This isn't junk science like anthropogenic global warming.Actually it is, just not as politically useful.....yet. There are as many studies one way as the other but the evidence in humans, as opposed to the lab rats upon which most of the doom and gloom studies are based, doesn't support the thesis that HFCS is any worse than sucrose. It's the overconsumption of either that is a problem.
Metabolic effects of fructose and the worldwide increase in obesity.
Physiol Rev. 2010 Jan;90(1):23-46.
"There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption."
Just one of many.
"While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C(6)H(12)O(6)), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption."
I can see why you didn't want to print the whole abstract. There's enough indirect evidence.
Thanks for the link which linked the original article. Here's the conclusion:
VI. Perspectives The potential danger of fructose consumption and its links to various metabolic disorders have been widely documented. Deleterious effects of high fructose intake on body weight, insulin sensitivity/glucose homeostasis, dyslipidemia, and atherosclerotic disease have been identified, and potential mechanisms have been proposed (Fig. 7). These effects, in humans, were often documented at very high levels of fructose intake, however, and some important questions remain to be addressed. Among the numerous deleterious effects of fructose, which ones are directly relevant for human daily nutrition? Most human studies addressing specifically the effects of fructose have administered large doses, often as a supplementation to an isocaloric diet. Nevertheless, there is solid evidence that fructose, even at moderate doses, can cause hypertriglyceridemia. Moreover, although data are scarcer, the fact that fructose may increase intrahepatic lipids and lead to insulin resistance in experimental settings raises some concern. Studies aimed at delineating the dose threshold at which fructose starts to chronically exert such effects remain to be performed. In addition to that, in everyday life, fructose cannot be blamed as the only culprit for all metabolic disorders. Indeed, a high fructose consumption most of the time clusters with additional “risky” behaviors, such as a hypercaloric diet, a diet rich in saturated fat, or low physical activity. Thus which part of metabolic disorders can be attributed to fructose and which results from interactions with other risk factors? Long-term intervention and longitudinal studies may help bring some clues to these issues.
Fig. 7. Potential relationships of high fructose intake with human diseases.
Isocaloric diets mean that the experimental group with more fructose got the same number of calories as the control group.
It's not just an increase in type 2 diabetes over time. This latest study finds about 20 % more in countries that allow HFCS versus no HFCS. Now there are two more diagnoses since HFCS cama on the scene: maturity onset diabetes of the young, MODY, and non-alcoholic fatty liver disease, NAFLD.