And the obesity wars drone on: it’s the sugar, it’s the fat, it’s the paucity of playgrounds, it’s the prevalence of too-thin models and TV and gaming and chips and texting. It’s the lack of parental discipline and self-restraint.

But wait: what if we accepted that “the environment”--the catch-all phrase for the above--just can’t be changed, or at least not fast enough to make a difference? And what if we just accepted that people will, by and large, continue to do as their genetic backgrounds direct them: eat as much as they can, and move as little as they must?

Slowly that heretical notion is taking root in the field of nutritional sciences. There, researchers are slowly and painstakingly shifting their inquiry to a more basic issue: homeostasis--the body’s innate capacities to recover from any kind of disturbance--and how we can strengthen those balancing mechanisms.

Call these whitecoats the flexocrats.

Theirs is not a difficult premise to understand. Consider: The human phenotype--the body our genes and environment dictate--has been shaped by evolution to adapt, to bend and flex and return to balance when confronted with a challenge, be it a Big Gulp or bad air. You eat a huge hit of sugar, your body pumps out insulin to make it possible for your cells to use it and return to balance. It’s an intricate, elegant system that worked just fine until we engineered an environment that made sugar virtually free and almost everywhere present. Then the system crashed, and we got our intertwined epidemics of obesity and diabetes.

Traditional public health folks have responded to these public health problems in two ways: change the environment - ban Big Gulps! - or change the behavior - stop eating and start moving! Reduce your risks!

Flexocrats say: rather than spending all our time making people do what is not in their nature, why not find ways to make our native metabolisms respond to the assault better? It’s a way to even the playing field and give us a fighting chance as we enter the unnatural arena of eating less and moving more.

Consider the current (and, no doubt, very temporary) consensus talking point: that sugar consumption, not obesity, causes type two diabetes. ( Actually, they both do, but given the current “obesity does not equal diabetes” media phase we’re now in, we’re not able to handle such a staggering concept.) The current public health model would hence look to any number of “solutions,” a reasonable but politically impossible one being the regulation of sugar.

The donuts are not the problem. It is you. Just kidding, you look pretty good. But that is not from the donuts either. Credit: Shutterstock

A pheno-flexo-crat (that sounds even cooler!) would say something completely different: What, in our innate bodily system of self-regulation, can we tweak or reprogram - using everything from breast-feeding routines to fortification of the food supply - to let us simply take that sugar assault in metabolic stride? No, that wouldn’t mean you could eat like a pig all the time, but it would give your body a buffer when you did. (And, face it, you’re going to!)

Predictably, some of the most robust flexocratic findings come from the world of laboratory rodents, our principal, if flawed, medical stand-ins. At Spain’s sunny University of the Balearic Islands (UIB), a huge program is studying the mechanisms of glucose control. In one experiment, lactating rat mommies were put into one of two regimens, one in which they ate normally, and one in which they ate 20 percent less than normal.

The results: the offspring in the calorically-restricted group were dramatically less likely to develop insulin resistance and diabetes than their traditionally fed counterparts, regardless of how they ate later in life. “It was shocking,” said Jadwiga Konieczad, a doctoral student who oversaw the study. “It’s obviously not something for humans to try yet, but the result was so strong, so dramatic, that it may lead to us rethinking our current dogmas about how to feed infants. Maybe we can make them tougher to the realities of modern life.”

In the realm of food supply supplementation, (not “healthy eating”), Swedish researchers have focused on the flexibility-inducing components of non-traditional grains--barley and rye and the like. At frigid Lund University, the preeminent diabetes scholar Inger Bjorck is tinkering with tiny, concentrated concoctions of rye. In one experiment Bjorck added the compound to the evening meals of one group of human type 2 diabetics; a control group ate an un-supplemented meal. The next day, both groups ate a normal (not a “heart-healthy”) breakfast - ham, eggs, toast and the like.

Two hours later, Bjorck recorded the blood sugar and insulin levels in both groups. Finding: The patients who’d eaten the little rye supplement the night before registered the healthy  levels of a non-diabetic; the control group’s response remained impaired and diseased. “We don’t know why it works,” Bjorck says. “But we have some idea. We think it involves some kind of gastric memory, maybe driven by fermentation in the gut, that we, as humans, once possessed, but which we lost when we began consuming our modern wheat mono-culture.”

What about reprogramming fat itself? After all, fat is not “bad.” Fat cells act like tiny endocrine organs. They are an essential part of our homeostatic toolkit, the way our body stores energy, fuels the immune system, and signals all kinds of beneficial processes. The problem is that modern life has accentuated, or perturbed, fat's bad qualities--its inflammatory, disease-causing signals. Yet new research, this also at UIB, has isolated a number of  potential additives that would "push" perturbed "bad" white fat cells into becoming more like brown fat cells, a form of fat that seems better equipped to handle the chronic over-consumption of sugar. This is not a try-this-at-home thing yet. Too much brown fat would likely make you so hot ( it partly works by increasing thermogenesis) you’d likely drink a Big Gulp.

Ben Van Ommen, a Dutch researcher who has led much of the EU's multi-million dollar investment in pheno-flex, explains that the new approach simply made sense. "About ten or fifteen years ago, all of us studying metabolism and fat saw the same thing: Sure, getting people to change and making the environment more healthful would be the best way to go, but it was simply not working. The dice were loaded against people. One day somebody said, 'look, the problem is not the donut, the problem is us--our body.'"

So far, few in the today’s world of public health have taken up the flexocrat cause. Think about it: it has no natural intellectual constituency. The vast “healthy lifestyle” industry - both private and public - would be threatened by it. The professional fatties would simply see another form of stigmatization and pseudo-eugenics. And such “unnatural” tinkering would also bring out the anti-nannies, the anti-pharmas, the truthers, the birthers, all three remaining anti-Trilateralists and, of course, those lonely, lonely Tea Party guys.
It would just be too "radical."

Yet Van Ommen points out that the flexocrat approach perfectly fits a nearly universally held definition of health. As articulated by one of its earliest 20th century proponents, the brilliant Johns Hopkins' pioneer Henry Sigerest, health “is not just the absence of disease. It is something positive, a joyful attitude to life, and a cheerful acceptance of the responsibilities that life puts upon the individual... A healthy individual is a man who is well balanced bodily and mentally, and well adjusted to his physical and social environment."

Greg Critser is the author of Fat Land: How Americans Became the Fattest People in the World. And you can read more of his articles here.