The Rise in Sugar Consumption in the U.S. – and the Obesity Equation
For years, sweets were marketed as innocuous treats for kids whose only drawback was cavities if you did not brush your teeth properly. A more nefarious role was alluded to much earlier: in the early 1900s, a British physician stationed in India, Sir Richard Havelock, pointed the finger to sugar as a possible factor in a remarkable rise of diabetes mellitus in the wealthy Indian population, but not in the poorer one. Likewise, in the early 1920s the New York City Public Health commissioner became concerned by a tenfold increase in diabetes - a lethal condition at that time - and found a strong linkage to sugar.1
By the 1950s, two competing theories were focusing on suspected causes for coronary heart disease (CHD), for which diabetes is a strong risk factor. The “fat theory” claimed fat and cholesterol as the main culprits, while the “sugar theory” pointed to sugar.
Anyone who has tracked with medical science through the centuries realizes that progress is not often clearly linear. Competing theories duke it out and eventually a winner emerges, sometimes to be challenged itself later as new discoveries are made again. Directed funding of a theory and systematic discrediting of the competing theory can throw a significant wrench in this process. We have seen this pattern for tobacco and lead - and sugar, too.
A recently published historical analysis revealed the agenda of the Sugar Research Foundation in the U.S. during the 1960s and 1970s, which was to feature the role of fat as a risk factor in CHD and downplay evidence that sucrose was a risk factor. This was in concert with systematic attacks on the theory of sugar as a dietary cause of CHD.2 The Foundation directly funded research and reviews in respected scientific journals to support those efforts. Furthermore, the U.S. sugar industry maintained that a lower fat intake meant there were “lost” calories, and those lost calories could be easily, tastily and “safely” replaced by an increased caloric intake of sugar. The intended business consequence for the sugar industry? More sugar sales!
We have since learned from these and similar findings. Medical journals are now much more aware of the importance of disclosing the sources of funding for the research studies they publish and any conflicts of interest with the researchers.
Obesity, too, has a strong risk factor for CHD. On the surface it seems easy to understand how obesity is related to CHD: too many calories in, not enough calories out. However, anyone who has tried dieting knows it is not as simple as that. Isolating the factors causing obesity is challenging. For example, excessive TV watching has been linked to obesity. But does excessive TV watching promote lower physical activity and result in lower calorie use, or do obese people just get fatigued more easily? Some evidence suggests the latter.3 The fuller answer lies in a complex relationship between obesity, satiety deficiency and chemical reward that is only now being slowly unraveled.
Sugar is a key molecular element in that equation. The two basic building blocks for sugar are glucose and fructose. Table sugar (sucrose) is made up of one molecule of glucose and one of fructose. A common substitute for sugar in the U.S. is high fructose corn syrup (HFCS), generally composed of 42% fructose and 50%-52% glucose. In the scientific arena, we are seeing an intense fight right now concerning whether or not HFCS is worse than table sugar. I will not open this can of worms here, but I can say that it is known that fructose does not behave in the body like glucose, especially in the insulin release and satiety pathways. Interesting developments on this front will come, again changing the course for future medical theories. Stay tuned for my next blog, “Sugar and Fat – and Diet Research,” highlighting recent diet studies and the challenging search for the “perfect diet.”
- R.J. Johnson et al., Advances in Nutrition, 2017 May 05.
- C.E. Kearns, et al., JAMA Intern Med., 2016 Nov 1.
- Ibid, at Note 1.