ALARMED BY THE stunning rise of obesity and type 2 diabetes in school-aged children, hundreds of millions of dollars were deployed to counterattack. The first choice in our arsenal was the beloved Eat Less, Move More approach, which sported a perfect record unblemished by success. Nevertheless, as nutritional authorities scrambled to do battle, only one diet plan got the call. The U.S. National Institutes of Health funded the HEALTHY study, a large three-year effort1 involving forty-two schools in grades six to eight. Half of the schools would receive a multicomponent intervention, while the other half continued their usual routines. The study encouraged certain nutritional and exercise goals, including
Our old friend—Eat Less, Move More. Not too bright, but as familiar as an old blanket. There were classroom-based programs, newsletters for parents, social marketing (branding, posters, in-school announcements), student events and incentives (T-shirts, water bottles). Both groups began with roughly 50 percent of the students considered overweight or obese. By the end of three years, the Eat Less Move More group brought that down to 45 percent. Success! The group that followed their usual habits finished at... 45 percent. There was no measurable benefit for the diet and exercise group. This weight-loss strategy was virtually useless.
But who hasn’t tried the Eat Less, Move More approach and failed? The HEALTHY study was only the latest in an unbroken string of failures.
OBESITY: NO LONGER JUST FOR ADULTS
DURING THE YEARS 1977 to 2000, the prevalence of childhood obesity skyrocketed in every age category. Obesity in children aged six to eleven increased from 7 percent to 15.3 percent. For children aged twelve to nineteen, it more than tripled, from 5 percent to 15.5 percent. Obesity-related diseases such as type 2 diabetes and high blood pressure, previously rare in children, are becoming more common. Obesity has metastasized from being solely an adult concern to being a pediatric one too.
Childhood obesity also leads to adult obesity and future health problems, particularly cardiovascular issues.2 The Bogalusa Heart Study3 concluded, “childhood obesity tracked into young adulthood,” which is obvious to almost everybody. Childhood obesity is a predictor of increased mortality,4 but is, most importantly, a reversible risk factor. Overweight children who became normal weight as adults have the same mortality risk as those who have never been overweight.5
Obesity has begun to afflict younger and younger children. In one study covering a twenty-two-year period ending in 2001, children of all ages show an increased prevalence of obesity, even in the zero- to six-month-old age range.6
That finding is especially interesting. Conventional calorie-based theories of obesity are unable to explain this trend. Obesity is considered an energy- balance problem, one of eating too much or exercising too little. Since six- month-olds eat on demand and are often breastfed, it is impossible that they eat too much. Since six-month-olds do not walk, it is impossible that they exercise too little. Similarly, birth weight has increased by as much as half a pound (200 grams) over the last twenty-five years.7 The newborn cannot eat too much or exercise too little. What is going on here?
Numerous hypotheses have been offered to explain newborn obesity. One popular theory suggests that certain chemicals (obesogens) in our modern environment lead to obesity, chemicals that are often endocrine disruptors. (That is, they disrupt the normal functional hormonal systems of the body.) Since obesity is a hormonal rather than a caloric imbalance, this notion does make some intuitive sense. Nonetheless, the majority of the data comes from animal studies.
For example, the pesticides atrazine and DDE may cause obesity in rodents.8 However, no data is available for humans. Without such data, it is difficult to conclusively determine whether a chemical is an obesogen or not. Furthermore, studies use concentrations of chemicals that are hundreds or even thousands of times greater than normal human exposure. While these chemicals are almost certainly toxic, it is difficult to know how it applies to the common human condition of obesity.
IT’S INSULIN
THE ANSWER IS simpler once we understand hormonal obesity theory. Insulin is the major hormonal driver of weight gain. Insulin causes adult obesity.
Insulin causes newborn obesity. Insulin causes infant obesity. Insulin causes childhood obesity. Where would an infant get high insulin levels? From his or her mother.
Dr. David Ludwig recently examined the relationship between the weights of 513,501 women and their 1,164,750 offspring.9 Increased maternal weight gain is strongly associated with increased neonatal weight gain. Because both the mother and the fetus share the same blood supply, any hormonal imbalances, such as high insulin levels, are automatically and directly transmitted through the placenta from the mother to the growing fetus.
