2004年印度洋海啸带来的应激暴露驱动甲状腺激素生理机能的长期变化

Stressful events are associated with long-term adverse health impacts, but the causal mechanisms linking exposures to disease remain poorly understood. One mechanism is persistent changes to hormonal signaling that regulate metabolic homeostasis. We examine the long-term impacts of stress associated with exposure to the 2004 Indian Ocean tsunami on levels of free triiodothyronine (FT3), a circulating measure of biologically active thyroid hormone, using data from the Study of Tsunami Aftermath and Recovery. Biomarkers are measured 20 years post-tsunami in a population-representative sample age 35y+ in 2024 who, at the time of the tsunami, were living along the coast of Aceh, Indonesia, the area hardest-hit by the tsunami. Because respondents were first interviewed before the tsunami and subsequently tracked regardless of migration, the sample avoids selection bias common in long-term disaster studies. We identify the causal effect of tsunami exposure using variation in community-level tsunami mortality, comparing communities within the same sub-district. We find that greater tsunami exposure reduced levels of FT3 20 years later. Exposure also altered relationships between FT3, body composition, and cortisol and increased cardiometabolic risk. These findings identify persistent alteration of thyroid hormone physiology as a potential pathway linking severe stressful exposures to long-term cardiometabolic disease risk.