Neuro-immune, metabolic, and oxidative pathways in depression due to hypothyroidism and Hashimoto's thyroiditis

Hypothyroidism is linked to depression and several metabolic alterations, including insulin resistance, dyslipidemia, and oxidative stress. This study investigates the impact of hormones, autoimmunity, metabolic, and antioxidant indicators on the severity of depression in patients with hypothyroidism.

Forty-six patients with hypothyroidism and seventy-four with Hashimoto's thyroiditis participated in this study, along with sixty healthy controls. Patients were categorized based on the Hamilton Depression Rating Scale (≥ 17) into those with depression and those without. The enzyme-linked immunosorbent assay method was employed to evaluate blood insulin and selenoprotein P (SePP). Graphite furnace atomic absorption spectrophotometry was employed to quantify serum selenium concentrations. Serum zinc and lipid profile indicators were measured using spectrophotometry.

Hypothyroidism and Hashimoto's thyroiditis are linked to increased atherogenicity, insulin resistance, and reduced antioxidant defenses, including selenium, SePP, and zinc. Both cohorts with thyroid dysfunctions demonstrate slight elevations in depressive symptoms. Individuals with hypothyroidism and heightened depressive symptoms demonstrated augmented insulin resistance, raised atherogenic indices, and markedly reduced levels of SePP relative to those with milder depressive symptoms. Elevated levels of thyroid-stimulating hormone and atherogenic index of plasma best predicted the severity of depression in hypothyroid patients.

The findings indicate that depression due to hypothyroidism is largely influenced by abnormalities in thyroid hormones, thyroid-stimulating hormone, metabolic pathways, and diminished antioxidant defenses. The observed results may be explained by the established impact of these hormones and biomarkers on cerebral functions, resulting in major depressive disorder.