Obesity Impact on SARS-CoV-2 Infection: Pros and Cons "Obesity Paradox"-A Systematic Review

Abstract

Background: During the last years, the COVID-19 pandemic meets the pandemic generated by obesity, raising many questions regarding the outcomes of those with severe forms of infection.

Methods: The present systematic review summarises and analyses the data providing evidence for or against the "obesity-paradox" in COVID-19 patients. After applying the inclusion and exclusion criteria, 23 studies were included. We also analysed the presumably underlying basic mechanisms.

Results: The patients with a body mass index (BMI) of 30-40 kg/m² presented severe symptoms that led to intensive care unit (ICU) admission but not increased death rate. Those with a higher degree of obesity, with a BMI higher than 40 kg/m², led to a rise in the death rate, particularly in young patients. Obesity was associated with a higher rate of ICU admission but was not determined as an independent predictor of increased mortality. In contrast, some studies suggest a strong association between obesity or morbid obesity and the risk of death.

Conclusions: The existence of "obesity-paradox" cannot be stated; our study presents obesity as a critical risk factor in the evolution of COVID-19.

Keywords: COVID-19; SARS-CoV-2 infection; intensive care unit; mortality; “obesity-paradox”.

Figure 1

Flow diagram of literature search, screening, inclusion and exclusion of studies.

Figure 2

The relation between SARS-CoV-2 infection and coagulation complications. Infection with SARS-CoV-2 stimulates the innate immune system by releasing proinflammatory cytokines. Interleukin (Il)-6, tumour necrosis factor (TNF)-α, interferon (IFN)-γ and C-reactive protein (CRP) interfere with the anticoagulant pathway and inhibit fibrinolysis. Due to all these mechanisms, coagulation is stimulated and ends with fibrin development.

Figure 3

Renin–angiotensin system: SARS-CoV-2 infection and implication of vitamin D. In SARS-CoV-2 infection, virus attachment to the ACE2 receptors blocks angiotensin II conversion into angiotensin 1,7 and leads to tissue injury reactions. Vitamin D function cascade [vitamin D3 is produced in the skin under ultraviolet radiation exposure, 25(OH)D3—25-hydroxyvitamin D (calcifediol, ergocalciferol), 1,25[OH]₂D3—1,25-dihydroxy vitamin D (calcitriol)] and vitamin D receptor (VDR) are implicated in the suppression of the renin gene expression, thereby inhibiting the renin-angiotensin system. Renin catalyses the conversion of angiotensinogen to angiotensin I, which is further converted to angiotensin II. Normally, angiotensin II turns into angiotensin 1–7—the tissue protector via MasR receptors.