Effects of acute psychosocial stress on the hypothalamic-pituitary-thyroid (HPT) axis in healthy women

Abstract Objective The individual set point of the hypothalamic-pituitary-thyroid (HPT) axis is largely genetically determined. Apart from this genetic predisposition, the HPT axis may also be malleable to environmental demands such as psychosocial stress. Indeed, previous research has indicated that critical life events often precede the onset of autoimmune thyroid diseases, and subtle abnormalities in HPT functioning are present in some patients with stress-related disorders such as depression. However, no studies have investigated whether exposure to psychosocial stress leads to an immediate activation of the HPT axis. Methods A total of N = 30 healthy women attended two laboratory appointments in a randomized order. An intravenous catheter was inserted at the beginning of each appointment. In the stress session, this was followed by the Trier Social Stress Test (TSST). Plasma samples to determine thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were taken at baseline and 20, 50, and 110 min after the TSST started. In the control session, participants rested and were instructed to read magazines, while the sampling schedule was maintained. Results There was a significant rise in TSH concentrations in response to the TSST, with a peak observed 20 min after stressor onset, and a steady decline thereafter. No such response was observed in the control session. The TSST did not increase T3 or T4. Conclusion The finding that acute psychosocial stress is able to elicit a significant increase in TSH is relevant to our understanding of a number of stress-related illnesses presenting with abnormalities of the HPT axis.