Opinion – Bruno Gualano: Bad skinny

While most of us struggle daily against modernities designed to make us fat, that slender fellow, averse to exercise and gluttonous with exultation, circulates unharmed. The infamous “thin of bad”.

Our schism with the saying-whose has its foundations there. After all, if our bodies were made to store fat and we live in a relentless environment of fattening, why do a lucky few escape the threat of obesity?

British biologist John Speakman (Abeerden University, UK) offers an interesting evolutionary explanation for the paradox.

Rather, it is important to say that the scientist does not share the adaptive view of obesity. This hypothesis considers that our efficient ability to accumulate fat would have represented an advantage to our hominid ancestors, protecting them from food shortages. From this scenario, a sparing genome would have been selected, which exposed to an abundance of food and insufficient movement, would predispose us to obesity.

In his critique of the thesis, Speakman argues that food insecurity would not have established itself as a vital factor in the evolution of our species. To illustrate the point, he cites the case of Homo erectus, who had meaty African herbivores, including elephants, on their menu. And he remembers that Homo sapiens himself, in his early days, had the habit of hunting more than he could eat – a hypothesis, by the way, that explains the extinction of several of its prey, and which, let’s face it, does not exactly match an environment of deprivation. of food.

According to the scientist, were the lack of food a decisive pressure on evolutionary success, excess weight would be a ubiquitous trait of our species. It is certainly not the case. Even in the United States—the country most beset by obesity—about 65% of people are not obese.

Speakman prefers a non-adaptive view of obesity, which presupposes the presence of a two-point control system, between which the individual’s fat and weight would be dammed.

The bottom point would have the function of preventing fat stores from exceeding critical levels, to the point of causing starvation and impairing reproduction and the immune response to pathological agents.

The superior, on the other hand, would operate against another threat to survival: excess weight. Indeed, heavier individuals —and of various species— were less successful throughout evolution, as (1) they needed more food to meet their energy demands and (2) they were easier prey for lack of mobility.

If this evolutionary scenario persisted, we could bet that obesity would be rare today. However, about 2 million years ago, profound social changes introduced new adaptations.

Our ancestors came to live in groups to protect themselves from predator attacks. Furthermore, the discovery of fire and weapons brought a substantial advantage to hominids against their tormentors.

In packs and armed, heavier and less agile individuals considerably increased their chances of getting rid of predation. Thus, the upper body weight control point would become dispensable for survival. And the genes responsible for such regulation would undergo unpredictable mutations. Consequently, some individuals would be more susceptible to obesity, and others practically immune to it – these, the lucky ones in the lottery of evolution.

An evolutionary thesis collates genetic, ecological, clinical, demographic, anthropological, behavioral, archaeological evidence, etc. Several premises are assumed to be true, but testing them in the laboratory is not always possible. It is, in short, an intricate and fascinating puzzle—one that needs to be reassembled whenever a piece doesn’t find its exact fit.

And the pieces have come together well for the maladaptive obesity hypothesis. It explains why that inconvenient pound we accumulate during the holidays — situated in a “neutral zone” between the two weight regulation points — does not stimulate an intense physiological response in order to eliminate it, unfortunately! And it also explains why some hot feet routinely exposed to poor diet and sedentary lifestyle do not become obese.

It remains to unravel the whole set of molecular, physiological and behavioral attributes that allow the “bad guy” to resist the obesogenic environment. It would be the harbinger of a revolution in the treatment of obesity.