As global climate change intensifies, heat waves are becoming more frequent, longer and more severe, emerging as an important environmental stressor on human health. Previous research has linked exposure to heatwaves to increased risks of cardiovascular and respiratory diseases, cognitive impairment, and mental health problems, while older adults are particularly vulnerable due to reduced thermoregulatory capacity and reduced physiological reserves.
At the same time, population aging is accelerating, making it increasingly important to understand how environmental factors shape long-term aging trajectories. Compared to chronological age alone, biological age provides a more comprehensive measure of multisystem physiological deterioration, and accelerated biological age is associated with chronic disease, functional decline, and mortality risk.
However, it remains unclear whether exposure to repeated heat waves accelerates whole-body biological aging and what biological mechanisms underlie this association. Given that heat stress can disrupt metabolic homeostasis, inflammatory responses, and organ function, investigating the association between heat wave exposure and accelerated biological aging and the metabolic pathways that may be involved is important to identify vulnerable populations and develop targeted climate adaptation strategies. ”
Dengyong Xu, author, researcher at Zhejiang University
This study used data from the China Health and Retirement Longitudinal Study (CHARLS), which included 2,318 middle-aged and older adults aged 45 and older, to assess the longitudinal association between heatwave exposure and biological age acceleration.
The researchers first applied the Kremera-Douval method (KDM) to integrate eight clinical biomarkers, including C-reactive protein, glycated hemoglobin, total cholesterol, triglycerides, blood urea nitrogen, serum creatinine, platelet count, and systolic blood pressure, to estimate biological age. Biological age acceleration was then calculated as biological age minus chronological age. Heatwave exposure was estimated using city-level meteorological data including the number of heatwave events and heatwave days in the 12-month period prior to biological age assessment in 2011 and 2015.
Twelve heat wave definitions based on different temperature percentile thresholds and event durations were used to test robustness. This study then applied a difference-in-differences design to examine whether within-individual changes in heatwave exposure were associated with accelerated changes in biological age while adjusting for baseline characteristics, lifestyle changes, weight changes, and changes in depressive symptoms, and further performed subgroup and sensitivity analyses. To investigate potential mechanisms, the researchers also analyzed liver transcriptome data from aged mice exposed to heat wave conditions, identified differentially expressed genes, integrated them with aging-related genes from public databases, and used protein-protein interaction and functional enrichment analysis to investigate molecular pathways potentially linking heat exposure and biological aging.
The results showed that exposure to heatwaves was significantly associated with accelerated biological aging in middle-aged and older adults. Of the 2,318 participants, mean age was 58.7 years, mean biological age increased from 57.3 years in 2011 to 62.3 years in 2015, and 58.8% of participants showed biological age acceleration during follow-up. Difference-in-differences analyzes showed that increased heat wave exposure was consistently associated with accelerated biological age, and the association was stronger under a stricter heat wave definition.
Under the most stringent HW12 definition (defined as at least four consecutive days of apparent temperature above the local 97.5th percentile), each additional heat wave event increases biological age acceleration by 0.531 years, and each additional heat wave day is associated with an increase of 0.057 years, which also increases the probability of accelerated biological aging. Subgroup analyzes showed strong associations among participants with BMI ≥ 23 kg/m², urban dwellers, and participants residing in southern China or subtropical monsoon regions, suggesting that metabolic status and living environment may shape vulnerability to heat exposure. Further biomarker analysis showed that heatwave exposure was associated with increases in total cholesterol and glycated hemoglobin, which may disrupt lipid and glucose metabolism. Transcriptome analysis of liver tissue from aged mice supported this mechanism and identified 29 heat wave-induced differentially expressed genes enriched in lipid metabolism, atherosclerosis, and insulin resistance pathways. Altogether, these findings suggest that repeated heat wave exposure can disrupt metabolic homeostasis and accelerate biological aging.
The importance of this study lies in linking climate change-related heat wave exposure to biological aging, suggesting that heat waves not only pose acute health risks, but may also influence aging trajectories through long-term physiological damage. By combining a national population-based cohort and transcriptome analysis of aged mice, this study found that repeated heat wave exposure is associated with accelerated biological aging, with stronger effects among individuals with higher BMI, urban dwellers, and those living in southern or subtropical regions, indicating that metabolic status and living environment jointly shape vulnerability to heat exposure.
Further biomarker and molecular analyzes pointed to perturbations in lipid and glucose metabolism, supporting a potential pathway from heat stress to metabolic dysregulation and accelerated biological aging. This study provides a new perspective for understanding the long-term effects of climate change on age-related health and highlights the need for targeted heat warnings, urban cooling measures, and community protection strategies for high-risk populations. However, this study is observational and cannot prove a direct causal relationship. Exposure to heatwaves is estimated using city-level meteorological data, which may not fully capture individual exposure. Biological age is mainly based on clinical biomarkers and needs to be further validated with molecular aging clocks and multi-omics data. And the sample size of the mouse transcriptome was limited. “In the future, we plan to conduct long-term follow-up studies in more regions and populations, combined with individual exposure monitoring and molecular mechanism verification, to more accurately assess the impact of heat waves on healthy aging.” Xu Dengyong said.
sauce:
Beijing Institute of Technology
Reference magazines:
Xu D. others. (2026). Exposure to heat waves accelerates biological aging through metabolic dysregulation. Cyborgs and bionic systems. DOI: 10.34133/cbsystems.0602. https://spj.science.org/doi/10.34133/cbsystems.0602
