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The role of adiposity, body mass index, aging and chronic comorbidities on the progression of COVID-19 illness. Is a ‘long COVID’ syndrome inevitable?


International Journal of Family & Community Medicine
Orien L Tulp,1,3 Andrew A Sciranka,2 Frantz Sainvil,2 George P Einstein1,3

Abstract

Age associated overweight and obese conditions now approach epidemic proportions in Westernized society, often beginning in childhood and extending throughout the lifespan. Excess adiposity is often linked to increased visceral fat deposition where it is associated with increases in the relative risks for developing severe complications of covid-19. Thus, excess adiposity, along with NIDDM, hypertension, respiratory, disordered bioenergetics and other comorbidities, may be added to a growing list of significant independent risk factors in the progression of complications in covid-19 illness in both vaccinated and unvaccinated individuals, and which may lead to the development of a syndrome of ‘long covid’ in a sizable proportion of those infected. In addition to excess adiposity, non-insulin dependent diabetes (NIDDM), hypertension, disordered bioenergetics, along with other commonly occurring age-related comorbidities contribute to a lengthy list of significant risk factors that often progress to complications in the development and treatment options for covid-19 illness. These complications may occur in both vaccinated and unvaccinated individuals and may lead to the development of a syndrome of ‘long covid’ in a sizable proportion of infected individuals.

The coronavirus causing Covid-19, SARS-CoV-2 has some similarities to the emergence of earlier reports of other zoonotic coronavirus illnesses including MERS and SARS which also caused respiratory illness in humans also with chronic symptoms of fatigue, musculoskeletal pain and psychiatric impairments. The origin of SARS-Cov-2 remains unclear, but appears to have originated in Wuhan, China in late 2019 as a local epidemic but within a few months had spread throughout the globe and was declared a pandemic by the WHO within three months of its first report to the WHO in December 2019. The virus enters mammalian organ systems via ACE2 receptors of receptive tissues of the respiratory, gastrointestinal, and other organs including the adipose tissue that can interact with the infective spike protein domains of the virus thereby permitting cellular entry. Once the adipose tissue becomes infected, the virus begins to replicate vigorously and initiates the release of inflammatory cytokines including IL-6, TNF and others which can contribute to an often-fatal cytokine storm. The common clinical symptoms include fever, coughing, musculoskeletal pain, and profound fatigue, and which often progress to hyperinflammation, a potentially serious cytokine storm, an acute respiratory distress syndrome (ARDS) and covid-related coagulopathy (CAC) and are often observed in overweight or obese individuals following SARS-CoV-2 infection in the absence of other comorbidities. While weight loss toward a normalization of BMI and an otherwise healthy weight is associated with smaller adipocyte size and corresponding adipocyte surface area can decrease the relative risks for other comorbidities over time, the risk reduction for COVID-19 following weight loss remains unclear. In conclusion, progressive increases in adiposity, overweight and obese conditions that increase visceral fat deposition and may progressively increase the relative risk for the most severe complications and dire outcomes of COVID-19 illness.

Keywords

overweight, hyperplasia, adulthood, preordained cell surface

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