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Ann Med
Ann Med
Annals of Medicine
0785-3890
1365-2060
Taylor & Francis

39253865
10.1080/07853890.2024.2399756
2399756
Version of Record
Review Article
Endocrinology
Racial and ethnic sleep health disparities in adolescents and risk for type 2 diabetes: a narrative review
E. L. M. Clark et al.
https://orcid.org/0000-0002-4922-7666
Clark Emma L. M. a
Gutierrez-Colina Ana ab
Ruzicka Elizabeth B. ab
Sanchez Natalia ac
Bristol Madison abc
Gulley Lauren D. ab
Broussard Josiane L. df
Kelsey Megan M. b
Simon Stacey L. be
Shomaker Lauren B. abc
a Human Development & Family Studies, College of Health & Human Sciences, Colorado State University, Fort Collins, CO, USA
b Pediatric Endocrinology, University of Colorado Anschutz Medical Campus and Children’s Hospital Colorado, Aurora, CO, USA
c Community & Behavioral Health, Epidemiology, and Global Health & Health Disparities, Colorado School of Public Health, Aurora, CO, USA
d Health & Exercise Science, College of Health & Human Sciences, Colorado State University, Fort Collins, CO, USA
e Pulmonology and Sleep Medicine, University of Colorado Anschutz Medical Campus and Children’s Hospital Colorado, Aurora, CO, USA
f Endocrinology, Diabetes and Metabolism, University of Colorado Anschutz Medical Campus, Aurora, CO, USA
CONTACT Emma L. M. Clark emma.clark@colostate.edu Human Development & Family Studies, College of Health & Human Sciences, Colorado State University, 1570 Campus Delivery, Fort Collins, CO, 80523-1570, USA
10 9 2024
2024
10 9 2024
56 1 239975627 11 2023
21 5 2024
9 7 2024
KnowledgeWorks Global Ltd.9 9 2024
published online in a building issue9 9 2024
© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group
2024
The Author(s)
https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

Abstract

Introduction

Sleep is an essential factor for health and wellbeing in people across the age spectrum; yet many adolescents do not meet the recommended 8–10 h of nightly sleep. Unfortunately, habitually insufficient sleep, along with the metabolic changes of puberty, puts adolescents at increased risk for a host of adverse health outcomes such as obesity and type 2 diabetes (T2D). Furthermore, individuals from historically minoritized racial and ethnic groups (e.g. Hispanic/Latinx, African American/Black) are more likely to experience shorter sleep duration compared to adolescents of White/European origin, placing them at even greater risk for disparities in T2D risk.

Methods

We conducted a literature review on the role of race and ethnicity in adolescent sleep health and its relation to cardiometabolic outcomes, specifically T2D. We use the minority stress model and the stress and coping theory as guiding theoretical frameworks to examine individual and societal level factors that may contribute to sleep health disparities and their downstream effects on T2D risk.

Results

This review highlights that the unique race-related stressors adolescents from minoritized groups face may play a role in the sleep and T2D connection on a biological, psychological, and social level. However, although there has been advancement in the current research on adolescent racial and ethnic sleep health disparities in relation to T2D, mechanisms underlying these disparities in sleep health need further investigation. Addressing these gaps is crucial for identifying and mitigating sleep health disparities and T2D among racial and ethnic minority youth.

Conclusion

We conclude with a discussion of the implications and future research directions of racial and ethnic disparities in sleep health and T2D prevention research. A comprehensive understanding of adolescent sleep health disparities has potential to better inform preventative and educational programs, interventions, and policies that promote sleep health equity and improve cardiometabolic outcomes like T2D.

