Gary Taubes says the “case against sugar isn’t so easily dismissed”:
My concern in my essay and my books is a simple and regrettable fact: the epidemics worldwide of obesity and diabetes that occur whenever populations pass through a nutrition transition from a traditional diet and lifestyle, whatever that may be, to a western one. Something is causing that, and because obesity and diabetes, particularly type 2, are intimately linked to insulin resistance, we should be looking ultimately and desperately for the cause of insulin resistance. Geneticists would say we’re looking for the environmental trigger that reliably and often dramatically increases the prevalence of the obese and diabetic phenotype, regardless of the underlying human genotype. And because insulin resistance, obesity, and diabetes are all intimately linked to heart disease, that trigger is almost assuredly going to be a cause of coronary heart disease as well.
But in this country, nutrition and chronic disease research from the 1950s onward was obsessively focused on a very different question: the dietary cause of heart disease in the United States and Europe. When the researchers decided on the basis of exceedingly premature evidence that dietary fat was the culprit, that drove all public health debates and thinking ever after. Even hypotheses about the cause of obesity and diabetes had to be reconcilable with the belief that saturated fat caused heart disease. As such, the evidence implicating insulin resistance in the disorder (and so the carbohydrate content of the diet) was delayed by 30 years in its acceptance, as I discussed in Good Calories, Bad Calories. Its implications are still not accepted because they clash with what remains of the dogmatic belief that saturated fat causes heart disease. And this all happened because researchers were asking the wrong question (and they got the wrong answer even to that): “why CHD in America now,” rather than “why obesity, diabetes, and insulin resistance in populations worldwide whenever they westernize?”
Now that we’re almost literally neck deep in obesity and diabetes, the right question is vitally important to answer. If the sugar hypothesis is wrong, it is critically important that it be refuted definitively. That can only happen on the strength of far, far stronger evidence than Dr. Guyenet provides in his somewhat flip and casual response. And if the sugar hypothesis is unambiguously refuted, whatever hypothesis steps up as the next prime suspect has to be very carefully considered. (i.e., not the simplistic notion that people eat too much and move too little). We need a hypothesis that holds the promise of explaining the epidemics everywhere.
In stopping an epidemic, nothing is more important than correctly identifying its cause. Where we are today with obesity and diabetes reminds me of where infectious disease specialists were through most of the 19th century, when they blamed malaria and other insect-born diseases on miasma, or the bad air that came out of swamps. That was mildly effective, in that it was an explanation for why the rich in any particular town preferred to build their homes on hills, high above the miasma and, incidentally, away from the swamps and lowlands and slums where the vectors of these diseases were breeding. But only by identifying the vectors and the actual disease agents do we help everyone avoid them and eradicate the diseases. Only by unambiguously identifying the cause can we effectively design treatments to cure it. The kinds of explanations that Dr. Guyenet and Freedhoff put forth – highly palatable foods or ultra-processed foods – are the nutritional equivalents of the miasma explanation. They sound good; they might help some people incidentally eat the correct diets or offer a description of why other people already do, but they’re not the proximate cause of these epidemics. And there is a proximate cause. We have to find it. I can guarantee it’s not saturated fat, regardless of the effect of that nutrient on heart disease risk. What is it?