This little girl couldn’t stop eating, what happened next changed our understanding of fat

Layla appeard to be a healthy newborn. But as she grew into her first year, something changed. Layla would finish a bowl of food and cry until she was given another. Her parents knew this was unusual, but suspected it was a temporary stage of development.

As Layla continued to grow, however, so did her appetite, and before long she was obese. The family tried to reduce her weight gain by cutting calories and encouraging more activity. It was to no avail, because Layla became inventive at finding food. She would burrow through the trash and break into locked cabinets. Once she even forced open a locked freezer and ate frozen fish. Even when they succeeded, limiting Layla’s food intake didn’t help her lose weight, it only served to increase her violent outbursts and her desperate search for food.

Fat BabyDoctors tested her for everything they could think of: a thyroid disorder, pituitary and adrenal glands abnormalities, Cushing’s syndrome, Prader-Willi syndrome, Bardet-Biedl and Alstrom’s syndromes. But all tests were negative. No one was sure what was causing Layla’s ferocious drive to eat and nothing seemed able to stop her.

Layla, it seemed, was destined for a lifetime of obesity.

At about that time, a very interesting study was being conducted that shed light on Layla’s problem. Researchers found that a group of mice with a specific gene mutation had unstoppable eating behavior and grew obese. The mutation was in a gene that made a hormone produced by body fat, and when the mice were given this hormone, they lost weight and not muscle or bone, just fat.

Researches found that this hormone sent the signal to the brain to stop eating. Mice with the gene mutation became obese because they always felt hungry–they never got the signal. Today, we call this hormone leptin and know that it plays a role in humans, as well.

One expert on Layla’s case (Dr. O’Rahilly) learned of this discovery, and he noticed many similarities to the child’s case. Like the mutated mice, she was extraordinarily obese, had an unstoppable urge to eat. He tested Layla’s leptin levels, and found he was correct — Layla was a human version of the mutation, she had no leptin! At last, there was an explanation for why Layla could not stop eating.

What happened next was no less than amazing. When O’Rahilly started administering leptin to Layla, her appetite decreased significantly. As O’Rahilly recalls, “She was eating a quarter compared to what she was normally eating. She went from being a completely focused eating machine into a normal kid.”

Further research would show that leptin not only reduces appetite but is also involved in metabolism. In addition to eating like gluttons, mice without leptin tend to move less and burn less fat. Without leptin, Layla was unable to burn fat normally, which is why even when her calories were restricted she could not lose weight.

Hormones matter much more to our weight and metabolism than we often give them credit. Before starting a diet it’s important to understand how our hormones really work. Here’s one example why: High fructose foods reduce the effect of leptin, and can lead to leptin resistance. With leptin resistance we are more hungry and gain weight.

There are many things you can do to promote fat-burning hormones such as growth hormone and testosterone and decrease the effects of fat-hoarding ones such as insulin. I discuss all of this at length in my book, The Secret Life of Fat.

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