Keywords

Sleep health disparities
adolescent
sleep
adolescent type 2 diabetes
social determinants of health
No funding was received.
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pmcOver 70% of U.S. high school students report insufficient sleep (<8 h) on school nights [1]. Adolescence is a vulnerable, developmental period for poor sleep health primarily due to biological factors (e.g. puberty, circadian rhythm changes, and shifts in natural sleep-wake cycles) along with psychosocial and environmental factors (e.g. academic/extracurricular demands and early school start times) that contribute to insufficient sleep [2]. These developmental changes typically lead to shorter sleep duration and reduced sleep quality, despite adolescents’ need for more sleep than adults [3–5]. Insufficient sleep during adolescence is associated with adverse cardiometabolic outcomes, such as poor insulin sensitivity, a key metabolic precursor that, in combination with insufficient insulin secretory capacity, is implicated in the chain to developing type 2 diabetes (T2D) [1, 6–14]. Puberty itself further heightens the risk, or potential, for developing T2D due to a transient and natural decline in insulin sensitivity during pubertal maturation [15]. Further, adolescents from historically underserved, minoritized groups are disproportionately at risk for poor sleep health and adverse cardiometabolic outcomes compared to adolescents of White/European origin [16]. Combined, these data highlight adolescence as a critical window to better understand the effects of sleep health on T2D risk [5], especially for youth from minoritized backgrounds who are already at greater risk.

Adolescent-onset T2D (<20 years of age) rates have increased annually by 5% over the last 20 years [17,18] and disproportionately affects individuals from racial and ethnic minoritized groups, including American Indian/Native American, Black/African American youth, and Hispanic/Latinx [17, 19]. Moreover, the annual incidence rates of adolescent-onset T2D has been increasing a faster rates for non-White/non-European adolescents, such as in American Indian/Native American adolescents (9%), Black/African American adolescents (6%), and Hispanic/Latinx adolescents (3%), compared to White/European adolescents (0.6%) [17, 19,20]. Adolescent-onset T2D has an aggressive disease course when compared to adult-onset T2D, with more rapid β-cell deterioration, greater health comorbidities, and earlier mortality [18, 21,22]. Unfortunately, effective prevention and treatment options for adolescent-onset T2D remain elusive, especially among adolescents from minoritized groups [22,23]. In addition to carrying a greater burden of T2D risk, adolescents from minoritized groups experience unique race-related stressors that have the potential to influence sleep health, via pathways such as disruptions in stress response and coping, which, in turn, potentially may propel T2D risk [24,25]. Although some research has been conducted on racial and ethnic health disparities in sleep in adults with T2D [26–29] as well as on racial and ethnic sleep health disparities in adolescents without diabetes [30], no work to date has considered the extent to which sleep health disparities may affect T2D risk in adolescents from minoritized groups.

To address this important gap, in this review, we draw on the minority stress model [25] and stress and coping theory [31] to explore adolescent and minority stress factors that may play a role in sleep health and its relation to T2D risk. The minority stress model theorizes that individuals from historically marginalized social backgrounds may experience excess stress and its associated adverse health consequences, which are uniquely related to their status as a minoritized individual [25]. Moreover, according to the transactional theory of stress and coping, an individual constantly appraises and evaluates stimuli in their daily environment, which may be appraised as potentially favorable and/or stressful, resulting in a coping response dependent on the situation [31,32]. Thus, a critical examination of unique race-related stressors that contribute to sleep health disparities among adolescents from minoritized groups could further our understanding of T2D prevention in a group in highest need for effective prevention efforts. In this review, we will first examine biophysiological and structural/societal stress factors that may contribute to sleep health disparities in adolescents at risk for T2D. Next, we will examine how disruptions in the stress system as a result of these stressors may be a mechanism that contributes to adolescent sleep health disparities and risk for T2D. We will conclude with a discussion of the implications and potential directions for future research on sleep health disparities and T2D prevention research.

