The National Institutes of Health describes the childhood obesity epidemic as “a devastating public health crisis.” In just thirty years, obesity rates in American children in have doubled, reaching 18% as of 2012. An excess of body fat places these children at increased risk of diabetes, cardiovascular disease, and cancer. But how did we get here? A controversial hypothesis published in Mayo Clinic Proceedings has proposed a new way to answer the question—and it doesn’t begin with the usual suspects.
“The greatest lie in public health is ‘We are what we eat,’” says Edward Archer, a postdoctoral researcher at the Nutrition and Obesity Research Center at University of Alabama at Birmingham. Instead, “We are what our body does with what we eat,” which is determined by body composition, he says. “And your body composition was determined by your mom’s physical activity and her body composition.”
This is key to Archer’s “Maternal Resources Hypothesis”: obesity can be programmed from the womb. “The nine months before birth are incredibly important for the health trajectories of the child forever,” Archer says. This process has been impacted by societal changes, he says, such as decreased physical activity since the late twentieth century. When expectant mothers are less physically active, Archer says, more energy is carried to a developing fetus as sugars and fat. This stimulates greater fat cell production in the baby’s body, Archer says, and “Individuals who have a larger fat mass will gain a larger amount of fat mass from the same amount of calories.”
Archer views this process as a competition between cells in the body, which he says is a unique factor of his hypothesis. Cells involved in basic metabolic processes, cells used in physical activity, and fat cells, or “adipocytes,” all use different strategies to compete for the same energy resources. Adipocytes find strength in numbers, Archer says: the more there are, the more they consume. If enough fat cells are present, they can out-compete other cells for energy, perpetuating obesity.
Archer’s hypothesis elicits both intrigue and doubt from obesity experts. While competition between cells is “an interesting concept,” says Dr. Charles Burant, professor of internal medicine at the University of Michigan and director of the Michigan Metabolomics and Obesity Center, he sees metabolism differently. Fat cells are the only place to store excess energy. When adipocytes can’t store any more fat, other tissues are negatively affected, so “you actually want the adipocytes to win most of these competitions.” While Dr. Burant doubts whether or not babies are actually born with higher numbers of fat cells, he says that fat cells tell the brain “how much energy is there.” More fat cells could mean “more signals to the brain to feed those fat cells,” Dr. Burant says. This is what Archer argues: “We literally have more fat cells screaming for energy,” he says.
As for “The intrauterine programming—I’m actually a fan of that,” Dr. Burant says. “Obese mothers probably impart some programming on the fetus.” But he says prenatal programming can be complex, and “even caloric restriction in utero will cause obesity.” And while Archer argues that “environment itself overwhelms any variability” in genetics, Dr. Burant disagrees. “He’s totally wrong about that,” Dr. Burant says. “I think the data is quite solid…There’s a high degree of genetic predisposition for obesity.”
Archer’s rejection of food as a major player in obesity also meets resistance. Dr. Lawrence Cheskin, director of the Johns Hopkins Weight Management Center, says reduced physical activity is part of the problem, but “changes in our typical diet” also play a role. Dr. Burant even argues physical activity “is probably not a large contributor” to the epidemic. The main problem, he says, is “excessive caloric intake.” Food has become far more accessible and palatable, he explains. “You’re giving crack to somebody…And you can’t withdraw from food addiction.”
But everyone seems to agree that environment plays a major role in the epidemic. School and home culture are both important, says Amar Kanekar, assistant professor in the Department of Health, Human Performance, and Sport Management at University of Arkansas at Little Rock. If physical activity early in life can prevent morbid obesity and health risks even in those predisposed towards obesity, as Archer argues, change might need to be significant. Archer and Dr. Cheskin both say schools have decreased physical activity requirements for children, and note that some families may feel unsafe walking or exercising outside in some neighborhoods. Many other factors play a role, says Dr. Cheskin—stress, advertisement of food, serving sizes, and more. Dr. Cheskin says that it will take “a systems-wide analysis” to understand how to intervene in the epidemic. “There’s a million different factors that go into it, which is why it’s extraordinarily difficult to change.”