Social determinants of health, health disparities, and adiposity
Introduction
Social determinants of health (SDoH), or the socioeconomic, environmental, and psychosocial conditions in which individuals spend their daily lives, have clear and significant effects on obesity as a cardiovascular (CV) disease (CVD) risk factor.1 Obesity is a complex, multifactorial disease defined by the World Health Organization as abnormal or excessive accumulation of adipose tissue that negatively impacts overall health.2 Obesity is associated with the development of CVD at younger ages with poorer long-term outcomes.3 From a clinical standpoint, obesity is commonly defined by a body mass index (BMI) at or above 30 kg/m2, with a BMI between 30 and 34.9 kg/m2 defining Class 1, 35 and 39.9 kg/m2 indicating Class 2, and 40 kg/m2 or higher categorized as Class 3 obesity.3 However, BMI has significant limitations as it does not consider adipose tissue distribution and varies in predictive accuracy of adiposity and CVD risk by age, sex, race, and ethnicity.3 Waist circumference and waist-to-hip ratio are accessible, more precise measures of visceral adiposity and may more accurately predict CVD risk.3
Independent of its definition, obesity prevalence has steadily increased in the U.S. and globally over the last 40 years, with the National Health and Nutrition Examination Survey (NHANES) estimating obesity among 41.9% of adults aged 20 and over based on pre-pandemic data from 2017 to 2020.4,5 There are notable racial, ethnic, and socioeconomic disparities in obesity; increasing obesity prevalence and disparities also persist in pediatric populations.4 The coronavirus disease 2019 (COVID-19) pandemic highlighted the converging epidemics of obesity, CVD, and social inequities globally, with obesity and CVD being independent risk factors for COVID-19 severity and lower-resourced populations most impacted by adverse SDoH having the highest COVID-19 mortality rates.6 These patterns underscore the importance of understanding the impact of SDoH on obesity as a CVD risk factor and addressing these exposures over the life course given that weight status in childhood is predictive of having overweight or obesity in adulthood.7 With half of the U.S. population projected to have obesity by 2030,8 it is especially critical to understand the relationship between SDoH and adiposity-related physiologic pathways to inform the design and implementation of multi-level obesity interventions that target both the individual and related adverse SDoH in at-risk communities. Moreover, understanding the interplay between social and biologic factors in adiposity can aid in clinical practice, particularly in obesity treatment and primary CVD prevention.
In our previous work, we presented a health equity-focused SDoH framework (Fig. 1) that outlined elements of structural health determinants and antecedents of social position which shape lived experiences, define disparities in access to health-promoting resources, and promote differences in CV health behaviors to subsequently produce disparate CVD outcomes.1 Further, we discussed the biology of adversity, highlighting the possible biologic pathways through which structural and intermediate social determinants of CVD get under the skin to influence CV health. In this review, we focus on the social determinants of adiposity; that is, we describe the socioeconomic, environmental, and psychosocial conditions that facilitate the development of obesity. Additionally, we summarize physiologic mechanisms that may link SDoH with adiposity to highlight the biologic consequences of adverse social, environmental, and psychosocial factors in obesity. Finally, we present implications for practice and future research to mitigate obesity and adverse adiposity-related CVD outcomes.
Section snippets
Structural racism and racial discrimination
Structural racism and racial discrimination are upstream factors that strongly influence SDoH, including income, education, and housing access.1 One of the health manifestations of structural racism is observed in the relationship between racial and ethnic residential segregation and obesity. Residential segregation can be measured in a variety of ways including using U.S. Census data to determine the racial and ethnic composition of neighborhoods. For instance, researchers have used spatial
Biology of adversity and the adipo-cardiology consequences
We have highlighted research connecting SDoH to obesity, but the biologic mechanisms linking these relationships need to be further elucidated. Here, we explore studies evaluating connections between SDoH as sources of chronic stress and stress-related biomarkers; specifically, we focus on potential mechanisms by which these relationships might result in increased adipose tissue accumulation. Additionally, we focus on how SDoH and obesity alter adipose tissue homeostasis through immune system
Individual and clinical care interventions
Current guidelines for treating obesity focus on the individual and provide a continuum of options that include lifestyle interventions, pharmacologic therapies, and bariatric surgery, with treatment choices dependent on obesity severity. However, racial, ethnic, and socioeconomic disparities in access to these treatments exist. For lifestyle interventions, the availability, accessibility, and affordability of nutrient dense and health conscious foods and PA resources are major concerns for
Future directions
Ultimately, it is an imperative for future interventions to target at-risk individuals and neighborhoods with the goal of enhancing equity. To achieve this, future interventions must be multi-level, backed by federal, state, and local level initiatives, and informed by residents' lived experiences and contextual factors of everyday life. For instance, interventions must be purposefully tailored at the clinical, institutional, and structural levels of society to enhance equity in obesity and CVD
Conclusions
In conclusion, SDoH are intricately linked to obesity and subsequent CVD risk. However, the mechanisms through which SDoH amplify the risk for developing obesity and CVD are understudied and not fully understood. In particular, the complex biologic pathways through which adversity promotes obesity and CVD must be further elucidated. Furthermore, we show some of the limitations seen with current interventions at the individual- and population-level. To address these limitations, multi-level
Funding
The Powell-Wiley Laboratory is funded by the Division of Intramural Research of the National, Heart, Lung, and Blood Institute and the Intramural Research Program of the National Institute on Minority Health and Health Disparities.
Declaration of Competing Interest
None.
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Authors contributed equally.