Stephen O’Rahilly, a prominent expert on obesity and other metabolic disorders — who struggles with his own weight — lost about 20 pounds in the six months before becoming ill with COVID-19. He believes the weight loss probably protected him from serious disease, and maybe even saved his life.

“My experience with the virus wasn’t so terrible,” says O’Rahilly, co-director of the Wellcome Trust-MRC Institute of Metabolic Science at the University of Cambridge in Britain, who said modest diet changes and exercise helped him shed the weight and probably enabled him to escape the worst effects of COVID-19, the illness caused by the novel coronavirus.

“No need for [intensive care], just five days in hospital, quick recovery, back in full-time work and playing vigorous singles tennis within three to four weeks of discharge,” he says.

If anyone needed a reason to lose weight, the novel coronavirus provides a powerful incentive.

Obesity, a significant public health problem among American adults and children, is one of the risk factors for severe disease and death related to COVID-19. Others include older age and underlying medical conditions such as heart disease and diabetes, both of them related to obesity.

Obesity grew from 30.5% to 42.4% among American adults between 2000 and 2018, while severe obesity rose from 4.7% to 9.2%, according to the Centers for Disease Control and Prevention. Obesity contributes to heart disease, stroke and Type 2 diabetes, which increase risk.


Researchers do not know why obesity worsens COVID-19. They are trying to discern the reasons, with several ideas under study. “It’s clear that we need to think more deeply about what it is about the obese state that makes COVID-19 more deadly,” O’Rahilly says.

But they agree that one way to likely reduce the risk is to do what O’Rahilly did: drop some excess pounds.

“Age remains the strongest risk factor for COVID-19, also being male or having specific medical conditions, but as we cannot change age or being a male, weight may be the major modifiable risk factor for severe COVID-19,” says Naveed Sattar, professor of metabolic medicine at the University of Glasgow’s Institute of Cardiovascular & Medical Sciences.

“Some countries, such as the U.K., have now started to take a stronger approach to the prevention and management of obesity,” Sattar says, with a public campaign to encourage its citizens to lose weight as a means to prevent severe COVID-19 disease.

Sattar says that, among other things, being seriously overweight makes it more difficult to breathe, increasing the disease’s harm on the lungs.

“When people carry extra weight, this can lessen their lungs’ ability to extract oxygen from the air, and excess weight also impairs the heart and blood vessels’ ability to deliver this oxygen around the body, as blood vessels become stiffer and blood pressure levels go up with obesity,” he says.


Obesity causes the blood to become thicker or stickier than normal, Sattar says, a condition made worse by the virus. This increases the possibility of blood clots. “Also, severe COVID-19 reactions appear linked to the body’s immune response going into overdrive, and some speculate that this is greater in those with excess body fat,” he says.

O’Rahilly thinks that disruptions in the body’s metabolism caused by obesity may be the prime reason being overweight contributes to severe COVID-19.

“Explanations around ‘heavy chests’ and upper airways narrowed by fat just don’t cut it,” he says. “We have to look closely into the metabolic effects associated with obesity. Only then will we possibly find paths to interventions that can really be protective.”

The virus enters the deep parts of the lung through ACE2 receptors, proteins attached to cells in the lung and elsewhere, which is the reason for lung inflammation and the formation of small local clots.

Most people who die of COVID-19 cannot get enough oxygen into their bodies through their lungs. This happens because the thin layer of lung cells that oxygen must pass through becomes damaged and swollen by the virus.

“This is further complicated by the fact that the blood supply to the parts of the lungs that normally take up oxygen is blocked off by tiny clots, which are a really striking feature of COVID-19,” O’Rahilly says.


Obesity can influence several steps in this process.

“Obesity is strongly associated with a ‘sick’ metabolic state called insulin resistance,” O’Rahilly says, referring to a condition in which the tissues that normally handle glucose in the body become less responsive to insulin, prompting the levels of insulin in the blood to climb higher to compensate. This “is often the prelude to obese people becoming diabetic,” he says.

Insulin resistance causes increases in inflammation-producing molecules, he says, and is associated with rising blood levels of a protein that attacks cells infected with virus. An excess of that protein, complement component 3, causes excessive inflammation and small clots in blood vessels.

“In fact, in COVID-19, there is good evidence that complement is involved in the damage seen to lung tissues, and its small blood vessels,” O’Rahilly says. “Obesity and insulin resistance may be ‘loading the gun,’ with too much complement, predisposing one to greater damage when the virus comes along.”

Obesity also prompts a reduction of adiponectin, a hormone secreted by adipose tissue, which is where the body stores fat. Obese people tend to have low levels, while thin people have more. Adiponectin protects the lung blood vessel linings from inflammation, he says. Along with the formation of “stickier” platelets, which start clots, obesity also increases levels of another protein, plasminogen activator inhibitor 1, that prevents clots from breaking down.

“All of the above effects of insulin resistance are well established and replicated — their impact on the worse outcome of COVID-19 in the obese remains theoretical but highly likely in my view,” O’Rahilly says.

Candida Rebello, a postdoctoral researcher at the Pennington Biomedical Research Center, agrees that multiple factors probably are involved in obesity’s dangerous effect on COVID-19 — citing insulin resistance, chronic inflammation of fat tissue and the effects of the pressure of excess fat around the lungs — but she speculates that leptin, an appetite-regulating hormone produced by fat cells, also may play a role.


“When fat stores are low, leptin signals to the brain to increase appetite,” she explains. “However, when fat stores increase, leptin increases. When fat stores are increased — as in obesity — a condition called leptin resistance develops where the brain does not receive a signal to lower appetite. The fat cells continue to secrete leptin in an effort to convince the brain to lower appetite, causing blood levels of leptin to rise.”

Typically, the body secretes leptin to meet its needs, she says.

“When leptin levels are out of balance, as occurs in obesity, the immune response could be ineffective, insufficient or misdirected,” she says. “Viral replication increases and its clearance reduces. Damage to tissue can precipitate a new response and a spiraling effect that can cause a lot of damage to tissues and organs.”

Research is still underway, but there’s no need to wait for it, O’Rahilly says. People can start by taking in fewer calories than they are burning. That’s enough for insulin resistance to start to improve.

“[This] may be something that most overweight people can take on board,” he says, “even before they see much of a change on the scales or in their clothes.”