intain a certain body weight," explains Friedman. The way the system works is that the more fat you have, the more leptin your body makes and the less hungry you feel. The ultimate goal is to shut down the appetite of individuals with a lot of fat, so they eat less and stop gaining weight. And vice versa. If you lose weight, your body produces less leptin and your appetite increases. The fact that the body possesses this mechanism has an evolutionary origin: "It would be very dangerous to have no fat, because you would risk dying of starvation, but it would also be dangerous to be too fat, because you would be at the mercy of predators. So the system tries to maintain an optimal level."
The lab also discovered that leptin "circulates in the blood and acts on centers in the brain to regulate appetite, just as Coleman predicted," adds Friedman, an admirer of his colleague's work: "His observations were very non-obvious. There were probably thousands of scientists looking at the same problem, but he was the one who got it right."
The discovery of leptin opened up a whole new field of research into the causes of obesity, propelled by a radical change of mentality in society and science: "Before people thought that how much we ate was completely a matter of willpower," Friedman reflects, "but we now know that body weight, in humans and other animals, is regulated by cells in the brain that receive important signals such as leptin and then unconsciously regulate appetite. And this system is absolutely crucial for the survival of any species."
This means, ultimately, that obesity is "in the mind": "As well as leptin and the leptin receptor, we know that 10 percent of morbidly obese individuals carry defects in genes that regulate food intake, metabolism and body weight. And all these genes act on the brain, which tells us that the main reason people get fat is an alteration of their brain chemistry."
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