"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.
From the full article as well:
"Altogether, epidemiological studies at this stage provide an incomplete, sometimes discordant appraisal of the relationship between fructose or sugar intake and metabolic/cardiovascular diseases. Part of the discordances may be explained by the fact that intakes of sugar, fructose, fruit juices, or sweetened beverages were often not recorded individually, which precludes an accurate calculation of total fructose intake. In addition, fructose is essentially consumed as either sucrose or HFCS, with the consequence that glucose intakes essentially varies with fructose intake. Confounding factors (i.e., interrelationship between sugar intake and intake of other nutrients, association with physical activity and life-style) are important and difficult to control for. At present, there appears to be strong evidence that consumption of sweetened beverages is associated with obesity, at least in children and adolescents. There is at present not the single hint the HFCS may have more deleterious effect on body weight than other sources of sugar. Regarding the relationship between fructose or sucrose intake and cardiovascular risk factors or type 2 diabetes, the evidence is even sparser. Given the number of confounding variables, there is clearly a need for intervention studies in which the fructose intake of high fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term intervention studies however suggest that a high-fructose intake consisting of soft drinks, sweetened juices, or bakery products can increase the risk of metabolic and cardiovascular diseases. There is, however, no objective ground to support that moderate intake of fructose, or of fructose consumed with fruits or honey, is unsafe."
I can see why you didn't want to print the whole abstract. There's enough indirect evidence.
You dishonor yourself with such snidery. Goodbye, Sir.