The concept of sleep health is multidimensional, with definitions in pediatric populations that typically focus on six key dimensions: sleep duration (i.e. total amount of sleep obtained), sleep continuity or efficiency (i.e. ease of falling asleep and returning to sleep), sleep timing (i.e. when sleep occurs during the day), alertness/sleepiness/napping (i.e. how well wakefulness is maintained), the subjective assessment of satisfaction/quality of sleep, and sleep behaviors (i.e. bedtime routines and usage of electronic devices) [33,34]. The current review paper will focus on sleep duration, which is in line with the existing evidence regarding racial and ethnic sleep disparities in adolescents. While the socially defined constructs of race (i.e. a socially determined construct that categorizes individuals based on shared physical traits, which can result in a sociopolitical hierarchy) and ethnicity (i.e. a characterization of individuals based on their shared cultural ancestry and history) [35,36] hold no biological meaning, they are important terms to include in order to study racism, health disparities, and social inequities [37]. Finally, in this review, we will focus on the cardiometabolic risk of T2D and T2D-adjacent risks, such as insulin sensitivity and secretion.

Theoretical framework

Given the literature reviewed, to date, and drawing on the Meyer [25] minority stress model and the stress and coping biopsychosocial theoretical framework [31], Figure 1 depicts a conceptual model of how biophysiological-level stress factors and societal-level stress factors may be experienced by adolescents from minoritized groups, potentially contributing to sleep health disparities and T2D. Adolescents from minoritized groups face unique race-related stressors, both biophysiologically and societally. Some biophysiological stressors are a result of normative biological maturation (e.g. puberty) that all adolescents experience; however, other societal stressors are uniquely experienced as a result of being part of a minoritized group (e.g. discrimination). These varying sources of adolescent and minority stress together have the potential to disrupt the body’s stress system, which helps maintain the body’s homeostasis [38,39]. In theory, if the stress system is disrupted through increased types of stressors and/or through a higher severity of potential race-related stressors (e.g. systematic racism and discrimination), it is possible that this disruption can lead to deficiencies in sleep duration that disproportionately affect adolescents from minoritized groups, and therefore disproportionately increase T2D risk. Identification of underlying explanatory mechanisms for the association of sleep impairment with T2D among adolescents from minoritized groups is essential to mitigate health disparities.

Figure 1. Theoretical model of health disparities and T2D risk in adolescents from racial and ethnic minoritized groups.

Note. This theoretical model represents a small piece of racially and ethnically minoritized adolescents’ biophysiologically and socially determined stressors in relation to type 2 diabetes (T2D) risk; however, this is not a comprehensive list of all stress risk factors in this community.

Sources of adolescent and minority stress

Biophysiological stress factors

Adolescence is a vulnerable period for poor sleep and worsened insulin sensitivity

Many adolescents experience chronic, insufficient sleep [40,41]. According to the ‘Perfect Storm’ model, insufficient sleep during adolescence may result from the maturation of sleep bio-regulation systems in conjunction with evolving psychosocial factors [2]. Specifically, adolescents experience changes in the sleep/wake homeostasis process that enable them to stay awake longer which is accompanied by a physiological shift in circadian rhythm that delays sleep and wake onset [42]. Cortisol naturally secretes in a circadian pattern in which highest concentrations are in the early morning and at midnight [43]; however, this circadian rhythm, regulated by the central and peripheral nervous systems, is highly sensitive, such that even slightly elevated chronic stress with elevated evening cortisol levels, in conjunction with an increased sensitivity to glucocorticoids in the evening, have the potential to influence the development of metabolic challenges in adolescents [43,44]. Thus, early school start times, academic pressures, and social commitments can compound this shift in adolescent sleep resulting in further insufficient sleep and metabolic risk (i.e. worsened insulin sensitivity) for this already at-risk population [42, 45].

