Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Epidemiology and Population Health

Outcomes of COVID-19: disparities in obesity and by ethnicity/race

COVID-19 outcome disparities are rapidly becoming apparent for people with obesity and multiple black, Asian, and minority ethnic (BAME) groups. Researchers have reported differences in COVID-19 hospitalization and mortality rates by race/ethnicity in the United Kingdom (UK) [1, 2] and United States (US) [3, 4]. Numerous minority ethnic groups in these countries live with a greater burden of obesity and other chronic diseases. This is particularly significant as obesity has emerged as a risk factor for severe COVID-19, the disease caused by novel coronavirus SARS-CoV-2 [3, 5]. We synthesize a range of potential biological, socioeconomic, behavioral, and sociological contributors to the disparate outcomes for people with obesity and minority ethnic groups in COVID-19.

Initial retrospective cohort analyses have demonstrated higher rates of hospitalization and intensive care, including invasive mechanical ventilation, for patients with obesity [5, 6]. Though these observational results do not assess mortality outcomes and adjust for few comorbidities, they signal potential biologic vulnerability for a large proportion of people worldwide living with obesity. Obesity rates are significantly higher among Hispanic and African Americans, as well as black, Bangladeshi, and Pakistani groups in the UK, than their white counterparts [1, 7]. The overlap of COVID-19 risk signals between obesity and ethnicity therefore is of consequence.

The most comprehensive epidemiology on ethnicity and COVID-19 currently available is from the UK [1, 2]. BAME individuals comprise over 30% of hospitalized, critically ill patients with COVID-19 [2]. The Office for National Statistics highlights stark ethnic disproportionalities in COVID-19 mortality odds, over four- and threefold for black and Bangladeshi/Pakistani individuals respectively compared to white individuals [1]. Indeed, the first ten UK physicians to die from COVID-19 were all of BAME background. Though US national data are limited, states and municipalities report a disproportionate burden of COVID-19 cases, hospitalizations, and deaths among Hispanic and African Americans [4, 8]. In Norway and Sweden, cases among Somalis are seven- to ten times expected based on population [9].

Ethnic differences in economic status, underlying health conditions, density of residence, and household crowding all contribute to the unequal impact of COVID-19. For example, the English Housing Survey noted household overcrowding in 30% of Bangladeshi, 16% of Pakistani, and 2% of white British households [1]. The mortality gap between the most and least deprived areas is greater for COVID-19 than that normally observed for all-cause mortality, highlighting the importance of socioeconomic status [1]. However, adjustments for age, geography, educational attainment, level of deprivation, and self-reported health only partially attenuate the higher odds ratios of COVID-19 mortality for black individuals (1.9), Bangladeshi/Pakistani men (1.8) and women (1.6) compared to white individuals in the UK [1]. Further inclusion of data on socioeconomic status and specific medical conditions such as obesity (absent from this model) will enhance our understanding of the joint and independent contributions of ethnicity, class, and preexisting comorbidities in COVID-19.

Sociodemographic patterns in COVID-19 may diverge from other viral pathogens. While the 2009 H1N1 influenza hospitalized disproportionate numbers of ethnic minorities, differences in mortality were not observed among hospitalized minority versus non-minority patients [10]. BAME disparities in COVID-19 intensive care mortality rates were similarly not observed in a recent historical cohort of patients critically ill with pneumonia from other viral pathogens [2].

One biologic hypothesis for observed associations between ethnicity, obesity, and worse COVID-19 outcomes is vitamin D deficiency [11]. The anti-inflammatory and anti-microbial properties of vitamin D include maintenance of tight junctions and reduced production of inflammatory cytokines [11]. Massive cytokines release (“storm”) has been implicated in severe COVID-19. Vitamin D supplementation in randomized, placebo-controlled studies has demonstrated reduced risk for acute respiratory tract infection, and associations between vitamin D deficiency and acute respiratory distress syndrome have been reported [12]. Non-white ethnicity and obesity are each independently associated with hypovitaminosis D [13], offering one plausible explanation for higher COVID-19 burden in these groups.

In addition to differential rates of comorbidities such as diabetes and cardiovascular disease across ethnic groups, pathophysiologic differences in inflammation may also be significant. The chronic low-grade inflammatory state of obesity is well-defined elsewhere, but inflammatory changes may not be consistent across race/ethnicity. Hispanic and African American children have higher risk of low-grade inflammation compared to white peers, an effect only partially mediated by parental education and body mass index (BMI) [14]. During a weight loss intervention among healthy female participants with overweight (BMI 27–30 kg/m2), fewer markers of inflammation decreased among African American compared to white patients [15]. It has been proposed that there may be a genomically influenced response to viral pathogens to explain the potential interaction of ethnicity-related factors on SARS-CoV-2 infection and subsequent outcomes [16]. In this model, one’s health state, health behaviors, and social behaviors interact with factors such as comorbidity burden and control in disease outcomes. Comprehensive data which include ethnic background should be evaluated to better understand biological factors that contribute to the disproportionate burden on certain segments of the population.

