expressed in heart, lungs, kidneys, and intestines, thereby providing a multimodal entry point for the virus to infiltrate the body. Preliminary unpublished data indicate that ACE-2 receptor concentrations are higher in adipose tissue in comparison with lung tissue, suggesting that adipose tissue might be vulnerable to SARS-CoV-2 infection (preprint data available from https://www.preprints.org/manuscript/202002.0315/v1). This presents a risk for adverse outcomes for obese patients with more adipose tissue and a greater number of ACE-2 receptors in comparison with their non-obese counterparts. Alterations of adipose tissue distribution and function linked to obesity have been shown to promote production of pro-inflammatory cytokines and induce chronic systemic inflammation. 7 Increased production and release of cytokines further exacerbates activation of kinase receptors, triggering a positive feedback loop of inflammation and metabolic dysfunction. Amongst obese patients with COVID-19, this heightened inflammatory response may put them at greater risk for a cytokine storm, an over-response of the immune system characterised by uncontrolled release and attack of cytokines on the body's own tissues and organs. Although obesity-specific clinical data are lacking, general findings provide evidence supporting the cytokine storm concept with COVID-19 non-survivors having significantly higher concentrations of interleukin-6, a pro-inflammatory cytokine that regulates homeostasis and inflammation, compared with survivors. 8 Research will need to explore these mechanisms in the context of the obesity paradox, the epidemiologically observed inverse relationship between obesity and mortality amongst select medical and surgical populations (interestingly, with surgery being a pro-inflammatory event). 9 Furthermore, it is well documented that elevated concentrations of inflammatory biomarkers amongst obese patients are linked to increased risk of co-morbidities, including cardiovascular disease, diabetes mellitus, metabolic syndrome, and liver disease. 7 The presence of these co-morbidities in COVID-19 patients has been shown to be associated with greater vulnerability to multi-organ injuries. 10 Ultimately, many patients die from complications that stem from these underlying illnesses, providing yet another reason for clinicians to be hyper vigilant when treating and monitoring obese patients with COVID-19. As research surrounding COVID-19 continues to evolve, it is crucial to consider obesity as a potential risk factor for adverse outcomes. A better understanding of the pathophysiological contributors linking obesity with severe-tocritical COVID-19 disease will not only help inform medical management of obese patients, but also aid in the development of successful therapeutics to prevent and treat COVID-19.

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