A tale of two pandemics: obesity and COVID-19.

To the Editor:

We are in the midst of the greatest global threat to human health of this century. As of 5 June 2020, the COVID-19 pandemic has resulted in nearly 6.6 million documented infections and ~390 000 lives lost. The clear inequality in infection burden and COVID-19 disease severity has illuminated another pre-eminent threat to public health, obesity. Mirroring findings from the 2009 H1N1 influenza pandemic, obesity is a risk factor for hospitalization, severity of disease and mortality upon infection with SARS–CoV-2. The advances made in understanding the molecular consequences of obesity and other metabolic disorders in the context of influenza virus will undoubtedly translate to our new viral foe.

In the first wave of SARS–CoV-2 infections centred in New York City, USA, those under 60 with obesity Class I [body mass index (BMI) = 30–35 kg/m2] had a 2.0 times greater odds of admission to the hospital, with odds even greater for those with obesity Class II or greater [BMI > 35 kg/m2; odds ratio (OR) = 2.2, confidence interval (CI) = 1.7–2.9]. These findings are echoed in cohorts worldwide. In a retrospective study centred in France, the prevalence of obesity was 1.35 times higher in hospitalized COVID-19-positive patients compared with the general public (CI 1.08–1.66, P = 0.0034) and higher in comparison to non-COIVD-19 intensive care patients.

Upon hospitalization, obese patients are also more likely to need intensive care. BMI, albeit an imperfect measure of health, is also a predictor of disease severity. Obese patients were found to have a 2.91 greater odds of severe or critical disease severity compared with non-obese cases and is associated with a longer median hospital stay of 23 [interquartile range (IQR) = 17–30] vs 18 (IQR 13–24) days in a case-controlled adult cohort centred in three Chinese hospitals. Preliminary retrospective analyses suggest Class II obesity is a predictor of mortality (OR = 3.78, 1.45–9.83), but additional investigation is needed.

The double threat of a viral and obesity pandemic is daunting. As has been studied in the context of influenza virus, obesity perturbs baseline cellular metabolism and the antiviral response to infections. Initial reports also suggest the expression of the SARS–CoV-2 receptor (angiotensin converting enzyme-2, or ACE-2) is significantly higher in overweight compared with lean bronchial sections, warranting further empirical studies on the cellular consequences of obesity for SARS–CoV-2 pathogenesis.

COVID-19 is not just a disease of the elderly. The first pandemic of the 21st century uncovered the sinister relationship between obesity and morbidity upon viral infection—trends that continued for subsequent seasonal influenza outbreaks. Today, COVID-19 has exploited our increasingly obese world in its global spread. The looming fall and winter influenza season in the Northern hemisphere may coincide with the second or even third wave of SARS–CoV-2 infections and compound the burden on our already overextended health infrastructure. Curbing the universal obesity epidemic will undoubtedly ripple into the control of viral disease. As much of the world’s population are on the cusp of re-opening society, it is important to consider national and local demographics and how they may shape future outbreaks and potential waves of SARS–CoV-2 infections.

Conflict of interest

None declared.