Immediately after the recommendations were published, they came under intense criticism for their screening and treatment methods, particularly drugs like semaglutide and Alexandra’s chosen surgery. Critics say these approaches are too aggressive, expose children’s bodies to unnecessary surveillance and manipulation, and can distort how children see themselves, and that the treatments have more to do with obesity than obesity itself. He also argued that it could lead to eating disorders that can cause great damage. Some critics objected to the controversial measurement BMI, arguing that doctors shouldn’t diagnose obesity in children at all. However, Hampl emphasizes that “treatment decisions are really in the hands of the family, not the doctor.”
In June, Alexandra waited in the pre-surgery area holding a stuffed white puppy with floppy ears and a red blanket with a gray hedgehog printed on it. Although she was nervous, she said, pointing to her mother, “she wasn’t as nervous as she was.” Gabriella nodded and said, “I think she’s overthinking it.” Her father sat quietly next to her as Alexandra tried to keep her busy by drawing in a sketchbook and eventually burying her face in a stuffed animal.
tenacity of Weight comes from our biology. Rudolf Leibel, director of pediatric molecular genetics at Columbia University Medical Center, said humans evolved to resist losing body fat to avoid extinction. Scientists are still trying to understand how it evolved. The “thrifty gene” hypothesis, which has been around for more than half a century, states that we gain weight (and continue to maintain that weight) to survive periodic starvation. In 2008, John Speakman, a prominent British biologist, proposed the “drift gene” hypothesis. As human survival became less dependent on escaping predators, random genetic mutations made it possible for the upper limit of body weight to rise. Right now, our brains may be adjusting our weight to stay within the upper and lower limits, but our brains may be fighting hard to stay above the lower limits. After all, hunger poses a more immediate danger than obesity. “Chronic calorie restriction does not chronically reduce body fat levels,” Liebel says. But that level could be pushed up “because of the environment,” he added.
Stephen Guynet, a neurobiologist and author of The Starving Brain, said our brains “subconsciously protect that high body weight.” And the brain may even slow down our metabolism to do so. The hypothalamus, located deep in our brains, is the master of this tightly regulated system. They are cone-shaped, about the size of an almond, and are responsible for determining whether you are hungry, prompting you to increase your food intake accordingly, or decrease your intake if you are satisfied. It also helps control your metabolism. The hypothalamus responds to signals sent from parts of the body such as fat cells and the intestines. For example, signals such as leptin, an important hormone that Liebel helped discover. Leptin increases when body fat increases and tells the brain to stop eating.
A small number of children who are severely obese are born with leptin deficiency. The genetic mutation was identified by Professor Sadaf Farooqi from the Institute of Metabolic Sciences at the University of Cambridge. Their appetite seems bottomless. Although rare, Farooqi cited the extreme effects of this mutation as a clear indication of the “very strong” influence biology has on appetite. When Farooqi treated children with this deficiency with leptin injections, their intake of leptin decreased. Too much leptin caused them to stop eating altogether. “You can literally control how much they eat by the amount of leptin you give them,” she says. In other words, appetite is not completely within our conscious control or willpower. Ghrelin, the hunger hormone, increases when food intake is restricted, causing you to eat more. Another important hormone, insulin, helps turn the food we eat into energy and controls things like blood sugar levels that affect how much we eat.