Good Calories, Bad Calories

This problem is exacerbated in the study of nutrition, obesity, and chronic disease because significant observations emerge from so many diverse disciplines. Indeed, the argument can be made that, to fully understand obesity alone, researchers should have a working familiarity with the literature in clinical treatment of obesity in humans, body-weight regulation in animals, mammalian reproduction, endocrinology, metabolism, anthropology, exercise physiology, and perhaps human psychology, not to mention having a critical understanding and familiarity with the nuances of clinical trials and observational epidemiology. Most researchers and clinicians barely have time to read the journals in their own subspecialty or sub-sub-specialty, let alone the dozens of significant journals that cover the other disciplines involved. This is a primary reason why the relevant science is plagued with misconceptions propagated about some of the most basic notions. Researchers will be suitably scientific and critical when addressing the limitations of their own experiments, and then will cite something as gospel because that’s what they were taught in medical school, however many years earlier, or because they read it in The New England Journal of Medicine. Speculations, assumptions, and erroneous interpretations of the evidence then become truth by virtue of constant repetition. It is my belief that when all the evidence is taken into account, rather than just a prejudicial subset, the picture that emerges will be more revealing of the underlying reality.

One consequence of this sub-specialization of modern medicine is the belief, often cited in the lay press, that the causes of obesity and the common chronic diseases are complex and thus no simple answer can be considered seriously. Individuals involved in treating or studying these ailments will stay abreast of the latest “breakthroughs” in relevant fields—the discovery of allegedly cancer-fighting phytochemicals in fruits and vegetables, of genes that predispose us to obesity or diabetes, of molecules such as leptin and ghrelin that are involved in the signaling of energy supply and demand around the body. They will assume rightfully, perhaps, that the mechanisms of weight regulation and disease are complex, and then make the incorrect assumption that the fundamental causes must also be complex. They lose sight of the observations that must be explained—the prevalence of obesity and chronic disease in modern societies and the relationship between them—and they forget that Occam’s razor applies to this science, just as it does to all sciences: do not invoke a complicated hypothesis to explain the observations, if a simple hypothesis will suffice. By the same token, molecular biologists have identified a multitude of genes and proteins involved in the causation and spread of cancer, and so it could be argued, as well, that cancer is much more complex than we ever imagined. But to say that lung cancer, in over 90 percent of the cases, is caused by anything other than smoking cigarettes is to willfully miss the point. In this case, if refined carbohydrates and sugars are indeed the reasons why we fatten—through their effect on insulin and insulin’s effect on fat accumulation—and if our goal is to prevent or remedy the disorder, the salient question is why any deeper explanation, at the moment, is necessary.