The association of obesity and COVID-19

Research on the pandemic of Covid-19 has demonstrated that there is a higher risk of contracting the disease, increased severity, and poorer outcomes in individuals who are obese.  The International Journal of Obesity (IJO) has received a number of papers dealing with some aspect of this association.  The papers in this collection cover a range of topics including data documenting the nature of the association, but more importantly, addressing the mechanisms behind the increased risk in people with obesity. 

There are many factors involved in increasing the risk of Covid-19 for people with obesity. Rebello et al (1), Kim and Nam (2), and Chippetta et al (3) address the broad topic of inflammation associated with obesity and discuss some of the potential mechanisms of increased inflammation.  Rebello et al (1) summarize the knowledge available early in the course of the pandemic and focus on the potential role of leptin in altering several pathways critical to the inflammatory response.  Kim and Nam (2) address the factors leading up to “cytokine storm” in severely ill individuals and what therapeutic measures might be taken to prevent or to treat this serious condition.  Chiappetta et al (3) provide data on interleukins and CRP in SARS-CoV-2 infected patients, how the distribution of adipose tissue may alter the degree of inflammation, and how the mixture of different interleukins increases or suppresses inflammation.  Hu et al (4) in a series of patients from China early in the pandemic showed that the presence of obesity and of abnormal liver function tests predict more severe illness and a greater mortality. 

Townsend et al (5) address the epidemiological aspects of the pandemic and point out that early studies of Covid 19 and obesity did not take race/ethnicity into account.  When examined, it is clear that some Black, Hispanic, Asian and Minority Ethnic groups tend to have higher rates of infection and mortality.  Potential explanations are advanced that some minority/ethnic groups have a higher rate of poverty and may have a higher percentage of individuals working in the service industries, which may expose them more frequently to the possibility of infection.  During the 2009 H1N1 influenza epidemic the rate of hospitalization was greater in minorities, but there were no differences in mortality, in contrast to that seen with Covid-19 (6). This suggests that SARS-CoV-2 has some fundamental differences from influenza and that social factors do not completely account for the increased mortality.  Presumably other factors, including physiological factors, are playing a role.  Vitamin D deficiency is associated with increased inflammation and is known to be more prevalent with obesity and in individuals with darker skin.  With Covid-19 there appears to be a higher prevalence of disease and increased mortality in individuals with darker skin leading Townsend et al (5) to hypothesize that lower levels of Vitamin D due the combination of darker skin and obesity may put them at higher risk. 

In a very provocative article about the potential mechanisms of increased inflammation in the lungs of patients with severe Covid-19 and obesity, Cinti et al (7) point out that SARS-CoV-2 infects adipose tissue and can cause inflammation and death of adipocytes, liberating fat into the extracellular space.  They demonstrate that the lungs of two very obese patients contained fat emboli in the lungs. Since fat emboli produce a major inflammatory response in the lungs, this may be a factor for some patients who are severely ill with pulmonary disease and difficulty breathing.

Finally, Demidowich et al (8) show that colchicine is capable of reducing inflammation in adipose tissue and propose that it should be tried in patients with obesity and Covid-19 to reduce the cytokine storm.

The pace of Covid-19 and coronavirus research is accelerating and as more papers dealing with this disease in patients with obesity become available, they will be added to this collection.  Investigators with new insights or hypotheses relating to this topic are encouraged to submit their research to IJO.

Richard L. Atkinson and Ian A. Macdonald

Editors-in-Chief, IJO

References:

1.      Rebello, C.J., Kirwan, J.P. & Greenway, F.L. Obesity, the most common comorbidity in SARS-CoV-2: is leptin the link?. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0640-5

2.      Kim, J., Nam, J. Insight into the relationship between obesity-induced low-level chronic inflammation and COVID-19 infection. Int J Obes 44, 1541–1542 (2020). https://doi.org/10.1038/s41366-020-0602-y

3.      Chiappetta, S., Sharma, A.M., Bottino, V. et al. COVID-19 and the role of chronic inflammation in patients with obesity. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0597-4

4.      Hu, X., Pan, X., Zhou, W. et al. Clinical epidemiological analyses of overweight/obesity and abnormal liver function contributing to prolonged hospitalization in patients infected with COVID-19. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0634-3

5.      Townsend, M.J., Kyle, T.K. & Stanford, F.C. Outcomes of COVID-19: disparities in obesity and by ethnicity/race. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0635-2

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

7.      Cinti, S., Graciotti, L., Giordano, A. et al. COVID-19 and fat embolism: a hypothesis to explain the severe clinical outcome in people with obesity. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0624-5

8.      Demidowich, A.P., Levine, J.A., Apps, R. et al. Colchicine’s effects on metabolic and inflammatory molecules in adults with obesity and metabolic syndrome: results from a pilot randomized controlled trial. Int J Obes (2020). https://doi.org/10.1038/s41366-020-0598-3