Food and Behaviour Research

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What if sugar is worse than just empty calories? An essay by Gary Taubes

Taubes, G. (2018) BMJ 360 j5808. doi: 10.1136/bmj.j5808. 

Web URL: View this and related research articles via PubMed here


Doctors have long suspected sugar is not simply a source of excess calories but a fundamental cause of obesity and type 2 diabetes. 

Gary Taubes argues we must do more to discourage consumption while we improve our understanding of sugar’s role.

The following is only a brief extract from this article, but in it, the author highlights the reasons why most medical and public health authorities failed to spot that there might be a causal link between excessive sugar consumption and the epidemics of obesity, Type 2 diabetes and related conditions.

Why was sugar missed?

To propose sucrose as a major cause of the epidemics of obesity and diabetes requires an explanation for why mainstream medical and nutrition authorities have only recently come to consider the possibility seriously. This becomes clear with the benefit of hindsight.

After Emerson and Larimore suggested sugar as the prime suspect in 1924, the hypothesis was rejected in the US by Joslin himself, whose textbook The Treatment of Diabetes Mellitus was becoming the bible in the discipline, and in the UK by Harold Himsworth, the future director of the Medical Research Council.

As a young physician in his 20s, Himsworth initially argued that sugar was healthy for people with type 2 diabetes because it “must be given” to treat diabetic coma, and that apparently shaped his thinking.6 He then decided that dietary fat was the cause of diabetes, based largely on two observations: his patients with diabetes reported consuming relatively fatty diets, while people in Japan tended to consume very low fat diets and had very low rates of diabetes.14

Joslin was swayed by Himsworth’s observations as well as the Japanese experience, assuming incorrectly that all carbohydrates are alike in how they are metabolised—whether from rice or sugar. So a population that ate a carbohydrate rich diet and had low rates of diabetes provided compelling reason to believe, so Joslin argued, that sugar was not a cause.15 (Neither Joslin nor Himsworth apparently considered the fact that the Japanese diet also contained relatively little sugar.)

With such influential authorities arguing that sugar was benign, it took on the aura of undisputed truth. Just as other physicians and nutritionists in the 1960s, led by the British researchers Peter Cleave and John Yudkin,16 began to suggest that sugar was indeed a likely cause of obesity, diabetes, and now heart disease as well, diabetes specialists would assume that the possibility was unworthy of their attention. This attitude was reinforced by the growing conviction among these authorities that heart disease could be adequately explained by the saturated fat content of diet, leaving no role for sugar. The two hypotheses were widely considered mutually exclusive.17

This in turn gave the sugar industry the ammunition to defend its product. Beginning in the mid-1960s, the industry engaged in a successful public health campaign based on hiring influential researchers, most prominently Fred Stare, the founding director of the nutrition department at the Harvard School of Public Health, to write articles and authoritative reports disseminating their belief that dietary fat was the primary evil in American diets and that sugar was indeed benign.18

By 1980, dietary guidelines from the US Department of Agriculture were advising consumers simply to “avoid too much sugar”—a statement that could be said about any food. By 1985 the guidelines stated dogmatically that “too much sugar in your diet does not cause diabetes.” A subsequent series of authoritative US and UK government reports institutionalised the hypothesis that dietary fat and serum cholesterol were the agents of heart disease, and that we should worry about the fat content of our diets and not the carbohydrates—sugar or otherwise. Evolving science on insulin resistance and metabolic syndrome that implicated the sugar content of diet remained on the fringes of nutrition discussions.


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