Here’s what I thought was the most interesting research news about COVID-19 to emerge this week. On Wednesday, a team from the southern California arm of the health-care giant Kaiser Permanente (KP) published a new study on obesity and COVID-19 using data from their insured patients. KP is a little like Canadian medicare in a private American form: it provides customers with all-in “capitated” care for a set price.
Unlike much of Canadian public health care, however, KP is capable of making timely research use of the patient data it collects routinely. A country with state single-payer medicare really ought to have the advantage in this regard, but we pretty obviously don’t, and our provinces also lag behind the European countries whose health-care systems we think of ours as being kin to. But I digress.
Kaiser Permanente, in the ordinary course of business, had gathered very good data on the health characteristics of 6,916 patients who had contracted COVID-19 between the beginning of the epidemic and the start of May. Researchers there wanted to know how obesity affected the risk of dying. The ordinary problem here is that anything might affect the risk of dying from COVID-19, and “anything” includes a lot of other stuff that is correlated in the population with obesity: diabetes, diet, hypertension, low socioeconomic status, you name it.
So to study the strict effect of being fat on COVID-19 risk, you would ideally be able to throw every possible variable into a multiple-regression blender and pluck out body mass index (BMI) from the resulting statistical smoothie. This procedure can never be perfect, but KP has a lot of variables and a pretty decent blender.
It was obvious already that obesity is related to COVID-19, but what fell out of the Kaiser Permanente model is that obesity is both a dominant and an independent risk factor for COVID-19 mortality. Factor out hypertension and the effect of obesity survives; so too with sex, age, race, smoking status, heart failure, history of myocardial infarction, proxies for socioeconomic status, all manner of vascular disease, asthma, diabetes, you name it. (Unlike some studies of COVID-19 risk factors based on health records, by the way, this one was able to incorporate actual A1c measurements from diabetic patients.)
Kaiser Permanente’s patients aren’t an ideal proxy for America’s or the world’s population as a whole. As the authors of the study point out a bit smugly, everybody in the sample shared the privilege, and in the U.S. it probably is a privilege, of being KP customers. (The paper, incidentally, is published in the Annals of Internal Medicine , a first-class, peer-reviewed journal.) But the sample grouping is otherwise quite diverse, and the findings raise the possibility that obesity, when it comes to COVID-19, is dangerous in itself.
That is to say, fat folk aren’t necessarily in greater danger just because they are more likely to be poor, or have bad habits, or suffer diabetes or high blood pressure. The fat itself might be an issue, clinically.
It ought to be pointed out that the relationship they found between BMI and mortality risk is “J-shaped,” which is not surprising. The patients in the KP sample who were underweight according to the commonly accepted criteria — having a BMI of under 18.5 kg/sq. m — faced risk estimated to be 81 per cent higher than persons of “normal” weight, although the confidence bounds of this estimate were very wide. And you do have to be quite big to be in extreme danger. The estimate of excess risk for persons with a BMI in the 35-39 kg/sq. m range was just 16 per cent. (For someone six feet in height, a BMI of 39 is about 288 pounds. To qualify as underweight at the same height you would have to weigh 136 pounds or less.)
Over that line, however, the added risk takes off like a jet. In the 40-44 BMI range, the point estimate is 168 per cent, and at 45-plus it’s 318 per cent. And there are just a lot more 40-pluses in the United States, and for that matter in Canada, than there are under-18.5s.
The journal regarded the paper as being important enough to have a famous cardiologist, David Kass of Johns Hopkins, write an accompanying editorial . Kass’s task was to envision ways in which obesity could have a direct effect on COVID-19 mortality risk. He certainly didn’t have any trouble. Setting aside diabetes and high blood pressure, Kass observes that obese persons have poorer immune systems and bad endotheliums (that’s the cellular layer on the interior surface of blood vessels, now treated as a bodily organ in its own right). Their metabolisms are screwy and they often don’t breathe well at night or in prone position.
Fatty tissue even has a high amount of the “docking” protein that the COVID-19 virus uses to break into cells — a higher amount than the lungs, Kass says, possibly allowing fat to “serve as a viral refuge and replication site, prolonging virus shedding.” Sure, I noticed the main study partly because I have my own spare tire, but I wasn’t prepared for the mental image of the SARS-CoV-2 virus using my navel as some sort of military redoubt. This year just keeps getting weirder.
National Post
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