Obesity and COVID-19: renin–angiotensin as a mediator of morbidity and mortality

“LONG COVID”—A hypothesis for understanding the biological basis and pharmacological treatment strategy

“…The virus then crosses the alveoli–blood barrier and because of the widespread cellular distribution of its target ACE‐2 results in other organs such as heart, liver, kidney, and CNS becoming infected, provoking an immune response and organ failure, covered in Lumbers et al 32 This can be fatal particularly in elderly adults with comorbidities such as hypertension, type 2 diabetes, and obesity 4 . The United States among others have reported that young adults with obesity are more likely to require hospitalization and develop more severe disease than non‐obese young adults, 6 consistent with the known increased distribution and activity of the renin–angiotensin system in obesity 38 . For patients who survive, there is increasing documented incidences of up to 50% people with a lack of return of taste and smell sensations for at least 6 months, chronic fatigue, respiratory impairment, and behavioral effects described as “brain fog” or depression.…”

“…4 The United States among others have reported that young adults with obesity are more likely to require hospitalization and develop more severe disease than non-obese young adults, 6 consistent with the known increased distribution and activity of the renin-angiotensin system in obesity. 38 For patients who survive, there is increasing documented incidences of up to 50% people with a lack of return of taste and smell sensations for at least 6 months, chronic fatigue, respiratory impairment, and behavioral effects described as "brain fog" or depression. By common usage, this has been described as "LONG COVID.…”

“…It is generally accepted that one useful strategy is to explore the ability of existing approved drugs to treat patients with COVID-19 disease and its complications such as "LONG COVID"-an approach referred to as treating the host. 37,38 However, this approach requires a thorough analysis of the pathophysiology of the disease, the dose-response curve in humans for the specific decision, and a clinical understanding of the patient group to be treated. As chronic inflammation due to elevated proinflammatory cytokines have been identified in "LONG COVID," antiinflammatory drugs could be considered.…”

“…Drug development is a very slow process with generally 10+ years elapsing between identifying a promising candidate in preclinical animal models and taking that through to an approved drug. It is generally accepted that one useful strategy is to explore the ability of existing approved drugs to treat patients with COVID‐19 disease and its complications such as “LONG COVID”—an approach referred to as treating the host 37,38 …”

The interacting physiology of COVID‐19 and the renin‐angiotensin‐aldosterone system: Key agents for treatment

“…9 Thus it is not surprising that obesity also induces a more severe inflammatory response and worse outcomes in patients with COVID-19. 10 Some patients infected with SARS-CoV-2 experience a hyperinflammatory response known as a "cytokine storm." It is this overwhelming release of pro-inflammatory cytokines and, in the case of COVID-19, suppressed levels of anti-inflammatory cytokines that causes the severe lung and tissue damage seen in COVID-19.…”