Societal stress factors

Adolescents from minoritized backgrounds may experience shorter sleep duration

Despite variations in sleep duration among adolescents from historically minoritized racial and ethnic groups, the extant literature overall suggests that adolescents from minoritized backgrounds are more likely to sleep less than adolescents of White/European origin, placing them at even greater risk for disparities in T2D risk [46]. For example, one study found that Black/African American adolescents, self-reported sleeping approximately 20 min less per week than their White/European comparisons [13, 47]. Similarly, a study using actigraphy found Black/African American adolescents slept 32 min less on weekdays and 41 min less on weekends than White/European adolescents [48]. This sleep difference was further confirmed in another study using wrist actigraphy, in which Black/African American adolescents slept on average ∼26 min per night less than White/European adolescents [49]. Moreover, another recent investigation using actigraphy to measure sleep showed that Black/African American adolescents slept less than Asian adolescents and Hispanic/Latinx adolescents by approximately 35 min per night [50]. Additionally, Asian American adolescents self-reported sleeping 18–24 min less per weeknight than White/European and Hispanic/Latinx adolescents [51]. Conversely, another study found that Black/African American and Hispanic/Latinx adolescents self-reported shorter sleep duration than White/European and Asian adolescents [16]. However, although past research has found these sleep health disparities in adolescent minoritized groups, there is limited research on why these disparities may exist.

Social determinants of sleep health disparities

Sleep health disparities may be partially explained by socially determined health factors [52]. Social determinants of health are non-medical factors/conditions in which people are born, live, learn, work, and grow that influence an individual’s health and quality of life, and these social determinants can drastically exacerbate health inequities [53]. In line with unique societal stress factors outlined in the minority stress model [25] and environmental stressors explained in the stress and coping theory [31], many individuals from racial and ethnic minoritized groups compared to individuals of White/European origin in the U.S. experience lower education quality and live in lower income, racially segregated areas [54–57]. Additionally, individuals from racial and ethnic minoritized groups typically experience reduced financial security, less access to healthcare, and fewer opportunities for economic growth [58–61]. As individuals from racial and ethnic minoritized groups have a higher likelihood of residing in disadvantaged, potentially unsafe neighborhoods compared to those of White/European origins, the disproportionate adverse effects of stress in these environments may directly and indirectly influence sleep health disparities [62–64].

Sleep health disparities experienced by adolescents from minoritized groups, compared to adolescents of White/European origin, may also be partially explained by socially determined health factors, such as socioeconomic status (SES) [52]. Indeed, research suggests that race and ethnicity and SES are associated with disparities in health status and sleep health outcomes [65,66]. Importantly, research further supports a connection between adolescent SES and sleep health in which adolescents with lower SES backgrounds experience poorer sleep outcomes, such as shorter sleep duration measured both subjectively via self-report and objectively using actigraphy, compared to those of higher SES backgrounds [67,68]. Other variables relating to SES (i.e. parental shift work, limited sleeping space, and threats to physical safety) may also interfere with adolescent self-reported sleep health [69]. Literature reviews further documented sleep disparities in which children and adolescents from racial and ethnic minoritized groups with less access to quality education and financial resources experience shorter sleep duration (measured using self-report, parent-report, and actigraphy) than White/European groups [30]. These racial and ethnicity-related social disparities may compound already existing excess stress during adolescence, contributing to sleep health disparities in adolescents from minoritized groups [70]. Although there has been mounting concern over the issue of SES and sleep health in adolescence, it is necessary to further investigate salient, underlying factors for sleep impairment among racial and ethnic minority youth, accounting for SES, to identify and mitigate the disparities in sleep health, obesity, and T2D in adolescents.

Disruptions in the stress system

Disruptions in the body’s stress system as a result of these biophysiological and unique structural/societal stressors may be a potential mechanism that contributes to adolescent sleep health disparities and their risk for adverse cardiometabolic health outcomes. According to the minority stress theory, individuals from historically marginalized social backgrounds experience excess stress, and associated negative health consequences, uniquely related to their minority status [25]. For example, racial and ethnic discrimination can further compound the adverse effects of stress by increasing stress exposures and by creating potential barriers to access health, educational, social, and financial resources [71,72]. Relatedly, perceived racial discrimination is associated with an increased risk of self-reported sleep disturbance in adults [73]. Moreover, individuals from minoritized groups may experience unique stigma-related stressors leading to increased emotional dysregulation and mental health concerns [25], and emotional dysregulation and mental health concerns are also linked to worse sleep. Although all racial and ethnic groups experience stress, there are significant racial disparities in stress wherein individuals from minoritized groups self-report greater levels of stress compared to White/European individuals [74].