We also acknowledge the complex roles of behavior and sociology. Occupational exposures contribute to ethnic disparities in SARS-CoV-2 [1]. Public health communication may not prepare minority citizens to respond to SARS-CoV-2 due to language or other structural barriers to access [9]. Similar access issues exist in health messaging for obesity and other chronic diseases. Individual choice and self-referral patterns also play a role. A holistic view does not attribute observed differences to any single factor.

Published retrospective cohort analyses of obesity and COVID-19 have not adjusted for ethnicity [3, 5], and analyses of ethnicity and COVID-19 have not adjusted for differences in obesity rates [1, 2]. Studies to date have incompletely parsed obesity from comorbidities such as diabetes and cardiovascular disease as risks for COVID-19. A critical knowledge gap remains to understand the interaction between ethnicity, obesity, and class in COVID-19 outcomes. We have presented several plausible biological, socioeconomic, and behavioral factors, which may inform the observed disproportionalities. The degree to which obesity and ethnicity are additive, multiplicative, mediators or confounders—and the degree to which obesity increases risk independent from its many comorbidities—have significant implications for our medical and public health response.


  1. 1.

    Coronavirus (COVID-19) related deaths by ethnic group, England and Wales: 2 March 2020 to 10 April 2020. United Kingdom Office for National Statistics. 2020.

  2. 2.

    Intensive Care National Audit & Research Centre. ICNARC report on COVID-19 in critical care. London: ICNARC; 2020.

  3. 3.

    Garg S, Kim L, Whitaker M, O’Halloran A, Cummings C, Holstein R, et al. Hospitalization rates and characteristics of patients hospitalized with laboratory-confirmed coronavirus disease 2019—COVID-NET, 14 states, March 1–30, 2020. MMWR Morb Mortal Wkly Rep. 2020;69:458–64.

    CAS  Article  Google Scholar 

  4. 4.

    Owen WF, Jr, Carmona R, Pomeroy C. Failing another national stress test on health disparities. JAMA. 2020.

  5. 5.

    Simonnet A, Chetboun M, Poissy J, Raverdy V, Noulette J, Duhamel A, et al. High prevalence of obesity in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) requiring invasive mechanical ventilation. Obesity. 2020.

  6. 6.

    Lighter J, Phillips M, Hochman S, Sterling S, Johnson D, Francois F, et al. Obesity in patients younger than 60 years is a risk factor for Covid-19 hospital admission. Clin Infect Dis. 2020.

  7. 7.

    Byrd AS, Toth AT, Stanford FC. Racial disparities in obesity treatment. Curr Obes Rep. 2018;7:130–8.

    Article  Google Scholar 

  8. 8.

    COVID racial data tracker 2020. COVID Tracking Project. 2020.

  9. 9.

    Masri L. COVID-19 takes unequal toll on immigrants in Nordic region. Reuters. 2020. World News.

  10. 10.

    Tricco AC, Lillie E, Soobiah C, Perrier L, Straus SE. Impact of H1N1 on socially disadvantaged populations: systematic review. PLoS ONE. 2012;7:e39437.

    CAS  Article  Google Scholar 

  11. 11.

    Grant WB, Lahore H, McDonnell SL, Baggerly CA, French CB, Aliano JL, et al. Evidence that vitamin D supplementation could reduce risk of influenza and COVID-19 infections and deaths. Nutrients. 2020;12:988.

    CAS  Article  Google Scholar 

  12. 12.

    Martineau AR, Jolliffe DA, Hooper RL, Greenberg L, Aloia JF, Bergman P, et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 2017;356:i6583.

    Article  Google Scholar 

  13. 13.

    Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31:48–54.

    CAS  Article  Google Scholar 

  14. 14.

    Schmeer KK, Tarrence J. Racial-ethnic disparities in inflammation: evidence of weathering in childhood? J Health Soc Behav. 2018;59:411–28.

    Article  Google Scholar 

  15. 15.

    Fisher G, Hyatt TC, Hunter GR, Oster RA, Desmond RA, Gower BA. Markers of inflammation and fat distribution following weight loss in African-American and white women. Obesity. 2012;20:715–20.

    CAS  Article  Google Scholar 

  16. 16.

    Pareek M, Bangash MN, Pareek N, Pan D, Sze S, Minhas JS, et al. Ethnicity and COVID-19: an urgent public health research priority. The Lancet. 2020;395:1421–2.

    CAS  Article  Google Scholar 

Download references


This work is supported by the following sources of funding: National Institutes of Health and Massachusetts General Hospital Executive Committee on Research (ECOR)(FCS), National Institutes of Health NIDDK P30 DK040561 (FCS) and L30 DK118710 (FCS).

Author information



Corresponding author

Correspondence to Fatima Cody Stanford.

Ethics declarations

Conflict of interest

The authors report no competing interests related to this manuscript. TKK reports consulting fees from Gelesis, Novo Nordisk, and Tivity Health unconnected to the present work.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Townsend, M.J., Kyle, T.K. & Stanford, F.C. Outcomes of COVID-19: disparities in obesity and by ethnicity/race. Int J Obes 44, 1807–1809 (2020).

Download citation

Further reading


Quick links