On one side of the scale are the genes you inherited from your parents. On the other is how many hours you actually sleep. For a long time, it seemed genetics pulled harder. But a new study covering more than 200,000 people shows that real sleep can tip the balance, especially when it comes to excess weight and diabetes.
The authors analyzed data from the All of Us research program, which includes medical records, genomes, and fitness tracker data from people in six different ancestry groups. They looked for links between 455 genetic variants affecting chronotype (whether you're a night owl or an early bird) and sleep duration, and 3,414 diseases or traits. The strongest signal came from variant rs1421085 in the FTO gene: its link to obesity, diabetes, and cardiovascular issues appeared in Europeans, Americans, and Africans.
Next, the researchers built polygenic risk scores, a kind of overall genetic score for sleep, and compared them with real data on weight, waist circumference, and blood sugar. They found that the higher the genetic tendency for short sleep, the greater the risk of obesity and diabetes. But when actual sleep duration was taken into account (measured by Fitbit devices in 7,655 people), the genetic contribution almost completely disappeared. In cross-sectional comparisons, real sleep explained 85.6% to 99.9% of the association, and in longitudinal observations of the same people over time, it explained 7.1% to 44.0%.
The difference between genetic data averaged across all groups and results for individual populations is a reminder: there are no universal 'sleep genes.' What works for one group may be silent in another. So the study underscores the importance of population-specific approaches. In the end, the scale tips not so much in favor of genes, but in favor of how we manage our hours of rest.
as written by the authors arXiv:2605.23521
Sleep traits are shaped by genetic and environmental factors and may influence many health conditions. The All of Us Research Program, which includes EHR, physical measurements, genomic data, and wearable data across ancestry groups, provides an opportunity to study genetic and non-genetic contributors to sleep-related health outcomes. We examined associations between genetic predispositions to chronotype, sleep duration, and short sleep and health outcomes across ancestries, as well as the role of measured sleep duration. We used All of Us genome-wide association study results, including ancestry-specific and meta-analyses for 3,414 phenotypes, to identify phenotypes associated with 455 sleep-related SNPs. Cross-sectional and longitudinal analyses (n = 212,529) evaluated associations between polygenic risk scores (PRS) and anthropometric and metabolic measures from EHR. A subgroup analysis (n = 7,655) assessed sleep duration using Fitbit data. Across six ancestry groups, SNP analysis identified 61 phenotypes linked to 29 sleep-trait-associated SNPs. The chronotype SNP rs1421085 in FTO showed the strongest associations with obesity, diabetes, and cardiovascular conditions, mainly in European, American, and African groups. PRS analysis showed that higher predisposition to shorter sleep duration was associated with increased risk of obesity and diabetes, with ancestry-specific variation. Measured sleep duration attenuated these associations, with relative contributions of 85.6%-99.9% in cross-sectional analyses and 7.1%-44.0% in longitudinal analyses compared with PRS. This study identified health conditions associated with genetic predispositions to sleep traits and suggests that actual sleep duration may play a prominent role in sleep-related health outcomes. Differences among meta-, pooled-, and ancestry-specific analyses highlight the importance of population-specific research.
The FTO gene, linked to obesity, is active in the brain and influences hunger, but its activity depends on circadian rhythms — which is why disrupted sleep can amplify cravings for calorie-dense foods.
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