There's one thing that many people may not realize, and even dogs may not realize: Labradors and humans share the obesity gene.

The research team spent more than a decade extracting DNA from dogs' saliva and came to a shocking conclusion. Labradors are not only notoriously gluttonous, but their genes for gaining weight are almost identical to those of humans.

In humans, genes determine the risk of obesity from 70% to 0%, with the rest attributed to lifestyle habits. In other words, some people have a hard time losing weight no matter how hard they try, while some people have a hard time gaining weight even if they eat casually.

The same logic is true for Labrador. The influence of genes is so strong that even with the same feeding method, some dogs are always slim, while others are as fat as piglets.

It's actually quite understandable. Dogs, like humans, have evolved through a cycle of "food scarcity-food scarcity", with the body's mechanisms to store as much fat as possible in order to survive in response to possible periods of famine. This mechanism relies on gene regulation.

Key genetic DENND8B is an example. DENND0B with a "problematic" version, means that the dog's body fat percentage will be 0% higher. In humans, the influence of this gene is so weak that it has not been taken seriously enough.

This time, the researchers found that DENND1B can directly affect the brain's appetite regulation.

This involves a hormone called leptin.

The role of leptin is simple and crude: the more fat, the more leptin is secreted, and the task of leptin is to "report" to the brain: "If you have enough fat, don't eat it anymore." ”

But the problem is with the receptors. Leptin is reported to the brain for "melanocortin receptors", and DENND1B will interfere with the signaling of this receptor, causing the brain to perceive the signal of satiety skewed, and the end result is that you eat more and accumulate more fat.

This directly explains why some dogs are hungry and hungry, desperately grabbing food, and even rummaging through Laji buckets to find food.

This is also confirmed by experimental data. Labradors with a higher risk of obesity at the genetic level have a more appetite than genetically normal dogs, harass their owners more often to eat, and can't stop when they see food. And dogs that are born with low risk will not gain weight easily even if the owner does not strictly control the diet.

This is very similar to humans.

Under the influence of obesity genes, the difficulty of weight control does not lie in the amount of exercise, but in the appetite itself. Some people are naturally more hungry and have more difficulty controlling their urge to eat. So, it's not that thin people have more perseverance, it's just that their genes don't need much perseverance at all.

Here's a very noteworthy phenomenon – guide dogs have a higher risk of genetic obesity. In other words, an excellent working dog is more likely to gain weight than an ordinary pet dog.

This is no coincidence. Because the biggest secret to training a guide dog is reward, and food is the most effective means of reward. Dogs can do anything to eat – and that's exactly what makes Labradors the best working dogs.

From an evolutionary point of view, Labrador is not a disadvantage, but an advantage. They have a natural appetite and are more easily driven by food, making them easier to train.

This explains why Labradors are naturally prone to obesity – their genes are selectively reinforced by humans for this food-driven trait.

On a deeper level, human society has been doing similar things.

Certain genes make it easier for people to hoard fat, which is a survival advantage in agrarian societies because famine can happen at any time. But in modern society, when there is an abundance of food and a sedentary life becomes the norm, this advantage has become a burden.

The essence of the problem of obesity is not just a matter of lifestyle, but a question of genetic adaptation to environmental changes.

DENND1B's discovery may be just the beginning. It points to a key fact that obesity is not just about not being able to control your mouth, but about the brain's regulation of food.

At present, existing anti-obesity drugs mainly target the "melanocortin receptor" pathway. The mechanism of action of DENND1B may provide new ideas for future obesity intervention.

But the question is, should this gene really be "fixed"? From an evolutionary point of view, it is naturally screened out. Labrador's gluttony helps them to be the best working dogs. And the obesity gene of human beings has helped countless ancestors survive in a long history.

Putting aside the aesthetic prejudice of modern society against "body", the existence of these genes is reasonable. But adapting to changes in the environment has always been a brutal process. The food supply in modern society is no longer the model of the past, and the speed of human evolution is far from keeping up with the speed of environmental change.

This may be the real root cause of the growing prevalence of obesity today. So, from a genetic point of view, it's not just a matter of weight loss, it's a matter of adaptation. Adapting to changes in the environment is fundamental.

For people, perhaps. For Labrador, the same is true.