by Laurent Glatz – for Athletic Carnivore
Obesity may not simply be a matter of losing control. In many cases, it could be an ancient biological program that modern environments keep permanently switched on.
This is what makes the topic so unsettling. We can keep repeating that people gain weight because they eat too much and move too little. This statement is short, moralizing, and reassuring for those who say it. But it poorly explains why so many people are constantly hungry, store fat easily, lose muscle, tire quickly, develop insulin resistance, and end up trapped in a body that seems to work against them.
The real question isn’t just: how many calories enter the body? The real question is: what biological signal do these calories trigger?
Fat as a Survival Strategy
In nature, fat is not a mistake. It’s a life insurance policy. An animal that must survive winter, migrate, hibernate, or endure famine benefits from rapidly accumulating energy. It benefits from feeling hungry. It benefits from slowing its energy expenditure. It benefits from temporarily becoming more insulin resistant to direct fuels toward storage.
In bears before hibernation, certain migratory birds, and animals facing seasonal scarcity, this mechanism makes perfect sense. The body activates survival mode: it eats more, stores faster, conserves energy, and protects its reserves. In this context, gaining weight is not a pathology. It’s an adaptation.
The problem arises when this program, designed for rare and limited periods, remains activated every day.
This is the hypothesis championed for several years by Dr. Richard Johnson around the “survival switch.” According to this view, some modern nutrients—especially fructose and refined carbohydrates—can activate metabolic pathways that tell the body: prepare for shortage.
Except winter never comes. The cupboards are full. Sugary drinks are available year-round. Desserts, cereals, juices, snacks, and flours have become permanent fixtures. The scarcity signal lights up in a world of abundance.
Fructose Tells a Different Story Than Glucose
Fructose has long been portrayed as a “more natural” sugar because it comes from fruit. This interpretation is too simplistic. Biology doesn’t judge a sugar by its cultural image but by its metabolic fate.
Glucose can be used by many tissues. Fructose, however, is primarily processed by the liver. Its metabolism rapidly consumes ATP, the cell’s immediate energy currency, which can create a paradoxical signal of energy deficit. In other words, even as the body receives energy, some cells interpret the message as a drop in availability.
This signal can promote hunger, liver fat production, increased uric acid, insulin resistance, and storage. It’s not just about “sugar that makes you fat.” It’s about a cellular message.
In an ancestral context, a very sweet fruit at the end of summer could signal an upcoming season of scarcity. The body had every reason to turn this signal into reserves. In the modern world, the same mechanism is hijacked: fruit juices, sodas, syrups, pastries, industrial sauces, cereals, and “healthy” sweetened products. The body receives the famine-preparation signal without ever encountering famine.
The Body Can Produce Its Own Fructose
What’s even more troubling is that fructose doesn’t only come from what we eat directly. When blood sugar rises sharply, a pathway called the polyol pathway can convert some glucose into fructose inside the body.
This changes the entire perspective. It’s not enough to blame table sugar or corn syrup alone. A diet very high in digestible starches—bread, pasta, rice, potatoes, cereals, and refined products—can also, in metabolically vulnerable individuals, indirectly feed this logic.
This is where many people lose track of their bodies. They say, “I don’t eat that much sugar.” Maybe. But if they live on a diet that keeps blood sugar high, insulin frequent, and the liver under pressure, the metabolic signal remains close.
The body doesn’t read slogans like “natural sugar,” “whole starch,” or “healthy energy.” It reads the load, the context, the frequency, the liver’s state, insulin, cortisol, muscle mass, sleep, and inflammation.
Uric Acid, Hunger, and Metabolic Lockdown
Uric acid is often reduced to gout. That’s important, but not enough. In the survival switch model, it becomes a metabolic player: a signal capable of amplifying cellular stress, insulin resistance, blood pressure, and storage.
Fructose increases uric acid production. Uric acid can disrupt mitochondrial function. Mitochondria produce energy less efficiently. The body interprets this deficit as danger. Hunger increases. Energy expenditure decreases. Storage becomes more likely.
It’s a loop. Not just a simple calorie addition.
And this loop explains why some people feel trapped in a body that demands more than it should. The problem isn’t always willpower. Sometimes it’s a metabolic terrain that acts as if winter is always coming tomorrow.
The Athletic Carnivore Approach: Reducing the False Scarcity Signal
This is where the Athletic Carnivore approach becomes interesting: it doesn’t just ask which foods are good or bad; it seeks to understand what those foods trigger in you.
A well-constructed carnivore or low-carb base removes much of the noise: less fructose, fewer refined carbs, fewer blood sugar spikes, less repeated insulin, less reactive hunger. The body can then stop constantly receiving the message: “store, conserve, prepare.”
The lion’s diet, in this logic, is not an extreme stance. It’s a dietary reboot: ruminant meat, salt, water. Few variables. Few conflicting signals. A way to see if the body regains a simpler reading of hunger, energy, and satiety.
Not everyone needs to stay strict. But many need to understand what sugar, modern fruits, juices, starches, and processed products tell their metabolism.
So the real question isn’t: why can’t I lose weight? It’s deeper: why does my body still believe it must store as if living in scarcity?
If our modern environment knows how to press a survival switch, then the first step isn’t punishment. It’s to stop pressing it.
Discussion around this article
Ask a question or add your feedback directly below the article. The comment appears on the page and can be removed from the admin area if needed.
No comment published yet. Start the discussion.