Stress and Thyroid Function—From Bench to Bedside

Abstract Experimental animal and human studies illustrate the effect of various stress forms on the thyroid gland and the regulation of thyroid hormones (THs) through the thyrotropic multiloop control circuit. The hypothalamic–pituitary–thyroid axis (HPT) axis is part of the physiological stress system and mediates key regulators of metabolic activity during stress response. Genetically characterized individuals are more affected in their response to stressors, and their psychological response is extremely amplified. This leads to significant increases in TH serum levels as soon as a negative stressor appears. Physical stressors are used to induce psychological stress (eg, physical exercise, starvation, sleep deprivation, hypoxia, and cold temperatures), all of which impact thyroid function. In addition, somatic illnesses may also affect the thyroid gland or may be related to a thyroidal dysfunction. As a psychosocial stressor in animal models, neonatal separation from the mother was used, affecting energy homeostasis and causing an increase in thyroliberin (TRH) expression in female rats and an increase in TRH degrading ectoenzyme in male rats. In mice with restrained stress, THs are important mediators of accelerated tumor growth. In human studies, isolated sexual abuse in childhood doubles the risk of thyroid dysfunction, with puerperal depression after sexual abuse in childhood increasing the risk for HPT axis disorders and elevated thyroid autoantibodies 4-fold. In addition, psychological illnesses influence thyroid function. In the future, laboratory studies with standardized induction of various stress forms are warranted to better understand stress-induced effects on the HPT axis and their corresponding mechanisms.