Sleep is a fundamental physiological process that plays a critical role in maintaining human health and overall well-being. It serves as a natural adaptation to the alternation of day and night, regulated by intricate neural mechanisms and following a strict rhythm (1). However, the fast-paced nature of modern life has resulted in significant changes in sleep patterns, posing a significant public health concern. Recent research has placed considerable emphasis on sleep duration and its impact on cardiovascular health (1).

Previous studies have highlighted associations between sleep duration and the prevalence of cardiovascular disease (CVD), suggesting a potential link between insufficient sleep and an elevated risk of CVD and all-cause mortality (2). Some researchers have even proposed sleep duration as a potential predictor of cardiovascular outcomes (3). Additionally, inadequate sleep duration has been linked to a higher risk of developing or dying from coronary heart disease (CHD) and stroke, although not for total CVD (4). On the other hand, an increased risk of CHD, stroke, and total CVD has been associated with long sleep duration (4). Both short and long sleep durations serve as predictors or markers and are associated with a heightened risk of all-cause mortality and cardiovascular events (4, 5). Nevertheless, studies focusing on healthy individuals (6) and middle-aged participants (7) have reported no significant association or correlation between sleep duration and mortality. It is crucial to consider various factors such as differences in research objectives, study designs, sample sizes, follow-up periods, and confounding variables that may influence these findings. Consequently, further investigations are warranted to comprehensively evaluate the relationship between sleep duration and all-cause and cardiovascular mortality.

Given the existing gaps in knowledge, our study aims to explore the association between sleep duration and all-cause and cardiovascular mortality using data obtained from a large cohort of participants included in the National Health and Nutrition Examination Survey (NHANES). As an observational study, our research contributes to the expanding body of evidence on this topic and provides valuable insights into the potential relationship between sleep duration and cardiovascular outcomes.

In this large, long-term study, we observed that the optimal sleep duration associated with the lowest risk of all-cause and cardiovascular mortality was approximately 7 h. These results confirm the findings from a previous cross-sectional study of sleep duration and cardiovascular health (17) and reinforce the detrimental impact of sleep disorders on cardiovascular health.

The American Academy of Sleep Medicine, the Sleep Research Society, and the National Sleep Foundation define “short sleep” as a duration of less than 7 h per night (18, 19). Although there is some variation in the definitions used across studies, it is important to note that our results align with the recommendation of 7 h of sleep per night as outlined in a 2015 consensus statement by the American Academy of Sleep Medicine and the Sleep Research Society (20). This statement emphasized that sleep durations below 7 h can impair immune function, affect metabolism, and have adverse effects on cardiovascular, cerebrovascular, and mental health. Furthermore, insufficient sleep has been associated with increased risks of obesity, diabetes, hypertension, heart disease, stroke, depression, and mortality (20). Several population-based cohort studies have consistently shown that individuals with shorter sleep durations are at higher risk of all-cause and cardiovascular death (21–23). Our findings reinforce these previous observations, indicating that a sleep duration of approximately 7 h represents a threshold for increased risk, with significantly shorter sleep durations corresponding to higher mortality risk.

Researchers have made efforts to elucidate the underlying mechanisms linking short sleep duration and increased cardiovascular risk. One potential mechanism involves metabolic dysregulation associated with inadequate sleep. Abnormalities in the release of peptides and leptin, which are involved in regulating energy intake, may contribute to this process. Peptides stimulate hunger and increase appetite, while leptin inhibits hunger and reduces appetite (24). Recent studies have demonstrated that shorter sleep durations can promote peptide release and inhibit leptin release, leading to increased food intake, weight gain, decreased insulin sensitivity, and elevated blood glucose levels, ultimately contributing to obesity and impaired glucose tolerance (25). Sleep duration has also been correlated with lipid metabolism. A recent study revealed a significant nonlinear association between short sleep duration and low high-density lipoprotein (HDL) levels and high triglyceride levels (26). Another proposed mechanism involves the neuro regulation of central body tissues. In individuals with insufficient sleep, increased stimulation of the cardiovascular sympathetic nerves results in heightened tension, reduced parasympathetic activity, elevated heart rate, and heightened reactivity, ultimately leading to increased blood pressure and vascular endothelial cell damage (27). Additionally, a study found that short sleep duration leads to decreased blood flow velocity in the cerebral basilar artery and midbrain, resulting in regional inadequate blood supply to the brain and triggering oxidative stress, inflammation, platelet dysfunction, and metabolic disorders (28).

The definition of “long sleep” is not well-defined, similar to “short sleep.” The consensus statement from the American Academy of Sleep Medicine and the Sleep Research Society stated that it remains uncertain whether sleep durations exceeding 9 h per night are associated with health risks for the general population, excluding individuals who are ill or have missed sleep (7). Recent Mendelian randomization studies have suggested a potential causal link between short sleep duration and CVD, but not for long sleep duration (29, 30). While our study found an increased risk of all-cause and cardiovascular mortality among individuals who slept more than 7 h per night, even after adjusting for covariates, we acknowledge that our findings do not establish a causal relationship. It is important to consider confounding factors in observational studies, such as conditions like depression, antidepressant use, or poor sleep quality, which can lead to longer sleep duration. These factors may confound the observed association, and the increased risk of CVD associated with long sleep duration could reflect underlying health conditions or residual confounding rather than a direct causal relationship.

