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The Perfect Storm: Coronavirus (COVID-19) Pandemic Meets Overfat Pandemic

ByCrossFitMay 14, 2020

Question: How extensive and significant are the links between excess adiposity — that is, too much body fat — and COVID-19 susceptibility?

Takeaway: “Overfat” impairs organ and immune function, increasing susceptibility to infectious disease. Given the generally high level of viral particles the average individual is exposed to each day, excess adiposity is a major threat to individual and public health.

This April 2020 review summarizes the links between excess body fat and infectious disease risk, then comments on the significance of the connections.

The average person is exposed to an estimated 1,012 new viral particles each day, making us  highly reliant on our immune systems to prevent infection and sickness (1). In the current COVID-19 pandemic, chronic conditions including diabetes, hypertension, cardiovascular disease, and chronic inflammation have been associated with increased disease severity and mortality across multiple populations and in both younger and older patients (2). Most of these conditions are associated with, exacerbated by, or directly caused by excess adiposity, which the review authors call “overfat” (3).

Figure 1: Potential relationship between body fat status and rates of infection

“Overfat” has been linked to increased vulnerability to infectious viral and bacterial diseases, impaired immune function, and impairments across a variety of organ systems (4). In previous epidemics, such as H1N1, and in seasonal influenza, excess weight has been an independent risk factor for impaired disease outcomes and disease-related death (5). For some conditions, obesity has also been found to reduce vaccine effectiveness (6).

Excess body fat has been linked to impairments in immune cell function, reduced antiviral responses, and increased viral shedding and transmission (7). Risk may be increased further in respiratory infections, specifically, as adiposity has also been associated with increased lung permeability and respiratory tissue breakdown, which may expedite broad lung tissue infection (8). Notably, these factors increase both individual and population risk, as they imply obese individuals are not only sicker when infected by a respiratory illness but also more likely to spread the disease to others. These and other factors are summarized in the figure below.

Figure 2: Illustration of the potential increased risk of death through virally driven hyperinflammation in overfat hosts. Excess adipose tissue promotes systemic inflammation and is characterized by infiltration and activation of immune cells secreting pro-inflammatory mediators, such as cytokines, adipokines, and chemokines, which secrete additional pro-inflammatory molecules. In addition to T cells and macrophages, these immune cells also include neutrophils, B1 and B2 cells, NK cells, and innate lymphoid cells.

The review authors argue that in the context of ubiquitous exposure to viral particles, the pandemic of excess body fat and its associated impact on inflammation, immune function, and viral response is “one of the greatest threats to global human health” (9). More optimistically, however, they conclude that the strength of our immune system — and thus our vulnerability to infectious disease — is, like chronic disease and physical impairment, largely within our control.


  1. The effect of obesity on chronic respiratory diseases: Pathophysiology and therapeutic strategies
  2. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study; Early transmission dynamics in Wuhan, China, of novel coronavirus-infected pneumonia; The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health — The latest 2019 novel coronavirus outbreak in Wuhan, China; An artificially simulated outbreak of a respiratory infectious disease; Prevalence of comorbidities in the novel Wuhan coronavirus (COVID-19) infection: A systematic review and meta-analysis; Clinical characteristics of coronavirus disease 2019 in China; Revisiting the global overfat pandemic; Overfat and underfat: New terms and definitions long overdue; Preliminary estimates of the prevalence of selected underlying health conditions among patients with coronavirus disease 2019 — United States, February 12-March 28, 2020
  3. Overfat adults and children in developed countries: The public health importance of identifying excess body fat
  4. Underweight, overweight, and obesity as independent risk factors for hospitalization in adults and children from influenza and other respiratory viruses; Risk factors for severe outcomes following 2009 influenza A (H1N1) infection: A global pooled analysis; Influence of obesity on pneumococcus infection risk in the elderly; Impact of obesity on influenza: A virus pathogenesis, immune response, and evolution; Associations of obesity and lifestyle with the risk and mortality of bloodstream infection in a general population: A 15-year follow-up of 64 027 individuals in the HUNT Study; A prospective study of age and lifestyle factors in relation to community-acquired pneumonia in US men and women; The prevalence of overfat adults and children in the US
  5. Adiposity and influenza-associated respiratory mortality: A cohort study
  6. Diet-induced obesity dramatically reduces the efficacy of a 2009 pandemic H1N1 vaccine in a mouse model 
  7. Adiponectin and Orexin-A as a potential immunity link between adipose tissue and central nervous system; Biochemistry of adipose tissue: An endocrine organ; Obesity-induced chronic inflammation is associated with the reduced efficacy of influenza vaccine; Obesity-induced changes in T-cell metabolism are associated with impaired memory T-cell response to influenza and are not reversed with weight loss
  8. The pathology of influenza virus infections; Predicting mortality in hospitalized patients with 2009 H1N1 influenza pneumonia
  9. The cellular and signaling networks linking the immune system and metabolism in disease

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