Activation of the body’s stress system by typical, everyday stressors will result in adaptive physiologic responses that help maintain the body’s homeostasis [38,39]. The body’s peripheral physiologic response to stress is governed by the hypothalamic-pituitary-adrenocortical (HPA) axis, including the hypothalamic corticotropin-releasing hormone (CRH) secreting neurons (located in the hypothalamus, pituitary, and adrenal glands) and brainstem, in conjunction with the body’s autonomic nervous system [38,39, 75]. Subsequently, when cortisol, an important glucocorticoid in the stress response system, reaches a specific level in the body, the body then typically employs a negative feedback system to return to its pre-stressed state by instructing the hypothalamus and pituitary to reduce their output of stress hormones. However, this negative feedback loop may be inhibited by chronic stress, like racism, therefore altering the normative regulation of stress hormones [39, 75]. The failure to appropriately inhibit the stress response can further increase allostatic load (i.e. the ‘wear and tear’ from chronic exposure to elevated or fluctuating neuroendocrine responses resulting from repeated or chronic environmental stressors) [75,76]. Moreover, adolescents from minoritized groups may become accustomed or conditioned to race-related life stressors in such a way that their distress cues and secretion of cortisol may become dysregulated [75].

Overall, highly stressful experiences often result in prolonged activation of the stress system [77–80], and in theory, racism and other race-related stressors can lead to lack of sleep and subsequently a disrupted stress system [25, 81]. Poor sleep health itself may also act as a stressor to alter the functioning of the HPA axis which could consequently alter cortisol output and lower insulin sensitivity [77–80, 82]. As poor sleep is a risk factor for T2D [83], understanding potential psychosocial variables that increase these adolescents’ risk for adverse health outcomes like T2D is essential.

Influence of stressors on sleep and T2D risk

Race-related stressors, sleep, and T2D

As adolescents from minoritized groups are disproportionately at risk for poor sleep health [16, 84] and adolescent-onset T2D [17], this is of particular concern because poor sleep health is also linked with adverse cardiometabolic outcomes like T2D [85]. In fact, among youth from minoritized groups, incident adolescent-onset T2D is rising at a faster rate than in White adolescents [17, 20], and adolescent onset T2D is associated with deleterious health consequences (e.g. rapid deterioration, greater health comorbidities, and earlier mortality) [22,23].

Racism and other race-related stressors may further influence sleep health and, in turn, adverse outcomes like T2D. Prior research in adult samples found that sleep health variables (i.e. sleep duration and sleep efficiency) measured with actigraphy partially explained racial disparities in adult cardiometabolic disease risk [85]. Other studies in adult samples suggest that sleep characteristics, measured with actigraphy, mediated a portion of racial and ethnic disparities in blood pressure [86] between Black/African American and White/European individuals. In adolescents, research supported an association between shorter sleep duration, measured with actigraphy, and increased insulin resistance with adolescents from minoritized groups compared to adolescents of White/European origin [10].

Interestingly, although individuals from racial and ethnic minoritized groups may experience more race-related stress compared to people of White/European origin, individual factors such as ability to cope and social support may serve as protective factors in the connection between origins from a minority group and minority-specific stressors like insufficient sleep [87]. Recent research investigated how sleep may help adolescents navigate race-related stress [50, 67]. For example, in a sample of adolescents from minoritized groups, adolescents who slept longer and better the night before (measured with self-report and actigraphy) experiencing higher than their typical levels of discrimination, engaged in better active coping strategies and reported higher well-being on days when they experienced discrimination [88]. These patterns indicate that sleep may be a salient mediating [85] and/or moderating [10] factor of race and ethnicity differences in cardiometabolic and T2D risk.

