NAA/Cr ratios were observed in the right thalamus and higher NAA/Cr ratios in the left cerebellum in both MDD with ED and MDD without ED compared to HCs. Neurometabolic factors and THs levels achieved an ROC curve area of 0.830 in differentiating MDD with ED from MDD without ED. In addition, serum FT3 and TT4 levels showed a positive correlation with NAA/Cr in the eft cerebellum in cases of MDD with ED.
Conclusions
Our findings reveal concurrent thyroid hormone irregularities and neurometabolic changes in the thalamic-cerebellum circuitry in MDD with ED, providing preliminary insights into the neurobiology of abnormal eating behaviors in depression. Given the cross-sectional design, these results are exploratory and require validation. Level of evidence Level IV, cross-sectional study.