The potential mechanisms underlying the association between long sleep duration and increased cardiovascular risk have also been investigated. An analysis of data from the Korea National Health and Nutrition Examination Survey (KNHANES) demonstrated a significant correlation between sleep duration of 9 h or more and low high-density lipoprotein cholesterol (HDL-C) levels (31). Another analysis found a positive correlation between longer sleep durations and increased levels of C-reactive protein (CRP) and interleukin-6 (IL-6) (32). In women, CRP levels were approximately 44% higher in those with habitual sleep duration of 9 h or more compared to those with 8 h of sleep after adjusting for age and BMI (33). CRP production is stimulated by IL-6, suggesting that the correlation between sleep duration and CRP levels may be secondary to the effect of sleep duration on IL-6 levels. Increased levels of CRP and IL-6 have previously been associated with an elevated risk of CVD and diabetes. Therefore, similar to short sleep duration, one potential mechanism by which long sleep duration may impact cardiovascular health is through the activation of inflammatory pathways. Insulin resistance may also play a role in the association between long sleep duration and cardiovascular risk. A study of nurses found that regular sleep durations exceeding 9 h were associated with a 47% increased risk of diabetes and a 57% increased risk of cardiac events (34, 35). Another recent study reported an increased risk of all-cause mortality among adult patients with type 2 diabetes who slept more than 7 h per night (36). Insulin resistance is a key risk factor for diabetes, and long sleep duration may contribute to an increased risk of insulin resistance through factors such as lack of physical activity, chronic inflammation, and disturbance of circadian rhythm. Furthermore, a prospective analysis of elderly individuals in China revealed that excessive sleep duration was associated with an increased risk of cognitive impairment, suggesting the need for early attention to neurodegeneration (37). Lastly, prolonged sleep duration may be associated with factors such as undiagnosed chronic conditions, depression, unemployment, low socioeconomic status, and reduced physical activity, which could further contribute to increased cardiovascular morbidity and mortality in these individuals (38).

A recent study found that both short sleep and long sleep were associated with an increased 10-year risk of CHD (39). However, a previous meta-analysis demonstrated that long sleep was more strongly correlated with adverse outcomes than short sleep, and the association between long sleep and mortality was not attenuated by improvements in health or lifestyle (40). In our study, the steep increase in the curve for all-cause mortality compared to cardiovascular mortality may be attributed to undiagnosed chronic complications among participants. This finding is highly consistent with previous studies that have reported an association between long sleep duration and increased mortality, particularly for non-cardiovascular cause (41, 42). Some researchers have even proposed using long sleep duration as a diagnostic tool for detecting subclinical or undiagnosed physical and mental disorders (43).

Our study had several strengths, including a relatively large sample size and a long follow-up period. However, it is important to acknowledge certain limitations inherent in our research. Firstly, while we were able to quantitatively measure the duration of sleep, the overall assessment of sleep is multifaceted and involves various aspects such as circadian rhythm, sleep initiation and maintenance difficulties, and sleep-related breathing disorders. Moreover, it is important to note that sleep patterns may change over time. Our study relied on a single assessment of sleep patterns at baseline, and we did not collect follow-up data to capture potential changes in sleep duration or quality during the study period. These aspects were not comprehensively captured in our study, which may have limited our understanding of the complexity of sleep patterns and their potential effects on health outcomes. Secondly, our study relied on self-reported sleep data, which introduces the possibility of memory biases and inaccuracies in reporting. Objective measures of sleep, such as polysomnography or actigraphy, could provide more precise and detailed information on sleep patterns and help overcome these limitations. Finally, while we made efforts to control for numerous confounding factors, it is possible that unmeasured confounders may exist. It is worth highlighting that our study did not include laboratory investigations such as inflammatory markers or hormone levels. As a result, our observations regarding potential underlying mechanisms remain largely speculative, and further research incorporating these measures is warranted to provide a more comprehensive understanding of the relationships between sleep duration and health outcomes.

In this large-scale, long-term study, we have further clarified the exact relationship between sleep duration and all-cause and cardiovascular mortality in American adults, demonstrating that the risk of all-cause and cardiovascular mortality was lowest when sleep duration was approximately 7 h. However, the pathophysiological mechanisms linking sleep disorders and negative prognosis require further investigation. Future studies should focus on understanding the underlying mechanisms and determining whether interventions targeting both sleep duration and quality can effectively reduce morbidity and mortality rates. These studies will be crucial in developing strategies to improve sleep-related health outcomes.