Insufficient sleep and T2D

Although sleep health may be an intervening variable in the connection between racial and ethnic health disparities in T2D risk, it is also possible that sleep health may be a potential predicting variable in this connection. Race-related stressors like lack of sleep may further compound an adolescent’s already existing risk for T2D [16]. Insufficient sleep may act as a stressor altering the functioning of the stress response system, potentially influencing cortisol output and insulin sensitivity, leading to T2D [77–80]. Specifically, stress-related physiologic responses (e.g. total daily cortisol output) may play a role in the associations of insufficient sleep duration or aspects of sleep disruption with insulin sensitivity [89–93]. Research investigating these connections found that longer sleep duration has been associated with greater insulin sensitivity in studies with adolescents and adults, whereas insufficient or short sleep may relate to acute and longer-term declines in insulin sensitivity, as well as decreased insulin secretory capacity, and consequently, a greater risk for T2D [26, 94,95]. In youth, literature supports the association between shorter sleep duration and poorer insulin sensitivity. For instance, findings from an observational, cross-sectional study of high school students indicated that shortened sleep assessed by actigraphy and self-report, particularly during the weekdays, was associated with lower insulin sensitivity [13]. Conversely, longer actigraphy-measured sleep duration, even after adjusting for adiposity, was related to better insulin sensitivity in a community cohort of healthy adolescents [10] and in a small sample of treatment-seeking adolescents with overweight and obesity [96]. Similarly, research utilizing self-reported sleep duration suggests that insufficient sleep duration cross-sectionally relates to poorer insulin sensitivity in adolescents with overweight and obesity [97]. Likewise, in an experimental study of healthy adolescent boys, shortening sleep, measured by polysomnography, acutely decreased insulin sensitivity [98]. A 2021 review of sleep and metabolic health concluded that existing evidence overall supports an association between short sleep duration and poorer insulin sensitivity in adolescents, but research into this area remains limited in scope and in need of more objective sleep measures combined with rigorous insulin sensitivity measures, such as the euglycemic hyperinsulinemic clamp [83]. Moreover, the underlying mechanisms that explain this connection are only beginning to be understood [10, 13, 99–101].

The sleep duration and insulin resistance connection may be explained through the impact of insufficient sleep on counter-regulatory hormones that influence insulin sensitivity (e.g. growth hormone, catecholamines, and cortisol) as well as the release of specific hormones that influence appetite regulation (i.e. leptin and ghrelin) potentially leading to increased eating and affecting insulin sensitivity, which can be impacted by changes in sleep duration, timing, and quality [102]. Furthermore, the sleep-wake cycle also helps to modulate glucose tolerance and insulin secretion [102]; therefore, shorter sleep duration can potentially disrupt these biological processes and increase the risk for decreased insulin sensitivity.

This research is a promising start in increasing our understanding of adolescent racial and ethnic sleep health disparities in relation to T2D; however, there are still existing gaps we must address, such as: (1) mechanisms underlying disparities in sleep health, (2) the role of race and ethnicity as mediators and/or moderators in the investigation of sleep health and T2D, and (3) potentially confounding factors that relate to stress, sleep, and social determinants of health. Overall, it is important to investigate salient, underlying factors for sleep impairment among racial and ethnic minority youth, accounting for SES, to identify and mitigate the disparities in sleep health, obesity, and T2D in adolescents.

Implications and future directions

Greater consideration of racial and ethnic health disparities in adolescent sleep health research may have important clinical implications for T2D prevention and intervention work. By paying particular attention to the unique race-related stressors adolescents from minoritized groups face, researchers and clinicians will be better able to address these stressors in prevention and intervention program development. Developing culturally tailored interventions is essential, and further research is needed to develop effective prevention programs that investigate race-related stress as a potential mechanism that leads to poorer sleep health and associated cardiometabolic health risks like T2D. In a recent study of Black/African American women with elevated insomnia, a culturally tailored internet-delivered cognitive behavioral therapy for insomnia (CBT-I) program was not only comparable to non-culturally tailored CBT-I in improving sleep, but also resulted in significantly higher completion rates compared to the non-culturally tailored version of CBT-I and a control patient education group [103]. Thus, prevention/intervention programs can be improved with cultural humility to better target race-related stress mechanisms, reduce sleep health disparities, improve sleep health, and reduce adolescent T2D risk.

