Study Puts New Light on Fructose as a Trigger for Type 2 Diabetes

Type 2 diabetes is a disease caused by something called insulin resistance. Insulin resistance occurs when cells shut down receptor sites on their surfaces that ordinarily react with insulin, so they aren't flooded with sugar. In type 2 diabetes, however, there is something very strange about insulin resistance. Insulin doesn't just help cells absorb sugar. It also helps cells absorb fat. Why should a disease that "turns off" insulin receptors for insulin's use in moving sugar "turn on" insulin receptors for insulin's use in moving fat? Shouldn't diabetics at least have the pleasure of staying skinny?

It turns out that consuming sugar makes cells "selectively" insulin resistant. Diabetic fat cells and liver cells lose their ability to absorb sugar so blood sugar levels soar, but keep their ability to soak up fat. Eliminating consumption of the kind of sugar known as fructose can alleviate this problem, but before you can do that, it helps to understand the interrelationships between sucrose, glucose, and fructose.

Sucrose, Glucose, and Fructose

Sucrose, glucose, and fructose are all common sugars. Sucrose is the sugar molecule found in table sugar. Glucose is the form of sugar our bodies use for fuel. Fructose is the super-sweet sugar found in fruit and corn syrup.

Glucose is essential to life, and our bodies usually make it from carbohydrates. However, the human body can also make glucose out of the amino acids digested from protein. That doesn't mean you don't need to eat any carbohydrates at all, because the process of turning amino acids into glucose releases urea, which "acidifies" the bloodstream. Your blood doesn't actually become acidic, but your kidneys have to find calcium and, ironically, other amino acids to keep it from becoming acidic. There is a metabolic cost to getting your glucose from protein foods.

Every molecule of sucrose is made from one molecule of glucose and one molecule of fructose. The body can't use sucrose, so it breaks it down with an enzyme called sucrase in the small intestine. When you eat table sugar, you are eating glucose, which your body can use easily, and fructose, which it cannot. Fructose whether it's from corn syrup or fruit or table sugar once it has been digested is one of the culprits in insulin resistance.

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The Complicated Way In Which Fructose Causes Insulin Resistance

Most of what scientists know about insulin resistance is derived from studies of animals, not humans, but the process through which fructose causes insulin resistance probably occurs something like this:

• Your liver combines glucose with water to make glycogen, a storage form of energy for times you aren't eating. This glucose can come from carbohydrate foods other than sugar, protein foods, or sugar. Your liver can also turn glucose into fat.
• Your liver can use a small amount of fructose directly for making energy. Up to 25 grams or 100 calories a day, whether it's from fruit, corn syrup, or table sugar, usually can be tolerated. If you consume more than that, however, your liver stores fructose as fat.
• When your liver has to store fructose as fat, it in effect says "No more!" and shuts down insulin receptors so sugar stays in your bloodstream.

The Downward Spiral of Insulin Resistance Into Type 2 Diabetes and What to Do About It

If the only thing eating too much fructose did to your body was to cause your liver to make too much fat, that would detrimental to your health, but not devastating. When non-alcoholic fatty liver disease, also known as non-alcoholic hepatic steatosis or NASH, causes the accumulate so much fat that it "infiltrates" liver tissue, there can be abdominal pain, nausea, vomiting, weakness, and depression. If the condition isn't addressed over a period of years, there can be fibrosis of the liver, cirrhosis of the liver, and in some cases liver failure or liver cancer. 

Fatty liver disease isn't the only problem that can result from the insulin resistance that is triggered by eating too much fructose. An even bigger problem with insulin resistance is that it causes even more insulin resistance. The liver shuts down to glucose, its usual fuel source, when it receives too much fructose. That glucose stays in the bloodstream. Other tissues in the body, especially the muscles, likewise shut down their insulin receptors as blood sugar levels go up. That makes blood sugar levels go up some more. The pancreas, in the early stages of type 2 diabetes, continues to try to make enough insulin to get blood sugar levels down, and from time to time it is successful.

If you don't eat for 10, 12, or 15 hours, such as overnight, then your blood sugar levels may temporarily fall to normal. Your fasting blood sugar test may not tell you anything is wrong. However, the very next time you eat, the process starts all over again. Eventually your the insulin-making beta-cells in your pancreas "burn out." They become depleted so that your pancreas can't make enough insulin to normalize blood sugar levels. Doctors used to give early-stage diabetics medications that forced the pancreas to make insulin, but these just made the process of "burn out" come all the earlier. Diabetics who never get their sugar habit under control reach a point that they have both type 1 and type 2 diabetes: They need injected insulin, but they need huge amounts of injected insulin because they are both insulin-dependent and insulin-resistant.

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The only way to avoid these problems is to stop eating sugar. Yes, a little sugar every day probably wouldn't be a problem. However, diabetics tend to fool themselves about the amount of sugar they actually eat. Most studies have found that dieters fail to remember about half of the calories they consume. If you can't discipline yourself to a single 100-calorie indulgence every day, it's better to give up sugar entirely so you don't feed the insulin resistance that can eventually make you dependent on large doses of insulin to stay alive.