Frontiers in Public Health
Despite the crucial role of sleep quality in hyperuricemia onset and progression, there is limited evidence on sleep interventions to improve outcomes for hyperuricemic individuals. This study aims to investigate the effects of sleep duration and sleep difficulties on all-cause mortality in this population.
We conducted a secondary analysis of the National Health and Nutrition Examination Survey (NHANES) data from 2007 to 2018, including 5,837 participants. We employed weighted multivariable Cox proportional hazard models to evaluate the independent predictive value of sleep duration and trouble for all-cause mortality. Restricted cubic splines and segmented Cox proportional hazard models were used to examine threshold effects.
During a mean follow-up of 6.5 years, 906 participants experienced all-cause mortality. After adjusting for confounders, both short (< 7 h; HR = 1.25; 95%CI: 1.04, 1.51; p = 0.018) and long (>9 h; HR = 1.50; 95%CI: 1.10, 2.04; p = 0.011) sleep durations were associated with increased all-cause mortality. The threshold analysis identified an optimal sleep duration of 7.23 h, and when sleep duration was below 7.23 h, it was inversely related to mortality (HR: 0.879; 95% CI: 0.788, 0.981; p = 0.022). Conversely, when sleep duration exceeded 7.23 h, it was positively associated with mortality (HR: 1.187; 95% CI: 1.066, 1.320; p = 0.002).
Sleep duration is U-shapedly associated with all-cause mortality among individuals with hyperuricemia in the United States. However sleep trouble was not associated with all-cause mortality. Maintaining optimal sleep duration helps improve the prognostic survival rates of those with hyperuricemia.
Text reproduced verbatim from Version of Record (source); DOI; CC-BY-4.0.
Yuanhui Dai, Xiangyu Sun, Ge Zhang, Chunying Cui, Xiaoli Wu, Yierzhati Aizezi, Kaisaierjiang Kadier. Association between sleep duration, sleep trouble and all-cause mortality in individuals with hyperuricemia in the United States. Frontiers in Public Health. 2025;13:1521372. https://doi.org/10.3389/fpubh.2025.1521372
Association between sleep duration, sleep trouble and all-cause mortality in individuals with hyperuricemia in the United States
A secondary linked-mortality analysis relates self-reported sleep to mortality in a complex-survey population with hyperuricemia. Associations and the fitted turning point are epidemiological estimates, not a survival-improving sleep prescription; sleep-trouble findings do not cover every diagnosed sleep disorder.
How are self-reported sleep duration and sleep trouble associated with linked all-cause mortality among the analyzed NHANES participants with hyperuricemia?
This secondary linked-mortality analysis examines self-reported sleep in a complex-survey population. The reported associations and fitted turning point are epidemiological estimates, not proof that prescribing a precise sleep duration improves survival. The sleep-trouble result should not be generalized to every diagnosed sleep disorder.
Raw participant counts and survey-weighted percentages are different quantities and must not be directly substituted for one another.
| Measure | Value |
|---|---|
| NHANES cycles | 2007–2018 |
| analytic participants | 5,837 |
| deaths | 906 |
| mean follow up | 6.5 years |
| analysis | Survey-weighted Cox |
Source locator: Methods 2.1 and 2.6; Results 3.1
This is an observational association, not a randomized intervention that shortens or extends sleep.
| Measure | Value |
|---|---|
| comparison | <7 h versus 7–9 h |
| model | Fully adjusted Model 3 |
| hazard ratio | 1.25 |
| reported 95 percent CI | 1.04–1.51 |
Source locator: Results 3.2; Table 2
The relative hazard is not an absolute-risk estimate or an individual prognosis.
| Measure | Value |
|---|---|
| comparison | >9 h versus 7–9 h |
| model | Model 3 |
| hazard ratio | 1.50 |
| reported 95 percent CI | 1.10–2.04 |
Source locator: Results 3.2; Table 2
This result for one self-reported indicator does not prove that all sleep disorders have no effect on mortality.
| Measure | Value |
|---|---|
| exposure | Self-reported sleep trouble |
| model | Model 3 |
| hazard ratio | 1.04 |
| reported 95 percent CI | 0.87–1.25 |
| P | 0.651 |
Source locator: Results 3.2; Table 2
The turning point is a model estimate from this dataset, not an intervention-validated sleep prescription or a precise target for every individual.
| Measure | Value |
|---|---|
| RCS nonlinearity P | <0.001 |
| estimated turning point | 7.23 h |
Source locator: Results 3.3; Fig. 2; Table 3
| Cohort | Role | n | Relationship |
|---|---|---|---|
| NHANES linked-mortality analytic cohort | analytic sample with hyperuricemia | 5,837 | Independent cohort |
In 5,837 NHANES participants with hyperuricemia, with 906 deaths and mean follow-up of 6.5 years, Model 3 associations were HR 1.25 (95% CI 1.04–1.51) for <7 h and HR 1.50 (95% CI 1.10–2.04) for >9 h versus 7–9 h. These survey-weighted associations are not intervention effects or individual absolute-risk estimates.
