Stressful exposure from the 2004 Indian Ocean Tsunami drives long-term changes in thyroid hormone physiology.

UNLABELLED: Stressful events are associated with long-term adverse health impacts, but the causal mechanisms linking these exposures to subsequent disease remain poorly understood. One plausible mechanism is persistent changes to hormonal signaling that regulate metabolic homeostasis. Here, 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. We measure biomarkers 20 years after the 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 most affected part of the Indian Ocean Basin. Because respondents were first interviewed before the tsunami and subsequently tracked regardless of migration, the sample avoids a major source of 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.

SIGNIFICANCE STATEMENT: Exposure to severe stressful events is associated with worse cardiometabolic health, but the biological mechanisms underlying these long-term effects remain poorly understood. Using the 2004 Indian Ocean tsunami as a natural experiment, we show that greater tsunami exposure causally reduces circulating free T3, the biologically active thyroid hormone, two decades later. Tsunami exposure also alters the normal relationships between free T3 and other metabolic measures and increases cardiometabolic risk, suggesting that persistent reductions of free T3 in response to stress may contribute to adverse cardiometabolic outcomes. Together, these results identify persistent changes in thyroid hormone physiology as a previously underexplored response to severe stressful exposure and a potential pathway linking such events to long-term metabolic disease.