Excess fructose consumption has been hypothesized to be a cause of insulin resistance, obesity, elevated LDL cholesterol and triglycerides, leading to metabolic syndrome. Fructose consumption has been shown to be correlated with obesity, especially central obesity which is thought to be the most dangerous kind of obesity. A study in mice showed that a high fructose intake increases adiposity.
Although all simple sugars have nearly identical chemical formulae, each has distinct chemical properties.
One study concluded that fructose "produced significantly higher fasting plasma triacylglycerol values than did the glucose diet in men..."
Fructose is a reducing sugar, as are all monosaccharides. The spontaneous chemical reaction of simple sugar molecules binding to proteins, known as glycation, is thought to be a significant cause of damage in diabetics. Fructose appears to be equivalent to glucose in this regard and so does not seem to be a better answer for diabetes for this reason alone, save for the smaller quantities required to achieve equivalent sweetness in some foods. This may be an important contribution to senescence (aging) and many age-related chronic diseases.
"The medical profession thinks fructose is better for diabetics than sugar," says Meira Field, PhD, a research chemist at United States Department of Agriculture, "but every cell in the body can metabolize glucose. However, all fructose must be metabolized in the liver. The livers of the rats on the high fructose diet looked like the livers of alcoholics, plugged with fat and cirrhotic." Fructose is almost entirely metabolized in the liver.
Excessive fructose consumption is also believed to contribute to the development of non-alcoholic fatty liver disease.
It has been suggested in a recent British Medical Journal study that high consumption of fructose is linked to gout. Cases of gout have risen in recent years, despite commonly being thought of as a Victorian disease, and it is suspected that the fructose found in soft drinks (e.g., carbonated beverages) and other sweetened drinks is the reason for this.
In order for the liver to process fructose, it must be phosphorylated by removal of phosphates from adenosine triphosphate (ATP). The ATP gets converted toadenosine monophosphate (AMP), then to inositol monophosphate (IMP), and finally to uric acid, the agent in gout.
Got that? Fructose, bad, for weight loss. What is not pointed out that fructose is metabolized in the liver to it's storage form, fat, visceral fat. Visceral fat comes out of storage about 1.3 to 1.5 time faster than sub-epidermal fat, gram for gram. That may also be the reason the last fat is the most difficult to lose. Fat and glucose puts on sub-epidermal.
But if we burn everything we eat each day, it does not matter so much. The objective of diet should be to never overflow the liver's storage. This is great in theory, but we still need to be able to do that. Therein lies the cravings that drive me to the food. Those are the part that I must address.