The 2007–2018 linked-mortality analytic sample comprised 5,837 participants and 906 deaths with mean follow-up of 6.5 years. Survey-weighted Cox analysis does not make raw counts interchangeable with weighted percentages.
Evidence: KF1
Model 3 gave HR 1.04 (95% CI 0.87–1.25), P=0.651, without a statistically significant association for the self-reported indicator. This cannot be generalized to all diagnosed sleep disorders.
Evidence: KF4
Restricted cubic splines gave nonlinearity P<0.001 and an estimated turning point of 7.23 h. This dataset-specific model estimate is not an intervention-validated prescription.
Evidence: KF5
| Row ID | Component | Context | Finding | Evidence Level | Scope | Source Locator | Evidence refs |
|---|---|---|---|---|---|---|---|
| evidence-sleep-hua-1 | Survey-weighted analytic population and mortality follow-up | Raw participant counts and survey-weighted percentages are different quantities and must not be directly substituted for one another. | The NHANES 2007–2018 analytic sample included 5,837 participants and 906 deaths, with a mean follow-up of 6.5 years and survey-weighted Cox analysis. | Survey-weighted human exposure–mortality association | Describes a complex-survey analytic sample; raw counts are not survey-weighted percentages. | Methods 2.1 and 2.6; Results 3.1 | KF1 |
| evidence-sleep-hua-2 | Short-sleep mortality association | This is an observational association, not a randomized intervention that shortens or extends sleep. | In fully adjusted Model 3, short sleep (<7 h versus 7–9 h) was associated with all-cause mortality at HR 1.25 (95% CI 1.04–1.51). | Survey-weighted human exposure–mortality association | Supports an adjusted short-sleep association, not benefit from changing sleep duration. | Results 3.2; Table 2 | KF2 |
| evidence-sleep-hua-3 | Long-sleep mortality association | The relative hazard is not an absolute-risk estimate or an individual prognosis. | In Model 3, long sleep (>9 h versus 7–9 h) was associated with all-cause mortality at HR 1.50 (95% CI 1.10–2.04). | Survey-weighted human exposure–mortality association | Supports an adjusted long-sleep relative hazard, not an individual absolute risk or prognosis. | Results 3.2; Table 2 | KF3 |
| evidence-sleep-hua-4 | Self-reported sleep-trouble association | This result for one self-reported indicator does not prove that all sleep disorders have no effect on mortality. | Self-reported sleep trouble did not show a statistically significant association with mortality in Model 3: HR 1.04 (95% CI 0.87–1.25), P=0.651. | Survey-weighted human exposure–mortality association | Applies only to the studied self-reported indicator, not the safety of all sleep disorders. | Results 3.2; Table 2 | KF4 |
| evidence-sleep-hua-5 | Nonlinear sleep-duration estimate | The turning point is a model estimate from this dataset, not an intervention-validated sleep prescription or a precise target for every individual. | Restricted cubic splines showed nonlinearity (P<0.001), with an estimated sleep-duration turning point of 7.23 h. | Survey-weighted human exposure–mortality association | Supports a data-derived turning point, not a prescribed personal sleep target. | Results 3.3; Fig. 2; Table 3 | KF5 |
The NHANES 2007–2018 analytic sample included 5,837 participants and 906 deaths, with a mean follow-up of 6.5 years and survey-weighted Cox analysis. Raw participant counts and survey-weighted percentages are different quantities and must not be directly substituted for one another.
Evidence: KF1
In fully adjusted Model 3, short sleep (<7 h versus 7–9 h) was associated with all-cause mortality at HR 1.25 (95% CI 1.04–1.51). This is an observational association, not a randomized intervention that shortens or extends sleep.
Evidence: KF2
In Model 3, long sleep (>9 h versus 7–9 h) was associated with all-cause mortality at HR 1.50 (95% CI 1.10–2.04). The relative hazard is not an absolute-risk estimate or an individual prognosis.
Evidence: KF3
Self-reported sleep trouble did not show a statistically significant association with mortality in Model 3: HR 1.04 (95% CI 0.87–1.25), P=0.651. This result for one self-reported indicator does not prove that all sleep disorders have no effect on mortality.
Evidence: KF4
Restricted cubic splines showed nonlinearity (P<0.001), with an estimated sleep-duration turning point of 7.23 h. The turning point is a model estimate from this dataset, not an intervention-validated sleep prescription or a precise target for every individual.
Evidence: KF5
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