The Obesity Code. Jason Fung
made a stunning transformation. While the guidelines still recognized the evils of sugar, refined grain was as innocent as a nun in a convent. Its nutritional sins were exonerated, and it was henceforth reborn and baptized as the healthy whole grain.
Was there any evidence? It hardly mattered. The goals were now the nutritional orthodoxy. Everything else was heathen. If you didn’t toe the line, you were ridiculed. The Dietary Guidelines for Americans, a report released in 1980 for widespread public consumption, followed the recommendations of the McGovern report closely. The nutritional landscape of the world was forever changed.
The Dietary Guidelines for Americans, now updated every five years, spawned the infamous food pyramid in all its counterfactual glory. The foods that formed the base of the pyramid—the foods we should eat every single day—were breads, pastas and potatoes. These were the precise foods that we had previously avoided to stay thin. For example, the American Heart Association’s 1995 pamphlet, The American Heart Association Diet: An Eating Plan for Healthy Americans, declared we should eat six or more servings of “breads, cereals, pasta and starchy vegetables (that) are low in fat and cholesterol.” To drink, “Choose . . . fruit punches, carbonated soft drinks.” Ahhh. White bread and carbonated soft drinks—the dinner of champions. Thank you, American Heart Association (AHA).
Entering this brave new world, Americans tried to comply with the nutritional authorities of the day and made a conscious effort to eat less fat, less red meat, fewer eggs and more carbohydrates. When doctors advised people to stop smoking, rates dropped from 33 percent in 1979 to 25 percent by 1994. When doctors said to control blood pressure and cholesterol, there was a 40 percent decline in high blood pressure and a 28 percent decline in high cholesterol. When the AHA told us to eat more bread and drink more juice, we ate more bread and drank more juice.
Inevitably, sugar consumption increased. From 1820 to 1920, new sugar plantations in the Caribbean and American South increased the availability of sugar in the U.S. Sugar intake plateaued from 1920 to 1977. Even though “avoid too much sugar” was an explicit goal of the 1977 Dietary Guidelines for Americans, consumption increased anyway until the year 2000. With all our attention focused on fat, we took our eyes off the ball. Everything was “low fat” or “low cholesterol,” and nobody was paying attention to sugar. Food processors, figuring this out, increased the added sugars in processed food for flavor.
Refined grain consumption increased by almost 45 percent. Since carbohydrates in North America tended to be refined, we ate more and more low-fat bread and pasta, not cauliflower and kale.11
Success! From 1976 to 1996, the average fat intake decreased from 45 percent of calories to 35 percent. Butter consumption decreased 38 percent. Animal protein decreased 13 percent. Egg consumption decreased 18 percent. Grains and sugars increased.
Until that point, the widespread adoption of the low-fat diet was completely untested. We had no idea what effect it would have on human health. But we had the fatal conceit that we were somehow smarter than 200,000 years of Mother Nature. So, turning away from the natural fats, we embraced refined low-fat carbohydrates such as bread and pasta. Ironically, the American Heart Association, even as late as the year 2000, felt that low-carbohydrate diets were dangerous fads, despite the fact that these diets had been in use almost continuously since 1863.
What was the result? The incidence of heart disease certainly did not decrease as expected. But there was definitely a consequence to this dietary manipulation—an unintentional one. Rates of obesity, defined as having a body mass index greater than 30, dramatically increased, starting almost exactly in 1977, as illustrated by Figure 1.2.12
Figure 1.2. Increase in obese and extremely obese United States adults aged 20–74.
The abrupt increase in obesity began exactly with the officially sanctioned move toward a low-fat, high-carbohydrate diet. Was it mere coincidence? Perhaps the fault lay in our genetic makeup instead.
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INHERITING OBESITY
IT IS FAIRLY obvious that obesity runs in families.1 Obese children often have obese siblings. Obese children become obese adults.2 Obese adults go on to have obese children. Childhood obesity is associated with a 200 percent to 400 percent increased risk of adult obesity. This is an undeniable fact. The controversy revolves around whether this trend is a genetic or an environmental problem—the classic nature versus nurture debate.
Families share genetic characteristics that may lead to obesity. However, obesity has become rampant only since the 1970s. Our genes could not have changed within such a short time. Genetics can explain much of the inter-individual risk of obesity, but not why entire populations become obese.
Nonetheless, families live in the same environment, eat similar foods at similar times and have similar attitudes. Families often share cars, live in the same physical space and will be exposed to the same chemicals that may cause obesity—so-called chemical obesogens. For these reasons, many consider the current environment the major cause of obesity.
Conventional calorie-based theories of obesity place the blame squarely on this “toxic” environment that encourages eating and discourages physical exertion. Dietary and lifestyle habits have changed considerably since the 1970s including
•adoption of a low-fat, high-carbohydrate diet,
•increased number of eating opportunities per day,
•more meals eating out,
•more fast-food restaurants,
•more time spent in cars and vehicles,
•increased popularity of videos games,
•increased use of computers,
•increase in dietary sugar,
•increased use of high-fructose corn syrup and
•increased portion sizes.
Any or all of these factors may contribute to the obesogenic environment. Therefore, most modern theories of obesity discount the importance of genetic factors, believing instead that consumption of excess calories leads to obesity. Eating and moving are voluntary behaviors, after all, with little genetic input.
So—exactly how much of a role does genetics play in human obesity?
NATURE VERSUS NURTURE
THE CLASSIC METHOD for determining the relative impact of genetic versus environmental factors is to study adoptive families, thereby removing genetics from the equation. By comparing adoptees to their biological and adoptive parents, the relative contribution of environmental influences can be isolated. Dr. Albert J. Stunkard performed some of the classic genetic studies of obesity.3 Data about biological parents is often incomplete, confidential and not easily accessible by researchers. Fortunately, Denmark has maintained a relatively complete registry of adoptions, with information on both sets of parents.
Studying a sample of 540 Danish adult adoptees, Dr. Stunkard compared them to both their adoptive and biological parents. If environmental factors were most important, then adoptees should resemble their adoptive parents. If genetic factors were most important, the adoptees should resemble their biological parents.
No relationship whatsoever was discovered between the weight of the adoptive parents and the adoptees. Whether adoptive parents were thin or fat made no difference to the eventual weight of the adopted child. The environment provided by the adoptive parents was largely irrelevant.
This finding was a considerable shock. Standard calorie-based theories blame environmental factors and human behaviors for obesity. Environmental cues such as dietary habits, fast food, junk food, candy intake, lack of exercise, number of cars, and lack of