HFCS’s connection to obesity, diabetes and heart disease lies in the way our bodies react to the substance. Unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production, both key processes in appetite regulation and fat storage. Instead, fructose forms the backbone for triacylglycerols. Elevated levels of triacylglycerols prevent leptin from reaching the brain and are linked to an increased risk of heart disease. Why does that matter? Without leptin, the brain doesn’t send out the signal to stop eating. There is no caloric difference between the two sugars, but glucose is readily absorbed and allows the brain to signal that we’ve had enough food.

Simply put, fructose leads our bodies to store more calories as fat, and leads us to overeat because we don’t feel full.

A USDA study that compared rats fed a high-fructose diet to those fed glucose found disastrous results from the fructose diet. The male rats did not reach adulthood, had anemia, high cholesterol and heart hypertrophy — which means their hearts enlarged until they exploded — and their testicles didn’t develop properly. Female rats were not as dramatically affected, but they were unable to produce live babies. The results were exacerbated by copper deficiency, a fairly common deficiency in Americans. Dr. Meira Field, who led the study, notes that while "every cell in the body can metabolize glucose … 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." Yum.