The leading cause of death in the world today is cardiovascular disease (CVD), including coronary heart disease (CHD), stroke, peripheral arterial disease, deep vein thrombosis, and pulmonary embolism (41, 42). By addressing modifiable risk factors, such as reducing excessive dietary salt, improving a poor diet, lowering obesity, avoiding excessive alcohol consumption, increasing physical activity, and improving socioeconomic conditions, premature deaths from cardiovascular disease can be prevented (43). This is the most cost-effective intervention for reducing cardiovascular disease-related morbidity and mortality and improving cardiovascular health.

According to the Coronary Artery Risk Development in Young Adults (CARDIA) cohort study conducted in Chicago, there is evidence of an association between objectively measured sleep duration and cardiometabolic disease (43). From this report, 18- to 30-year-old individuals were participated and were followed up for five years. The sleep metrics were measured using wrist actigraphy, and to measure the calcifications of their coronary arteries, a CT scan was used. After excluding the possible confounding factors, participants with a sleep habit of 5 hours or less had a sharp increase in their risk of developing coronary calcifications, which is in turn a risk factor for myocardial infarction. Women are more affected than men, although the possible justification of gender differences is not well stated. Similar to what was reported, individuals who regularly slept less than 5 or 6 hours were more likely to experience episodes of coronary heart disease and develop stroke in the long run than people who typically slept for about 6 to 8 hours each night (44). If the short sleep is accompanied by poor sleep quality, the risk is greater. In general, few studies have investigated the associations of objectively measured sleep duration with incident cardiovascular diseases (CVDs). A prospective cohort study of 12,770 people in the United Kingdom discovered that getting enough sleep is associated with a lower risk of cardiovascular disease in people with diabetes (45). A cross-sectional study involving a sample of 893 adults found that shorter sleep duration, as determined by wrist actigraphy, is associated with higher SBP and possibly cardiovascular risk. Objectively measured short sleep duration may therefore be a modifiable behavioral target for reducing cardiovascular risk (46). Yadav et al. also showed that objectively measured short sleep duration was consistently associated with the occurrence of hypertension in middle-aged participants (47). The findings were in line with previous studies carried out by Bertisch et al. which also reported that short sleep duration was associated with hypertension compared to individuals who had normal sleep duration (48). Another prospective study of 1715 Korean adults aged 40 to 70 years found that objectively short sleep duration is independently associated with the development of hypertension among middle-aged and elderly Korean adults (47). Thus, the study encourages clinicians and researchers to promote sound sleep practices in society by giving evidence that explains the association between objective short sleep duration and hypertension as a risk predictor of the incidence of cardiovascular disease.

Hypertension is a known risk factor for cardiovascular disease and leads to disability and death. It is often described as a “silent killer” because it rarely causes symptoms (49). Currently, studies prove a significant association between short sleep (less than 5 hours per night) and an increased risk of hypertension (19, 50). In the Penn State Cohort study, Bertisch et al. showed that objectively measured short sleep duration is a clinically significant risk factor for the development of hypertension independent of other risk factors such as age, race, obesity, diabetes mellitus, smoking, caffeine, or alcohol consumption (48). Using a cross-sectional, observational study design of 255 adult volunteers, Bathgate et al. reported that objectively measured short sleep duration of < 6 hr was associated with an increased risk of hypertension development as compared to individuals with a sleep duration of >6 hrs (51). However, no significant risk was observed using subjectively measured sleep duration groups in this study. Finally, this study concluded that objectively short sleep duration increased the likelihood of hypertension more than three times, taking into account possible confounding variables, and, in turn, increased the risk of cardiovascular disease (51).

