> Incidence of coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, and stroke
> People with the brightest nights (90-100th percentiles) had significantly higher risks of developing coronary artery disease (adjusted-HR range: 1.23-1.32), myocardial infarction (aHRs: 1.42-1.47), heart failure (aHRs: 1.45-1.56), atrial fibrillation (aHRs: 1.28-1.32), and stroke (aHRs: 1.28-1.30), compared to people with dark nights (0-50th percentiles).
> These relationships were robust after adjusting for established risk factors for cardiovascular health, including physical activity, smoking, alcohol, diet, sleep duration, socioeconomic status, and polygenic risk. Relationships of night light with risk of heart failure and coronary artery disease were stronger for women, and relationships of night light with risk of heart failure and atrial fibrillation were stronger for younger individuals in this cohort.
These relationships were *robust*.
The observed associations between nighttime light exposure and increased incidence of coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, and stroke may be driven by complex and multifactorial pathways. These cardiovascular conditions can arise from numerous interrelated long- and short-term physiological and behavioral factors, making it difficult to isolate the causal role of nighttime light exposure alone.
It is plausible to hypothesize that if individuals in the lower-exposure group were subjected to increased nighttime light exposure under controlled conditions—where all other lifestyle factors remained constant and stress levels were actively managed—their cardiovascular risk might not increase. This would suggest that ambient light exposure at night, in isolation, may not be a direct etiological factor.
Although the study adjusted for a broad range of established cardiovascular risk factors—including physical activity, smoking, alcohol consumption, diet, sleep duration, socioeconomic status, and polygenic risk—these adjustments do not capture acute or chronic variations in psychological stress. Since stress is a known contributor to cardiovascular disease, the inability to directly account for its temporal dynamics represents a potential limitation in the interpretation of these findings.