Relatedly, as race-related stress is uniquely connected to socially determined societal/structural factors, increased policy level research interventions that strive to improve access to health care and educational resources, to reduce potential threats to the community, and to target adolescent race-related stress exposure would be beneficial additions to the literature. Future research should also increase investigation into protective factors against the adverse health effects of poor sleep for adolescents from minoritized groups. For example, physical activity may be protective against the adverse effects of short sleep duration in adolescents, whereas low physical activity may increase an adolescents’ risk [49]. Good sleep hygiene may further help protect youth from insufficient sleep [104]. Some adolescents may also benefit from engaging in adaptive, coping strategies along with having access to safer environments that facilitate quality sleep [70]. Moreover, social support may protect minority adolescents, to some extent, from negative effects of discrimination on health behaviors like insufficient sleep [105].

It will be important to investigate individual-level differences (i.e. behavioral and physiological) in stress vulnerability which may be protective or aversive in influencing the association of sleep health characteristics with insulin sensitivity [106,107]. There is also an increasing need for researchers to use updated, comprehensive definitions and measures of the social construct of race and ethnicity that are both reliable and valid [37]. Along with being cognizant of culturally specific factors, it is essential for researchers to practice cultural humility and to be attentive to any experiences of perceived racial discrimination that could affect the acceptability of a program or intervention [108]. Additionally, it will be of great importance to appropriately represent different races and ethnicities with specific heritage-related details in future research (e.g. White, Black or African American, Hispanic or Latino, Asian, Native American, American Indian, Native Hawaiian, etc.) [109]. Finally, when designing prevention/intervention programs for adolescents from minoritized groups, it is important to view racial and ethnic health disparities from a biopsychosocial theoretical framework to help researchers identify, understand, and address factors that are associated with the inequitable distribution of health in these underserved communities [31].

Conclusion

Adolescents from minoritized groups that have been historically underserved, underrepresented, and economically marginalized are disproportionately at risk for both poor sleep health and cardiometabolic outcomes compared to adolescents of White/European origin [16]. Therefore, there is a critical need to investigate salient race-related stressors associated with sleep health disparities in adolescents from minoritized groups to better inform programs designed to prevent adolescent T2D, particularly for adolescents from minoritized groups who are most affected by poor sleep and T2D risk [110]. The increasing prevalence of adolescent insufficient sleep especially in racial and ethnic minoritized groups may be a mechanistic factor in the rise of adolescent T2D, yet research focusing on racial and ethnic health disparities in adolescent sleep and T2D research is lacking. Adolescents from minoritized groups experience unique race-related stressors that may contribute to sleep health disparities and risk for T2D; therefore, increased investigation into the connections between race-related stressors, sleep health disparities, and T2D risk in adolescents from minoritized groups can better inform targeted, preventative interventions for improving sleep health and preventing T2D in adolescents.

Author contributions

ELMC conceptualized the idea and wrote the original manuscript. AGC, EBR, and LBS assisted in interpretating, drafting, revising, and editing the original manuscript. NS, MB, LDG, JLB, MMK, and SLS reviewed, edited, and contributed to the interpretation of findings. All authors approved the final manuscript and agreed to be accountable for all aspects of the work.

Disclosure statement

MMK has relevant financial relationships in the bio-medical arena outside the submitted work with site investigators for clinical trials with no direct compensation. All other authors have no conflicts of interest to disclose.

Data availability statement

The data that support the findings of this study are available from the corresponding author, EC, upon reasonable request.
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