The cohort was recruited from 12 Southeastern states between March 2002 and September 2009 and was distinguished by its racial and socioeconomic diversity. It included 22,437 non-Hispanic Black or African American men, 9,609 non-Hispanic White men and 1,215 men from other racial groups. About 85% of participants were recruited through community health centers, while 15% came through population-based methods, and the authors described the population as predominantly low-income. Among the men who died from prostate cancer, most were between 50 and 69 years old at enrollment and had household incomes below $25,000; about 45% reported being current smokers.

Investigators used a baseline questionnaire to assess sleep separately on weekdays and weekends. Participants reported in full-hour increments how many hours they typically slept during a 24-hour period. The researchers calculated a weighted average using the formula [(weekday sleep duration × 5) + (weekend sleep duration × 2)]/7. Sleep measures were classified as less than six hours, six hours, seven to eight hours or at least nine hours, with seven to eight hours serving as the reference category. Participants also rated how often their sleep had been restless during the preceding week, ranging from rarely or none of the time to most or all of the time; the lowest frequency was the reference level.

Prostate cancer-specific mortality was determined through linkage with the National Death Index through December 31, 2022, while vital status was ascertained through the Social Security Administration. Prostate cancer deaths were classified using underlying-cause data from the National Death Index and the International Classification of Diseases, Tenth Revision code C61. Follow-up for each man began at enrollment and continued until a prostate cancer death or December 31, 2022, whichever occurred first. The researchers used multivariable Cox proportional hazards regression to estimate hazard ratios and 95% confidence intervals, and the proportional-hazards assumption was assessed with Schoenfeld residuals and considered satisfied.

The statistical models accounted for age, race and ethnicity, recruitment source, education, household income, body mass index, current employment, smoking, alcohol use, physical activity and several medical histories. The latter included diabetes, depression, hypertension, chronic obstructive pulmonary disease, asthma, stroke and benign prostate hyperplasia. Age was initially grouped into 40–49, 50–59, 60–69 and 70–79 years. Race and ethnicity were additionally examined as potential effect modifiers through separate analyses for non-Hispanic Black and non-Hispanic White men, with a Wald test used to assess sleep-by-race interaction. Most sleep and covariate variables had missing or unknown values below 3.6%, and the primary models used complete cases.

Weekend sleep produced the clearest result, while the study did not identify a consistent relationship for weighted average sleep, weekday sleep or restless sleep. For men reporting at least nine hours of weekend sleep, the adjusted hazard ratio for prostate cancer-specific mortality was 1.44 compared with seven to eight hours. By contrast, no consistent associations emerged for the other sleep measures. The available evidence also did not show that sleep characteristics interacted clearly with race or ethnicity. In other words, the analysis did not find a statistically clear indication that the sleep–mortality relationship differed between Black and White men.

Race-specific estimates for long weekend sleep pointed in the same direction but were less precise because each subgroup had fewer prostate cancer deaths. Among Black men, the hazard ratio was 1.36 for at least nine hours of weekend sleep versus seven to eight hours, with a 95% confidence interval of 0.93 to 1.99. Among White men, the corresponding estimate was 2.57, but its 95% confidence interval ranged from 0.98 to 6.75. Both intervals included a hazard ratio of 1, and the number of deaths among men in the longest-sleep category was small, particularly in the White subgroup. The stratified results therefore provide limited support for a similar pattern in both groups, not proof of distinct race-specific associations.

Several sensitivity analyses produced results consistent with the main analysis. Fine–Gray subdistribution hazard models, which account for death from other causes as a competing event, gave similar findings. The researchers also used multiple imputation for missing covariates under a missing-at-random assumption, generating 30 complete datasets while leaving the sleep exposures un-imputed; the resulting estimates were similar to those from the complete-case models. Additional adjustment for prostate-specific antigen testing, digital rectal examination, the Healthy Eating Index and family history of prostate cancer did not change the inferences. A further sensitivity analysis treated age as a continuous variable rather than a categorical one and retained the observed pattern.

The investigators cautioned that long sleep may function as a marker of underlying poor health rather than a direct cause of prostate cancer mortality. In their analysis, long sleep was more common among participants who were not currently working, who were current smokers or who reported a history of depression. They also noted that prolonged weekend sleep could reflect irregular sleep during weekdays, fatigue or a delay in circadian timing. These are possible explanations rather than mechanisms demonstrated by the study, which measured only sleep duration and restless sleep at baseline and did not directly evaluate why participants slept longer.

Several limitations constrain the findings. Sleep duration and restless sleep were self-reported, creating the possibility of exposure misclassification, and a single baseline assessment may not represent long-term sleep patterns. The study lacked information on sleep medication use, sleep disorders, shift work, snoring, chronotype and medical treatments that could affect sleep. The relatively small number of prostate cancer deaths, especially in extreme sleep-duration categories and race-specific groups, limited statistical power and produced imprecise estimates. The observational analysis also cannot determine whether longer sleep contributes causally to prostate cancer death or instead reflects other health conditions that influence survival.

Overall, the study offers a prospective signal linking unusually long weekend sleep with prostate cancer-specific mortality in a cohort composed largely of Black men recruited from low-income communities in the southern United States. It does not find a consistent relationship between sleep and prostate cancer death across the full range of sleep measures, and the race-stratified estimates remain statistically uncertain. The authors call for larger studies with more deaths, additional sleep characteristics and information about sleep medications and sleep disorders. Whether the observed weekend-sleep pattern is causal, a marker of underlying illness or a combination of both remains unresolved.

Subject of Research: Prospective associations of self-reported sleep duration and restless sleep with prostate cancer-specific mortality in Southern men

Article Title: Sleep duration and prostate cancer-specific mortality in the Southern Community Cohort Study

Article References: Anukam, D. C., Nianogo, R. A., Arah, O. A., Rao, J., Fowke, J. H., Hashibe, M., & Zhang, Z.-F. (2026). Sleep duration and prostate cancer-specific mortality in the Southern Community Cohort Study. Cancer Causes & Control, 37(11), Article 182. https://doi.org/10.1007/s10552-026-02256-8

Image Credits: AI Generated

DOI: 10.1007/s10552-026-02256-8

Keywords: prostate cancer mortality, sleep duration, weekend sleep, restless sleep, prospective cohort, Southern Community Cohort Study, Black men, health disparities, self-reported exposure, competing risks, Sleep, duration