As soon as the recommendations were announced, they were met with fierce criticism for their screening and treatment methods, especially drugs like semaglutide and the surgery Alexandra opted for. Critics claimed that these approaches are far too aggressive and subject children’s bodies to unnecessary scrutiny and manipulation, potentially distorting how they view themselves, and that treatments could lead to eating disorders that cause more damage than obesity itself. Some critics challenged B.M.I. — a controversial measurement — and argued that doctors should not be diagnosing obesity in children at all. But, Hampl emphasizes, “the decision for treatment is really in the hands of the families,” rather than the doctors.

In June, grasping her white stuffed puppy with floppy ears and her red blanket printed with gray hedgehogs, Alexandra waited in the pre-op area. She was nervous, but “not as nervous as she is,” she said, pointing to her mother. Gabriela nodded and said, “I think I’m thinking too much.” Alexandra’s father sat quietly beside her as she tried to keep busy by drawing in her sketchbook, eventually burying her face in her stuffed animal.

The tenacity of body weight can be traced to our biology. Humans evolved to resist losing body fat so that we don’t become extinct, says Rudolph Leibel, chief of the pediatric molecular genetics division at Columbia University’s medical center. Scientists are still trying to unravel that evolutionary process. According to the “thrifty gene” hypothesis, which has been around for over a half-century, we gain weight (and keep it on) to help us prepare for and survive periodic famines. In 2008, John Speakman, an eminent British biologist, coined the “drifty gene” hypothesis: As human survival came to depend less on escaping predators, random gene mutations allowed our upper weight limits to drift higher. Today our brains may be regulating our body weight so that it stays within a range between upper and lower thresholds — while perhaps fighting harder to keep us above the bottom one. After all, starvation poses more immediate danger than obesity. “You cannot get a person to chronically defend a lower level of body fat by chronically restricting their calories,” Leibel says. But, he adds, that level may be pushed up “by virtue of environment.”

Our brains are “nonconsciously defending that higher weight,” Stephan Guyenet, a neurobiologist and the author of “The Hungry Brain,” told me — and they are even capable of slowing down our metabolism to that end. The hypothalamus, seated deep in our brains, is the master of this tightly regulated system. Cone-shaped and no larger than an almond, it’s involved in determining if we’re hungry and accordingly prompts us to increase our food intake, or if we’re satisfied, decrease it. It also helps control our metabolism. The hypothalamus responds to signals sent from parts of the body including our fat cells and guts — signals like leptin, an important hormone that Leibel helped discover, which increases when body fat rises, telling our brains to stop eating.

A small number of children with severe obesity are born with leptin deficiency, a gene mutation identified by Sadaf Farooqi, a professor at the University of Cambridge’s Institute of Metabolic Science. Their appetites seem to be bottomless. Though it’s rare, Farooqi cites the extreme effect of this mutation as a clear illustration of the “very strong” impact that biology has upon appetite. When Farooqi treated children with this deficiency by injecting them with leptin, they reduced their consumption; too much leptin made them stop eating entirely. “We can literally control how much they’re eating by the dose of leptin we’re giving them,” she says. In other words, appetite is not entirely within our conscious control or willpower. Ghrelin, a hunger hormone, increases when food intake is restricted, making us eat more. Insulin, another important hormone, helps turn the food we eat into energy and controls things like blood sugar that influence how much we eat.