Fetal macrosomia is a term used for fetuses that are large for their gestational age. There are a number of risk factors, but chief among them are maternal gestational diabetes, maternal obesity and maternal weight gain. What do these conditions all have in common? High maternal levels of insulin. The high levels transmit to the developing fetus, resulting in one that is too large.
The logical consequence of too much insulin in the newborn is the development of insulin resistance, which leads to even higher levels of insulin in a classic vicious cycle. The high insulin levels produce obesity in the newborn as well as the six-month-old infant. The origins of both infant obesity and adult obesity are the same: insulin. These are not two separate diseases, but two sides of the same coin. Babies born to mothers with gestational diabetes mellitus have three times the risk of obesity and diabetes in later life, and one of the biggest risk factors for obesity in young adulthood is obesity in childhood.10 Those who are obese in childhood have more than seventeen times the risk of obesity going into adulthood! Even large-for- gestational-age babies whose mothers do not have gestational diabetes are also at risk. They have double the risk of metabolic syndrome.
The sad but inescapable conclusion is that we are now passing on our obesity to our children. Why? Because we are now marinating our children in insulin starting in the womb, they develop more severe obesity sooner than ever before. Because obesity is time dependent and gets worse, fat babies become fat children. Fat children become fat adults. And fat adults have fat babies in turn, passing obesity on to the next generation.
What has really hampered our ability to combat childhood obesity, though, is a simple lack of understanding about the true causes of weight gain. A singular misguided focus on reducing caloric intake and increasing exercise led to government programs that have almost no chance of success. We didn’t lack resources or willpower; we lacked knowledge of and a framework for understanding obesity.
SAME METHODS, SAME FAILURES
SEVERAL LARGE-SCALE STUDIES on prevention of childhood obesity were started in the late 1990s. The National Heart, Lung, and Blood Institute undertook the Pathways study11 at a cost of $20 million over eight years. Dr. Benjamin Caballero, director of the Center for Human Nutrition at the Johns Hopkins Bloomberg School of Public Health, led this ambitious effort involving 1704 children in forty-one schools. Some schools received the special obesity-prevention program while other schools continued their standard program.
Low-income, native American children at risk for obesity and diabetes received both breakfast and lunch at the school cafeteria, where “healthy” food lessons were immediately reinforced. Special exercise breaks were introduced in the middle of the school day. The specific nutritional goal was to reduce dietary fat to less than 30 percent. In a nutshell, this was the same low-fat, low-calorie diet combined with increased exercise that had failed so miserably as a remedy for adult obesity.
Did the children learn how to eat a low-fat diet? Sure did. Dietary fat started at 34 percent of calories and over the course of the study, fell to 27 percent. Did they eat fewer calories? Sure did. The intervention group averaged 1892 calories per day compared to 2157 calories per day in the control group. Fantastic! The children were eating 265 fewer calories per day. They learned their lessons extremely well, eating fewer calories and less fat overall. Over the course of three years, calorie counters expected a loss of approximately 83 pounds! But did the children’s weight actually change? Not even by a little bit.
Physical activity was no different between the two groups. Despite the increased physical education done in the schools, the total physical activity measured by accelerometer was not different—which should have been expected, given the known effect of compensation. Those children who were very active in school reduced their activity at home. Children relatively sedentary at school increased their activity once out of school.
This study was vitally important. The failure of the low-fat, low-calorie strategy should have prompted a search for more effective methods of controlling the scourge of childhood obesity. It should have prompted soul searching for the underlying cause of obesity and how to rationally treat it. So what happened?
The results were tabulated. The study was written. It was published in 2003 to thunderous... silence. Nobody wanted to hear the truth. The Eat Less, Move More approach, so adored by academic medicine, had failed yet again. It was easier to ignore the truth than to face it. And that’s what happened.
Other studies confirmed these results. Dr. Philip Nader from the University of California San Diego randomized 5106 grade three to grade five students to education with “healthy” food and increased exercise.12 Fifty-six schools received the special program, and forty schools (the control group) did not.
Once again, children receiving the extra indoctrination ate a lower-fat diet and retained this knowledge for years afterward. It was “the largest school- based randomized trial ever condu