I have a massive sweet tooth.  In the last 72 hours, I’ve had four Sprinkles cupcakes, half a bag of Trolli Apple Rings, about 3/4 of a pint of gelato, apple strudel with whipped cream and ice cream, plus hearty helpings of beer and wine.  And I’m undoubtedly leaving something out.

And, it looks like sugar is bad for us.  Not “rots your teeth and makes you hyper” bad for you. More like “causes diabetes, heart disease and cancer” bad for you.  Great.

It all starts with the way your body metabolizes things.  The fructose part of sugar and high fructose corn syrup is metabolized by the liver, while the glucose component is metabolized by every cell in the body.  The speed at which you eat the sugar also affects how the liver processes it.  If you eat it fast enough and in great enough quantities, the liver converts much of it to fat.  This presents several problems.  First of all, you’ll get fat, and nobody wants that, but that’s just the beginning.

When you eat any type of carbohydrate, like bread or Skittles, your pancreas secretes insulin to help control your blood sugar. Eventually, cells become resistant to insulin, so your pancreas has to pump out more and more of it.  Then, either your pancreas quits from exhaustion (literally called “pancreatic exhaustion”) or your cells become so resistant that they can’t produce enough to control your blood sugar.  That’s called diabetes.

Even if you don’t get diabetes, having chronically elevated levels of insulin leads to elevated levels of triglycerides (fats), higher blood pressure, and lower HDL (good) cholesterol, which makes cells even more insulin resistant.  These symptoms constitute what’s called metabolic syndrome.

As it happens, metabolic syndrome and insulin resistance are the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist who did much of the pioneering work on the subject, feeding them diets that are mostly fructose is an easy way to do it. It’s a “very obvious, very dramatic” effect, Reaven says.

By the early 2000s, researchers studying fructose metabolism had established certain findings unambiguously and had well-established biochemical explanations for what was happening. Feed animals enough pure fructose or enough sugar, and their livers convert the fructose into fat — the saturated fatty acid, palmitate, to be precise, that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The fat accumulates in the liver, and insulin resistance and metabolic syndrome follow.

Oh, and one more, minor little thing:

As it was explained to me by Craig Thompson, who has done much of this research and is now president of Memorial Sloan-Kettering Cancer Center in New York, the cells of many human cancers come to depend on insulin to provide the fuel (blood sugar) and materials they need to grow and multiply. Insulin and insulin-like growth factor (and related growth factors) also provide the signal, in effect, to do it. The more insulin, the better they do. Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes. Some do both. Thompson believes that many pre-cancerous cells would never acquire the mutations that turn them into malignant tumors if they weren’t being driven by insulin to take up more and more blood sugar and metabolize it.

So, essentially, my sweet tooth is slowly murdering me.