SAN FRANCISCO - Two seemingly benign nutritional maxims are at the root of all dietary evil: A calorie is a calorie, and You are what you eat. Both ideas are now so entrenched in public consciousness that they have become virtually unassailable. As a result, the food industry, aided and abetted by ostensibly well-meaning scientists and politicians, has afflicted humankind with the plague of chronic metabolic disease, which threatens to bankrupt health care worldwide.
The United States currently spends US$147 billion on obesity-related health care annually. Previously, one could have argued that these were affluent countries' diseases, but the United Nations announced last year that chronic metabolic disease (including diabetes, heart disease, cancer, and dementia) is a bigger threat to the developing world than is infectious disease, including HIV.
These two nutritional maxims give credence to the food industry's self-serving corollaries: If a calorie is a calorie, then any food can be part of a balanced diet; and, if we are what we eat, then everyone chooses what they eat. Again, both are misleading.
If one's weight really is a matter of personal responsibility, how can we explain toddler obesity? Indeed, the US has an obesity epidemic in six-month-olds. They don't diet or exercise. Conversely, up to 40 per cent of normal-weight people have chronic metabolic disease. Something else is going on.
Consider the following diets: Atkins (all fat and no carbohydrates); traditional Japanese (all carbohydrates and little fat); and Ornish (even less fat and carbohydrates with lots of fiber). All three help to maintain, and in some cases even improve, metabolic health, because the liver has to deal with only one energy source at a time.
That is how human bodies are designed to metabolise food. Our hunter ancestors ate fat, which was transported to the liver and broken down by the lipolytic pathway to deliver fatty acids to the mitochondria (the subcellular structures that burn food to create energy). On the occasion of a big kill, any excess dietary fatty acids were packaged into low-density lipoproteins and transported out of the liver to be stored in peripheral fat tissue. As a result, our forebears' livers stayed healthy.
Meanwhile, our gatherer ancestors ate carbohydrates (polymers of glucose), which was also transported to the liver, via the glycolytic pathway, and broken down for energy. Any excess glucose stimulated the pancreas to release insulin, which transported glucose into peripheral fat tissue, and which also caused the liver to store glucose as glycogen (liver starch). So their livers also stayed healthy.
And nature did its part by supplying all naturally occurring foodstuffs with either fat or carbohydrate as the energy source, not both. Even fatty fruits - coconut, olives, avocados - are low in carbohydrate.
Our metabolisms started to malfunction when humans began consuming fat and carbohydrates at the same meal. The liver mitochondria could not keep up with the energy onslaught, and had no choice but to employ a little-used escape valve called 'de novo lipogenesis' (new fat-making) to turn excess energy substrate into liver fat.
Liver fat mucks up the workings of the liver. It is the root cause of the phenomenon known as 'insulin resistance' and the primary process that drives chronic metabolic disease. In other words, neither fat nor carbohydrates are problematic - until they are combined. The food industry does precisely that, mixing more of both into the Western diet for palatability and shelf life, thereby intensifying insulin resistance and chronic metabolic disease.
But there is one exception to this formulation: sugar. Sucrose and high-fructose corn syrup are comprised of one molecule of glucose (not especially sweet) and one molecule of fructose (very sweet). While glucose is metabolised by the glycolytic pathway, fructose is metabolised by the lipolytic pathway, and is not insulin-regulated. Thus, when sugar is ingested in excess, the liver mitochondria are so overwhelmed that they have no choice but to build liver fat. Today, 33 per cent of Americans have a fatty liver, which causes chronic metabolic disease.
Prior to 1900, Americans consumed less than 30 grams of sugar per day, or about 6 per cent of total calories. In 1977, it was 75 grams/day, and in 1994, up to 110 grams/day. Currently, adolescents average 150 grams/day (roughly 30 per cent of total calories) - a five-fold increase in one century, and a two-fold increase in a generation. In the past 50 years, consumption of sugar has also doubled worldwide. Worse yet, other than the ephemeral pleasure that it provides, there is not a single biochemical process that requires dietary fructose; it is a vestigial nutrient, left over from the evolutionary differentiation between plants and animals.
It is therefore clear that a calorie is not a calorie. Fats, carbohydrates, fructose, and glucose are all metabolised differently in the body. Furthermore, you are what you do with what you eat. Combining fat and carbohydrate places high demands on the metabolic process. And adding sugar is particularly egregious.
Indeed, while food companies would have you believe that sugar can be part of a balanced diet, the bottom line is that they have created an unbalanced one. Of the 600,000 food items available in the US, 80 per cent are laced with added sugar. People cannot be held responsible for what they put in their mouths when their choices have been co-opted.
And this brings us back to those obese toddlers. The fructose content of a soft drink is 5.3 per cent. Of course, many parents might refuse to give soft drinks to their children, but the fructose content of soy formula is 5.1 per cent, and 6 per cent for juice.
We have a long way to go to debunk dangerous nutritional dogmas. Until we do, we will make little headway in reversing an imminent medical and economic disaster.
Robert Lustig is Professor of Pediatrics in the Division of Endocrinology, Director of the Weight Assessment for Teen and Child Health Program, and a member of the Institute for Health Policy Studies at the University of California, San Francisco.