Bariatric surgery at age 16
As soon as the recommendations were announced, they were fiercely criticized for their screening and treatment methods, especially drugs like semaglutide and the surgery Alexandra chose. Critics have argued that these approaches are far too aggressive and subject children’s bodies to unnecessary exploration and manipulation, potentially distorting the way they see themselves, and that treatments can lead to eating disorders that cause more damage than obesity itself. Some critics disputed BMI – a controversial measurement – and argued that doctors should not diagnose obesity in children at all. But, Hampl emphasizes, “the decision about treatment is really in the hands of the families,” and not in the hands of the doctors.
In June, Alexandra waited in the pre-operative room, holding her white stuffed puppy with floppy ears and her red blanket with gray hedgehogs. She was nervous, but “not as nervous as her,” she said, pointing to her mother. Gabriela nodded and said, “I think I’m thinking too much.” Alexandra’s father sat quietly next to her as she tried to keep busy by drawing in her sketchbook, eventually burying her face in her hug.
The tenacity of body weight can be traced back to our biology. Humans have evolved to resist losing body fat so we don’t go extinct, says Rudolph Leibel, chief of the division of pediatric molecular genetics at Columbia University Medical Center. Scientists are still trying to unravel that evolutionary process. According to the “thrifty gene” hypothesis, which has been around for more than half a century, we gain weight (and continue to gain weight) 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 became less dependent on escaping predators, random gene mutations caused our maximum weight limits to increase. Today, our brains may regulate our body weight to keep it within a range between the upper and lower thresholds – while perhaps fighting harder to keep us above the lower threshold. After all, starvation is a more immediate danger than obesity. “You can’t get someone to chronically defend lower body fat levels by chronically restricting their calories,” says Leibel. But, he adds, that level can be pushed up “thanks to the environment.”
Our brains “subconsciously defend that higher weight,” said Stephan Guyenet, a neurobiologist and author of “The Hungry Brain,” and they are even able to slow our metabolism to do so. The hypothalamus, located deep in our brain, is the master of this tightly regulated system. Cone-shaped and no bigger than an almond. It is involved in determining whether we are hungry and therefore encourages us to increase our food intake, or if we are 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 intestines – signals such as leptin, an important hormone that Leibel helped discover, which increases when body fat levels rise and tells our brains to stop eating.
A small number of children with severe obesity are born with a leptin deficiency, a gene mutation identified by Sadaf Farooqi, a professor at the University of Cambridge’s Institute of Metabolic Science. Their appetite seems bottomless. Although rare, Farooqi cites the extreme effect of this mutation as a clear illustration of the “very strong” impact biology has on appetite. When Farooqi treated children with this deficiency by injecting them with leptin, they reduced their consumption; too much leptin caused them to stop eating altogether. “We can literally control how much they eat by the dose of leptin we give 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, causing us to eat more. Insulin, another important hormone, helps convert the food we eat into energy and regulates things like blood sugar levels that affect how much we eat.