Eating Fructose is Far Worse than Eating Fat
However, the physiological problems of fructose metabolism extend well beyond a couple of pant sizes:
- Fructose elevates uric acid, which decreases nitric oxide, raises angiotensin, and causes your smooth muscle cells to contract, thereby raising your blood pressure and potentially damaging your kidneys.
Increased uric acid also leads to chronic, low-level inflammation, which has far-reaching consequences for your health. For example, chronically inflamed blood vessels lead to heart attacks and strokes; also, a good deal of evidence exists that some cancers are caused by chronic inflammation. (See the next section for more about uric acid.)
- Fructose tricks your body into gaining weight by fooling your metabolism—it turns off your body’s appetite-control system. Fructose does not appropriately stimulate insulin, which in turn does not suppress ghrelin (the “hunger hormone”) and doesn’t stimulate leptin (the “satiety hormone”), which together result in your eating more and developing insulin resistance. 
- Fructose rapidly leads to weight gain and abdominal obesity (“beer belly”), decreased HDL, increased LDL, elevated triglycerides, elevated blood sugar, and high blood pressure—i.e., classic metabolic syndrome.
- Fructose metabolism is very similar to ethanol metabolism, which has a multitude of toxic effects, including NAFLD (non-alcoholic fatty liver disease). It’s alcohol without the buzz.
These changes are not seen when humans or animals eat starch (or glucose), suggesting that fructose is a “bad carbohydrate” when consumed in excess of 25 grams per day. It is probably the one factor responsible for the partial success of many “low-carb” diets.
One of the more recent findings that surprised researchers is that glucose actually accelerates fructose absorption, making the potential health risks from HFCS even more profound.
You can now see why fructose is the number one contributing factor to the current obesity epidemic.