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.

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 (https://www.sciencealert.com/here-s-richard-feynman-s-simple-technique-for-sorting-science-from-pseudoscience) 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.'"

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.  

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.