Covid-19 and Obesity
From the early days of the coronavirus epidemic in China, we have been aware that older adults and people with underlying health conditions, such as diabetes and cardiovascular disease, are at greatest risk of severe illness and mortality caused by the virus, SARS-COV-2.
But when the epidemic spread to Europe, it quickly became apparent that overweight and obesity are also major risk factors for becoming critically ill with Covid-19. This was first noted in Italy (1), then in the UK, where 73% of the first 5,500 critically ill patients had overweight or obesity (2), and then the US. A recent publication in the Journal of the American Medical Association showed that, of 5,700 patients hospitalised with Covid-19 in the New York City area, 42% had obesity (3). Another study showed that, once hospitalised, patients aged below 60 with BMI > 30 are twice as likely to need critical care compared with patients with a BMI < 30 (4).
Given that hypertension and type 2 diabetes are two of the common comorbidities of obesity, this revelation was not surprising, but it also raised the question of whether obesity is an independent risk factor for critical illness or death from Covid-19, or if it is due just to the comorbidities. Data from Arthur Simonnet and colleagues in France showed that, of the Covid-19 patients in ICU, the need for ventilation rose with BMI, and this was independent of age, diabetes and hypertension – indicating that excess body fat itself increases an individual’s vulnerability to Covid-19 (5). Simonnet’s findings are supported by reports from the US that significant numbers of younger people with obesity, but otherwise healthy, are being hospitalised (6).
So how can obesity result in a worsening of symptoms and greater risk of death from Covid-19? One way is simply the physical presence of fat stores in the upper abdomen, which causes compression of the diaphragm and lungs, compromising respiratory function. However, probably the key factor is the effect that obesity has on the immune system.
In individuals with obesity, visceral adipose tissue in the abdominal cavity produces inflammatory cytokines that cause a chronic low-grade inflammatory state throughout the body. It is unclear how this affects the response to the viral infection in the lungs, but one theory is that inflammation caused by obesity occupies the immune system’s resources, reducing its ability to mount an effective response against the virus.
On the other hand, it has also been proposed that this constant activation of the immune system means that it over-reacts to the virus, causing excess inflammation and damage in the lungs (7).
There is also evidence that leptin may play an important role. Leptin is a hormone produced by adipose tissue, which is best known for its effects on reducing appetite by binding to receptors in the brain. In people with obesity, the CNS becomes resistant to leptin, so blood levels of leptin are high but it is ineffective at reducing appetite. However, T-lymphocytes, which are involved in the cell-mediated response to viral infections, also have leptin receptors and leptin deficiency or resistance can lead to dysregulation of cytokine production and increased susceptibility toward infectious diseases and inflammatory responses (8).
Research into the relationship between obesity and influenza viruses has been ongoing since the H1N1 ‘swine ‘flu’ influenza pandemic in 2009, and has shown that not only are individuals with obesity at increased risk of severe illness from the influenza virus, but they also respond less well to vaccines (9), and they are potentially more infectious because they shed virus for longer when infected (10).
When we add all this evidence up, it is clear that people with obesity are very vulnerable, not only to the current coronavirus, but also to influenza viruses and future viral pandemics.
Rising global obesity rates could be contributing to the spread of infection and are certainly putting added strain on already-stretched health services, highlighting the urgent need to tackle obesity and reverse this trend – something which governments and health systems around the world have so far failed to do.
Sources
- Mills J (2020) Obese people are ‘at higher risk from coronavirus’. Metro. Published online 23 March 2020. https://
metro.co.uk/2020/03/23/obese-people-higher-risk-coronavirus-12444395/ - Intensive Care National Audit Research Centre (2020) ICNARC report on COVID-19 in critical care. Published 17 April 2020. https://www.icnarc.org/Our-Audit/Audits/Cmp/Reports
- Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, and the Northwell COVID-19 Research
Consortium (2020) Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With
COVID-19 in the New York City Area. JAMA. Published online 22 April 2020. doi:10.1001/jama.2020.6775. - Lighter J, Phillips M, Hochman S, Sterling S, Johnson D, Francois F, Stachel A (2020) Obesity in patients younger than 60
years is a risk factor for Covid-19 hospital admission. Clinical Infectious Diseases. https://doi.org/10.1093/cid/ciaa415 - Simonnet A, Chetboun M, Poissy J, Raverdy V, Noulette J, Duhamel A, Labreuche J, Mathieu D, Pattou F, Jourdain M,
Lille Intensive Care COVID-19 and Obesity study group (2020) High prevalence of obesity in severe acute respiratory
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April 2020. doi: 10.1002/oby.22831. - Rabin RC (2020) Obesity Linked to Severe Coronavirus Disease, Especially for Younger Patients. New York Times. Pub-
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Mechanisms. Circulation. Published 22 Apr 2020. https://doi.org/10.1161/CIRCULATIONAHA.120.047659 - Maurya R, Bhattacharya P, Dey R and Nakhasi HL (2018) Leptin Functions in Infectious Diseases. Front. Immunol.
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(2018) Obesity Increases the Duration of Influenza A Virus Shedding in Adults. J Infect Dis. 218(9): 1378-1382.