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

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

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


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Clarke Read
May 15th, 2020 at 5:47 pm
Commented on: The Perfect Storm: Coronavirus (COVID-19) Pandemic Meets Overfat Pandemic

Tom, I think your comment is fair about the use of the term "overfat." That said, he consistently uses it to refer to a single condition or state - excess adiposity - and so I don't think there is any loss of content here. If you replace the term "overfat" with a statement about excess adiposity each time he uses it, the paper's conclusions still hold. On one hand, it's frustrating that the author is trying to coin an unnecessary term...on the other hand, it's not so frustrating that we need to dismiss his other arguments on that basis. He makes this distinction clear in arguing that we use adiposity, not obesity, as our marker for poor metabolic health - and so makes the same correction for lean individuals with high levels of visceral fat (i.e., the same group as Rob Lustig's TOFI - "thin on the outside, fat on the inside") and for large individuals with low levels of fat (i.e., the muscular who have obese BMIs but are lean) that many others before have. He's making the same argument, just using unnecessarily complicated language.

That said, there is utility in his precise focus on excess adiposity. As we've seen in many articles published linking various forms of poor metabolic health to adverse disease outcomes, the strongest links are not with obesity, but with conditions that track with insulin resistance and increased visceral fat - diabetes, impaired kidney function, hyperglycemia, etc. In other words, it is the various metabolic shifts that cause, occur alongside, or are consequences of, increased visceral fat that lead to increased vulnerability to acute disease. These consequences, as outlined here, include changes to immune function, an elevated inflammatory state, and even increased vial shedding, alongside changes in tissue function that increase viral susceptibility.

The figure with the three silhouettes illustrates some of the key clinical / public health points that follow. First, there is a meaningful share of the population - in the U.S., it's been argued as much as 40% of the population with a "healthy" BMI - that may perceive themselves to be at low risk, but who are at high risk because of metabolic distress that has not led to obesity. Second, it provides further - hopeful - support for the idea that we may be able to reverse this susceptibility, and so moderate disease risk, more quickly than we can resolve obesity. As CrossFit has repeatedly shown on these pages, diet and exercise interventions can rapidly reverse insulin resistance and its various consequences, alongside the buildup of visceral fat. It is consistent with the authors' arguments here that these rapid metabolic improvements would lead to a similarly rapid improvement in resistance to disease.

We are obviously FAR from anything that looks like robust clinical proof of any of these statements, but it provides a promising indication that there may be an element of disease vulnerability that is highly predictable, and highly and rapidly modifiable. If the case linking specific metabolic defects to acute disease vulnerability continues to build, it could - and arguably should - change the way we look at chronic disease, and shift the importance we place on disease mitigation at an individual and societal level. Simultaneously, it will give us tools to specifically, effectively and rapidly reduce disease risk in more vulnerable populations.

While the correlations and their implications are currently tragic, they are also empowering.

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Thomas Cusack
May 15th, 2020 at 4:57 pm
Commented on: The Perfect Storm: Coronavirus (COVID-19) Pandemic Meets Overfat Pandemic
Dr. Maffetone has studied "human biology, kinesiology, physiotherapy and Chinese medicine," and while he has decades of experience in sports and performance, he has very little formal or informal research background in immunology or infectious disease. As an ICU clinician in the middle of fighting this disease every day I absolutely agree that obesity is a risk factor for death, and that diabetes is a comorbidity that causes a general immunocompromised state, both making one's risk of sickness and death from COVID and from being in the ICU higher. However, I am not sure that terms "overfat" or "underfat" are useful ones, and this paper could be rewritten without those terms. Obesity and malnourishment serve and have widely understood meaning in the scientific literature and amongst the general population. This is all to say that while I agree with the hypothesis here and perhaps even the exceedingly broad strokes with which it is penned, I think this paper is more about trying to create novel language that is redundant. I agree with the ends but question the means here. There are much more rigorous scientific authors writing without vague graphics (Fig 2 for example featuring a coronavirus particle with a arrow pointing into fat with the words "Poor T cell and macrophage function" seems to imply that those cells have difficulty achieving motility in fat. This isn't the case. Macrophages love diving into and through the fat of overweight animals and people, which is why being fat is associated with chronic low level inflammation. The broader dysregulation of the immune system is far more complex, nuanced, and compelling even in brief summary than has been presented here.)
I keep coming back to this article ( which quotes the great Richard Feynman: "I finally figured out a way to test whether you have taught an idea or you have only taught a definition. Test it this way: You say, 'Without using the new word which you have just learned, try to rephrase what you have just learned in your own language. Without using the word 'energy', tell me what you know now about the dog's motion.' You cannot. So you learned nothing about science."

Science education aside, Feynman's advice is equally useful when it comes to testing out someone else's claims, as Simon Oxenham explains:

"If someone cannot explain something in plain English, then we should question whether they really do themselves understand what they profess. If the person in question is communicating ostensibly to a non-specialist audience using specialist terms out of context, the first question on our lips should be: 'Why?' In the words of Feynman, 'It is possible to follow form and call it science, but that is pseudoscience.'"

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Matthieu Dubreucq
May 15th, 2020 at 3:18 pm
Commented on: The Perfect Storm: Coronavirus (COVID-19) Pandemic Meets Overfat Pandemic

The more I study this pandemic the more I realize it puts society face to face with the problem of chronic disease. I hope this helps change things and people realize there is no pills you can take, only actions to be taken to get off the carbs, off the couch.

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Mothilal Jayathilake
June 20th, 2021 at 7:53 am

Exactly 100 percent true.

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Nathan Jenkins
May 15th, 2020 at 1:29 am
Commented on: The Perfect Storm: Coronavirus (COVID-19) Pandemic Meets Overfat Pandemic

It doesn't happen often, but here we are - CrossFit's modern science approach and the academy's post-modern consensus science are pointing to the same conclusion: COVID-19 is deadly primarily, almost exclusively, in the setting of existing chronic disease.

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Grant Shymske
May 15th, 2020 at 1:30 pm

Good observation.

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