We are close now to a strong agreement that the epidemic of chronic illness is diet related and that sugar and fructose is at the heart of it.
This chart showing sugar consumption is I think the smoking gun for looking at the role of sugar and now fructose in the epidemic of chronic illness.
This article – link here – is complete. It goes into depth on the process by which sugar and then fructose affects us and some people more than others. All who care about their health should read this. All who are in health care should too – for we have to acknowledge that, until now, we must have been wrong. Our failure to make progress is the proof.
Here are the facts about the load:
Sugar consumption continued to increase in the 1900s, with an overall doubling in the United States and the United Kingdom between 1900 and 1967 (34). By 1993, >110 million tons of sugar were produced worldwide (33). Whereas sugar intake continues to be marked in the industrialized nations, it is in the developing countries that the greatest increase in the rates of sugar consumption has been observed (35 ). By the early 1970s, an additional sweetener, high-fructose corn syrup (HFCS), was introduced in the United States, which had certain advantages over table sugar with relation to shelf life and cost. This sweetener, the composition of which is similar to that of sucrose, is used extensively to sweeten soft drinks, fruit punches, pastries, and processed foods. The combination of table sugar and HFCS has resulted in an additional 30% increase in overall sweetener intake over the past 40 y, mostly in soft drinks. Currently, consumption of these sweeteners is almost 150 lb (67.6 kg) per person per year (36), which has resulted in the ingestion of >500 kcal/d (37; Figure 1⇑).
Here they make the connection:
recent history in the United States has shown that, although a low-fat intake has been promoted, rates of obesity have continued to increase as sugar consumption has continued. In addition, recent studies showing that a low-carbohydrate, high-fat diet has no adverse cardiovascular effects (40, 41) suggest that it is time to revisit the causes of the cardiorenal disease epidemic. In 2002, Havel’s group (37) made the case that the fructose content of sugar may be the critical component associated with the risks of obesity and heart disease. Sucrose is a disaccharide consisting of 50% fructose and 50% glucose, and HFCS is also a mixture of free fructose and glucose of approximately the same proportion (55:45).
There are some striking epidemiologic associations between sugar intake and the epidemic of cardiorenal disease. For example, obesity was initially seen primarily in the wealthy, who would have been the only ones able to afford sugar. Also, the first documentation of hypertension, diabetes, and obesity occurred in the very countries (England, France, and Germany) where sugar first became available to the public. The rise in sugar intake in the United Kingdom and the United States (Figure 1⇑) also correlates with the rise in obesity rates observed in these countries. Furthermore, the later introduction of sugar to developing countries also correlates with the later rise in their rates of obesity and heart disease. A series of epidemiologic studies linked the ingestion of soft drinks to obesity, hypertension, and diabetes (42, 43) and the consumption of fruit juice and fruit punch to obesity in children (44, 45). Although these epidemiologic associations suggest a potential causal role, are there any direct experimental data to show that sucrose or fructose can induce obesity or hypertension?
Please invest the time to go further. Link here.