The Science of Health Disparities Research. Группа авторов

to the hypothalamus. For instance, sleep deprivation has been shown to downregulate leptin (a hormone associated with satiety) and upregulate ghrelin, a hormone associated with increased hunger [42]. The combined action of these hormones has considerable influence on the development of a host of chronic health conditions (e.g., obesity, type 2 diabetes). Additionally, hyperarousal of certain brain regions related to sleep deprivation is associated with hedonistic behaviors like sweet/salty food cravings. Furthermore, sleep disturbances often precede the onset of mood disorders, like anxiety and depression, which, for instance, exacerbate risk factors for suicide and depression relapse [43].

      2.5.1 Sleep Health Disparities and Allostatic Load

      Large racial/ethnic disparities in sleep and sleep disorders exist. Blacks (especially men) are nearly twice as likely as Whites to report short sleep duration [44]. Blacks are also over 60% more likely to report being long sleepers [45]. Evidence also suggests that Latinos compared to non‐Hispanic Whites may also be at higher risk for both a short and long duration of sleep [46].

      Furthermore, sleep architecture appears to differ by race. For instance, Blacks consistently have been shown, based on objective sleep measures, to experience less deep (or N3) sleep and more light sleep (N1 and N2), take more time to fall asleep, and spend less time in bed actually sleeping. Although there are believed to be many undiagnosed cases of sleep apnea (especially among minorities), the prevalence is highest among Blacks, and Black children are alarmingly, four to six times more likely than White children to have OSA [47].

Moreover, Blacks also experience more severe health consequences as a result of significantly higher rates of obesity and hypertension at the time of sleep apnea diagnosis [48]. Compared to Whites, Blacks, and Hispanics, Chinese individuals appear to have a stronger association of increasing BMI and waist circumference with sleep‐disordered breathing [49].

      Regarding insomnia, the results are mixed, but Whites seem to have the highest prevalence. These estimates may, however, be based on methodological issues related to varying insomnia definitions, the use of self‐reported data, and the need for a formal diagnosis that is highly influenced by healthcare access and utilization, which often varies by race and ethnicity. Sleep irregularities may also contribute to disproportionately high rates of chronic conditions, such as hypertension among Blacks. This may be due, at least in part, to a higher likelihood of nondipping blood pressure during deep or N3 sleep. Disproportionately poorer sleep may also contribute to disparities in metabolic health conditions, such as type 2 diabetes, by contributing to greater levels of insulin resistance and cardiovascular disease through pathways linked to higher levels of the circulating inflammatory cytokines described above. Therefore, preventing or minimizing the impact of modifiable environmental and social disturbances on sleep duration, quality, and timing could help mitigate racial/ethnic and socioeconomic disparities in common chronic health conditions associated with rising levels of allostatic load [12].

      Understanding the fundamental cause(s) of racial/ethnic differences in sleep, its contribution to allostatic load, and the combined influence on chronic health conditions across the lifespan is important. The ultimate goal of generating new knowledge in these areas is to provide strategies for intervention and disease risk reduction that will most efficiently reduce widespread health‐associated inequities. The upstream factors that could contribute significantly to racial disparities include physical and social environments and/or epigenetic influences.

      Racial groups have historically lived and continue to live in different environments—both physically and socially—and these differences in exposures to adverse conditions lead to differential levels of physiological dysregulation at multiple points across the life course. These differences likely contribute to an increased risk of acute and chronic health conditions. Experimental and observational studies demonstrate that the properties contributing to sleep are both intrinsic and extrinsic, and involve a broad complement of environmental as well as social factors, such as light, temperature, noise, air quality, diet/nutrition, medication use, physical activity, safety, and social cohesion. Adverse exposure to any of these and other factors can lead to insufficient or disturbed sleep [50]. Compared to Whites, Blacks and many other racial/ethnic groups have greater exposure to potentially health‐damaging environments and less access to health‐promoting goods and services that may influence their risk of both poor sleep and health. This could be due to living in less healthy urban neighborhoods or resource‐limited rural regions with higher frequencies of food deserts or swamps, and where there is less access to safe areas for recreational activity.

      2.5.2 Sleep Health Disparities and Genetics

Genetics is clearly another important factor to consider. Genes account for 31–55% of a person's sleep duration, with behavior and environment accounting for the remainder [51]. Although genetics is a major contributor to sleep in all individuals, modifiable environmental factors are likely to play a larger role than genetics in poor sleep and poorer health between races. For instance, racial residential segregation resulting in differential exposure to artificial light at night, noise, and safety concerns due to poverty, for example, may have a more profound impact on sleep than genetic differences. Moreover, single nucleotide polymorphisms with minor allele frequencies (which generally need to be functional and may still confer small risks) are likely to play a much smaller role than the environment in shaping racial variation in health and disease. It is now widely accepted that race, as distinct from ancestry, is a social construct whose distinguishing phenotypes (e.g., skin and eye color) are not strongly linked to lifestyle‐related health conditions that cause the majority of premature deaths in the United States [52]. In fact, the human genome project found that all humans are 99.9% the same (meaning that genetic variants overlap). There is more genetic diversity within (especially among people of African ancestry) than between racial categories—which are, again, socially constructed and have changed over time.

      Despite the large overlap of genetic variants across racial groups, studies should investigate how much (or how little) ancestral differences in genetic architecture (e.g., haplotypes, structural variation) contribute to observed differences in various sleep characteristics that affect health outcomes. These studies should also acknowledge that behaviors such as sleep are complicated and strongly influenced by nongenetic environmental factors. In fact, race could serve as a proxy/marker for relative advantage or disadvantage by identifying groups with more or less social and economic obstacles to health.

      Finally, gene expression can be modified without altering an individual's actual genetic code (known as epigenetics, or gene‐by‐environment interactions). Environmental factors such as diet/nutrition, as well as toxicants (e.g., phthalates, flame retardants, surfactants, bisphenol‐A, and fungicides like vinclozolin), can promote the epigenetic transgenerational inheritance of disease and phenotypic variation [53]. Epigenetics (especially in early life) may play an important role in racial differences in the relationship between sleep and many health outcomes influenced by sleep, since Blacks and Whites have historically been and currently are exposed to different physical and social environments across the life course.

      Behaviors and biological mechanisms along the pathway between sleep and suboptimal health outcomes are likely affected by the aforementioned upstream environmental and social factors, contributing to the often‐observed racial differences in risk, prevalence, and severity of both poor sleep characteristics and their downstream health sequelae.

      2.5.3 Methodologies in Sleep Research

Research focused on sleep and sleep disparities can advance the field by addressing important methodological challenges. For instance, studies should include more prospective designs to establish temporal ordering of sleep and health outcomes. Objective sleep measures, as obtained by wrist actigraphy and polysomnography (the gold standard), are needed to minimize hard‐to‐report sleep‐related behavior misclassification (e.g., sleep latency, snoring among individuals without a bed partner). Researchers should keep in mind that addressing sleep disparities at a population level to prevent subsequent poor health outcomes will require more racial/ethnic minority inclusion in studies, as well as scientific evidence (likely from multilevel research including individual,