Adipose tissue, or fat, is an active metabolic organ with a role in many processes, including immunity and inflammation. In people with a healthy weight, adipose tissue functions normally.
However, fat cells accumulate fat and become larger during weight gain, resulting in chronic low-grade inflammation in obesity that is associated with various complications, including type 2 diabetes, heart disease, respiratory diseases, and some cancers.
This inflammation causes a release of molecules called cytokines that trigger a response from the body’s immune system.
The metabolic changes and sustained low-grade inflammation in people with obesity leave them with an impaired immune response to infections and increased viral loads when infected by viruses, resulting in poorer outcomes and recovery from infections.
In a recent study at Maastricht University Medical Centre, researchers found that there are overlaps between the immunological disturbances in both COVID-19 disease and patients with obesity.
This could explain the increased disease severity and death risk in patients with obesity and COVID-19.
Since fat mass generally increases with aging, this finding might also partly explain the increased death risk in older patients.
The study was presented at the European and International Congress on Obesity (ECOICO 2020). One author is Associate Professor Gijs Goossens.
In COVID-19, the attempts of the immune system to eliminate the virus produce a constant stream of these cytokines, which can lead to an effect known as the ‘cytokine storm’, which can cause organ damage (e.g. lung injury), leading to poor outcomes and death.
Various research around COVID-19 is focusing on the renin-angiotensin-aldosterone system (RAAS) in the body since SARS-CoV-2 enters the host cells through the angiotensin-converting enzyme-2 (ACE-2), which is part of the RAAS system.
The RAAS, among other things, increases blood pressure and inflammation.
In obesity, the RAAS system is overactivated and may play a critical role in the increased susceptibility and worse clinical outcomes of COVID-19 in people with obesity.
In the study, the researchers suggest that the increased fat mass may contribute to increased RAAS activity and inflammation in obesity, thereby providing a critical link between obesity and the increased COVID-19 susceptibility and poorer disease outcomes.
Furthermore, it is also well documented that increased age is a major determinant of severe disease and COVID-19-related mortality.
Since aging is accompanied by changes in body composition, namely reduced muscle mass and increased fat mass, it is tempting to postulate that this may at least partly contribute to the poorer outcomes in older individuals infected by SARS-CoV-2.
The team says a detailed analysis of patients with COVID-19 is essential to identify people at increased risk of developing this disease, and better predict disease progression and outcomes.
In particular, the potential role of belly fat in the development of COVID-19 warrants further research.
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