With the U.S. government unwilling to impose mandates on obesity – which is implicated in the deaths of more than four times as many Americans as COVID-19 over the course of the past decade, if you believe the studies – it might be a good time to talk about a new and raging medical debate over what is fueling the country’s most visibly obvious epidemic.

And, no, we’re not talking about genes.

When it comes to body fat, some people might be more genetically inclined than others to pile on the blubber, but as Harvard University scientists studying obesity have noted “Genes Are Not Destiny.”

There have been genes linked to the tendency to add body fat, but as they write, “‘many people who carry these so-called ‘obesity genes’ do not become overweight, and healthy lifestyles can counteract these genetic effects.”

Or maybe not.

Dr.  David Ludwig, an endocrinologist and researcher at Boston Children’s Hospital and professor of pediatrics and nutrition at Harvard, has made a strong case for the problem being what we eat – not necessarily how much we eat or how much we exercise – that has kicked off something of a scientific firestorm.

Heretics

“Obesity Paper Has Diet Researchers Riled Up” is how the website MedPage Today headlined the situation on Tuesday in what it billed as an “exclusive” and “special report.”

The dietary hypothesis posted last month in The American Journal of Clinical Nutrition by Ludwig and a team of more than a dozen researchers from Cornell Medicine, the Univesity of Copenhagen, the National Institute on Aging, the University of British Columbia, the University of California’s Berkley and San Fransicso campuses, Harvard, Ohio State University, Duke University, Boston Children’s Hospital and a variety of research institutes is not exactly new.

But the credentials of the scientists now embracing the carbohydrate-insulin conundrum seem to have given it new weight.

The piece “stirred up tensions in the worlds of epidemiology, physiology, and nutrition,” wrote Sophie Putka at MedPage. “Doctors and researchers argued on Twitter; (and) commenters defended and derided related opinion pieces.”

What the Ludwig-led commentary did was question the simple, long-held and fundamental belief that obesity is merely about calories consumed and calories expended or what scientists call “the energy balance model (EBM).”

While the authors of the paper did not disagree with that model as a fundamental reality, they argued that it errors by merely restating “a principle of physics without considering the biological mechanisms that promote weight gain.”

There is really no denying the energy balance model. People who are placed on starvation diets or go on hunger strikes lose weight. None of them stay fat. It just doesn’t happen.

Real world

But few people in this country or elsewhere are put on starvation diets, and it takes amazing willpower to maintain a hunger strike, which makes energy balance much more complicated in the real world than in a theoretically simplified world.

In the real world, Ludwig and others argue, obesity is complicated by a diet now rich in carbohydrates and the response of the human body to this diet.

“Rapidly digestible carbohydrates, acting through insulin and other hormones, cause increased fat deposition, and thereby drive a positive energy balance,” they write.

Among those living the now-common “sedentary lifestyle,” a “positive energy balance” is not a positive. A positive energy balance leads your body to store fat in the interest of self-preservation for future periods when food supplies might be limited.

For most of human history – no matter whether you were a Neanderthal living in a European cave 100,000 years ago, a Dorset Eskimo living along the Arctic Coast 2,500 years ago, or an Athabascan Indian or gold prospector in Alaska only a century ago – this was a good thing.

Some body fat could help you get through those times when there was little or no food to be had. Now, however, with food readily available, the same accumulation of fat has become a liability.

It has been linked to heart disease, stroke, diabetes, some cancers, gallbladder disease and, lately, COVID-19, the disease caused by the pandemic SARS-CoV-2 virus.

A peer-reviewed study published at PLOS One on Tuesday reported that in the first wave of the pandemic in Sweden the obese were about twice as likely as their thinner countrymen to end up dead or with a prolonged length of stay (LOS) in an intensive care unit.

“A prolonged LOS reflects a more severe course of disease and is associated with greater functional impairment in survivors.,” they added…;”A prolonged LOS is an important factor not only for the individual patient but also as an important factor for health care, putting excess strain on ICUs during the COVID-19 outbreak.”

Obesity, once a human luxury, has become a curse in much of the modern world.

But Ludwig and his colleagues argue it’s not really our fault.

Well, sort of.

‘Vicious cycle’

They argue a carbohydrate-insulin model (CIM) has us trapped in a nasty feedback loop.

Basically, the theory is that when we eat foods with a high “glycemic load” – breads, pastries, potatoes, french fries, crackers, chips, etc. – we quickly convert them to body fat and having done so quickly grow hungry again.

Or to quote the study:

“Three hours after eating, most of the nutrients from a high-GL meal have been absorbed from the digestive tract. However, the persistent anabolic actions from this hormonal response slow the shift from uptake to release of glucose in liver and fatty acids in adipocytes.

“Consequently, total metabolic fuel concentration in the blood (from glucose, nonesterified fatty acids, and ketones) decreases rapidly in the late postprandial phase, possibly to concentrations below that in the fasting state.

“The brain perceives this signal as indicating that critical tissues (e.g., liver) are deprived of energy – a state of ‘cellular semistarvation’ as it has been termed – and may respond to the metabolic challenge with a counter-regulatory hormone response.

“Simultaneously, hunger and cravings for high-GL foods (i.e., those that rapidly raise blood glucose) increase, setting the stage for a vicious cycle.”

Probably the most controversial part of this view is that it suggests the low-fat diet craze has made the obesity problem worse rather than better through the years, although they do admit they could be wrong.

“In this review, we provide the most comprehensive formulation of the CIM to date, argue that the CIM better reflects knowledge on the biology of body weight control than the EBM, specify testable hypotheses to help resolve controversies, and call for constructive discourse among scientific camps on this question of critical public health importance,” they write.

It’s hard to disagree with that.

Full disclosure: The author of this story generally believes in the energy-balance model. Like most Americans, he has also struggled with weight. He has never seriously experimented with the carbohydrate-insulin model.

But a fishing buddy, who shall remain nameless, resorted to it years ago. It always seemed sort of silly when he visited a restaurant for lunch or dinner (back in the good old days when restaurant dining was safe), and ordered a hamburger sans bun and a salad instead of fries.

He’d generally sworn off bread and potatoes as having too high of a glycemic index. This form of dieting worked for him. He managed to get back to his old high-school weight years ago and has stayed there now since, which is no small accomplishment for a man in his 60s.

If only we could all claim the same.