Background: Sleep and circadian rhythm disturbances constitute modifiable risk factors for type 2 diabetes mellitus (T2DM). Meta-analytic evidence demonstrates that short sleep duration (9h) both increase T2DM risk (OR 1.28–1.48). Night shift work elevates risk dose-dependently (RR 1.40, 95% CI 1.15–1.71) across 1.16 million participants. Molecular mechanisms involve desynchronized clock genes (CLOCK, BMAL1, PER2, CRY1), mitochondrial dysfunction reducing oxidative capacity 20–30%, and altered melatonin signaling. Sleep extension interventions improve insulin sensitivity 17–45% within 1 week. Evening chronotherapy with glucose-lowering drugs demonstrates superior efficacy compared to morning dosing. CBT-I (cognitive behavioral therapy for insomnia) reduces T2DM incidence by 42% in prediabetic populations. Conclusion: Sleep and circadian optimization represent cost-effective, modifiable strategies for T2DM prevention. Personalized chronotherapy guided by genetic profiling and objective sleep/activity monitoring warrants implementation in clinical practice and public health policies.
Wojciech et al. (Wed,) studied this question.