The term “metabolic syndrome” refers to a group of metabolic risk factors including glucose intolerance, dyslipidemia, hypertension, and central obesity that are associated with an increased risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD), including glucose intolerance, dyslipidemia, hypertension, and central obesity (52). According to the Joint Interim Statement (JIS) harmonized, the following three components are required for the definition of Metabolic Syndrome (MetS), of which waist circumference is not a prerequisite: High resting blood pressure (≥ 130/85 mmHg) or on hypertension treatment; ≥ 5.6 mmol/l fasting blood sugar or on diabetes treatment: Elevated waist circumference (WC): Females ≥92 cm, males ≥86 cm; elevated triglycerides (TG): ≥1.7 mmol/l and reduced high-density lipoprotein cholesterol (HDL-C): men < 1.0 mmol/l, women < 1.3 mmol/l (53). Most previous studies exploring the relationship between sleep duration and MetS-related morbidity and mortality were inconsistent and underwhelming (54–56). For instance in In a cross-sectional study of Chinese children and adolescents, Duan et al. reported that objective short sleep duration is associated with higher odds of metabolic syndrome and abdominal obesity. However, the relationship between short sleep duration and MetS in children and adolescents has been inconsistent (56). In a population-based study, Fernandez-Mendoza et al. demonstrated the PSG and reported that objectively measured short sleep duration modifies the elevated risk of CVD mortality associated with MetS. Importantly, this is primarily caused by the high blood pressure and glucose dysregulation components of MetS, which suggests that objectively short sleep duration in those with MetS may be related to the degree of central autonomic and metabolic dysfunction (57). On the other hand, Cook et al. found a significant non-linear (U-shaped) association between short sleep duration and JIS-MetS risk (p = 0.0308) ( Table 1 ) (16). The findings of this study are consistent with the study conducted by Rae et al. (9). According to the authors, this was the first actigraphy-measured sleep and cardiometabolic health study from a rural South African setting. Future clinical trials should investigate whether long-duration sleep improves the prognosis of people with MetS.

The global prevalence of obesity has increased dramatically over the past few decades, and the World Health Organization has declared it a global epidemic (58). The rise in obesity is paralleled with a decrease in sleep duration. Most of the previous studies were predominantly cross-sectional; that is, they measured both sleep duration and the presence of obesity at the same time. Therefore, a possible relationship cannot support a causal association. More recently, however, objective measures of sleep using actigraphy and more specific measures of adiposity (fat mass versus lean body mass) appear to support the link between sleep deprivation and obesity (59). Experimental studies provide a good explanation of the plausible mechanism of how short sleep leads to obesity. Chronic short-term sleep results in increased energy intake and decreased energy expenditure by activating hormonal responses that regulate appetite and energy balance (60). During sleep deprivation, there are reciprocal changes in leptin, a hormone that regulates energy storage and satiety, and ghrelin, a hormone that increases appetite ( Figure 1 ) (61). These two hormones regulate the hunger and satiety of individuals.

Several epidemiologic and longitudinal studies have reported that short sleep duration is a risk factor for the incidence of obesity. For example, in sex-and age-stratified analyses, Sluggett et al. indicated that short sleep duration increased the likelihood of being overweight or obese in children and adolescents compared to longer sleepers (62). In contrast to this study, a cohort sleep laboratory study using polysomnography (PSG) showed that objectively measured short sleep duration is not significantly associated with obesity (63).

Type-2 diabetes is the most common type of diabetes in the world, and it is characterized by the body’s inability to use glucose from circulation, resulting in hyperglycemia. This is caused by peripheral tissue resistance to the action of insulin to take up glucose into the cell (insulin resistance) or inadequate pancreatic insulin production in response to a glucose load (64).

Currently, several studies have revealed that sleep duration is associated with poor glycemic control (17, 65, 66). In a sample of 384 Mexican adolescents from a birth cohort study, Chen et al. reported that objectively shorter sleep duration and later sleep midpoint was associated with higher insulin resistance (HOMA-IR). In linear regression analysis, they found that shorter sleep duration was associated with higher log HOMA-IR after adjusting for age, sex, and sleep midpoint. In the sex-stratified models, the associations between insulin resistance and short sleep duration were more evident among girls (17). Another prospective cohort study of nulliparous women recruited between 16 and 21 weeks gestation found that shorter sleep duration and a later sleep midpoint using the actigraphy sleep measuring tool were associated with an increased risk of gestational diabetes. This study concluded that short sleep duration is the sole contributing factor to gestational diabetes in nulliparous women (67). This research was consistent with a cross-sectional study done in the UK with 2848 adult participants, which showed a link between short sleep duration and the incidence of diabetes mellitus (64). According to a population-based study conducted in 2021 on a Taiwanese population, short sleep duration increased the risk of T2DM. This study found that women who sleep for shorter periods have a higher risk of developing type 2 diabetes, which has an impact on the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index (68). In this review, the authors observed that the association between sleep durations and increased CMR has been well-documented in higher-income countries (37). However, objective sleep measures are relatively limited in low-income countries such as Sub-Saharan Africa. The majority of sleep studies conducted in this region most frequently used self-reported sleep. Thus, little is known about the prevalence and consequences of sleep disorders in African populations, and their association with type 2 diabetes mellitus has not yet been well investigated, based on objective sleep measures, in most parts of African countries (37).