In an earlier blog post, I mentioned that food industry labels use many different names for sugar. The intent appears to be a) avoiding the generic label ‘sugar’ as the first ingredient by breaking up the different types of sugar, and b) misleading those who don’t know all those different names mean sugar.
However, there’s another side to the story, and it is potentially a deadly one. This is the story of how high fructose corn syrup came to be the darling of the food industry and contributed to an almost immediate rise in Type II diabetes.
Ever hear of the glycemic index? Even now it is cited when nutritional experts and journalists talk about ‘healthy’ food. Simply put, the developers endeavored to rank carbohydrates by the insulin response, or glycemic load, of a measured unit of each food. Trying to decide whether to have a serving of orange juice or an apple? The glycemic index will tell you they are approximately equal in glycemic load. However, that isn’t the end of the story. Like any tool, the GI chart is suitable for some uses, and not for others.
The flaw in the chart is that the measured unit is the same for every food, whether that unit (50 grams) is a reasonable serving or not. Another flaw is that it measured only carbohydrates. In fact, all food (including protein and yes, fat) provokes an insulin response to some extent. In fact, just putting food in your mouth provokes an insulin response, even if you don’t chew and swallow it. We focus on carbohydrates, because that class of macronutrient typically induces the highest glycemic response, with protein carrying a more moderate glycemic load, and fat the least of all.
Back to the sugar isn’t sugar idea. Fructose is a type of sugar found in fruit. The amount varies by fruit, but in most fruits its effect is mitigated by fiber and the fact that fructose does not circulate in the blood, like glucose. Therefore, since diabetes research was focused on blood sugar, fructose was deemed healthier.
One little problem stood in the way. Fructose was expensive to refine from fruit. As with other foods that have been accused of causing obesity or metabolic diseases, Mother Nature had already given us the protective factor, and when we only got fructose from fruit, we didn’t get more than our bodies could handle. So until researchers discovered how to make fructose a food additive that was cheap to use, we were safe from the more harmful effects of the innocent-seeming sugar.
But wait! Some bright scientist discovered a way to synthesize fructose from corn. And there was plenty of cheap corn. Now everyone was happy. The food manufacturers had a cheap way of flavoring everything, sneaking a little HFCS in here and there to make everything taste better, and loading it into foods and beverages that were supposed to be sweet. Presumably, we could eat – and drink – more of it, since it was low on the glycemic index. The result was a steady rise in the consumption of fructose, peaking in the year 2000 at an astounding 9 percent of total calories.
Here’s the rub. HFCS had a deadly secret. As it became clear that the rise in obesity was closely associated with the increased use of HFCS, investigators searched for the reason. It came down to insulin resistance. But how could that be, when fructose doesn’t require insulin to be metabolized?
In a word, fatty liver. You see, the liver is involved in processing and storing sugar for use as fuel, as well as in making new fat to store excess sugar for later use. In a much-simplified analogy, the liver is a factory with a limited amount of storage space. When the storage space is full, it ships excess fuel out to be stored offsite. When the fuel it has on hand is used up, then it brings back the fat, converts it back to glucose, and the body uses it in that form.
Fructose, on the other hand, cannot be directly used as fuel, and where glucose circulates in the blood for energy by direct use, fructose can only be changed into fat in the liver and stored there for later use when the liver uses it for gluconeogenesis (i.e, making new glucose for energy). Gluconeogenesis occurs only when there isn’t enough glucose circulating in the blood to be used for energy. Typically, that’s during fasting or when the subject is on a very low carbohydrate diet.
Excess fructose can’t be shipped offsite, either. It remains in the liver as fat, and soon, excess fat. When excess blood glucose knocks on the door, using insulin to seek admittance, the liver puts up a ‘closed’ sign. But the body wants the extra glucose out of the blood, so it knocks harder; i.e., it manufactures more insulin to force open the door. Are you beginning to see the problem? It’s a vicious cycle, with HFCS feeding it.
As we will see in other posts, Type II diabetes has long been thought of as a disease of excess blood sugar. However, that’s actually a symptom, not a cause. The cause is hyperinsulinemia; i.e., too much insulin circulating in the body, also called insulin resistance. Therefore, high fructose corn syrup can be said to be a direct cause of insulin resistance, leading to the current Type II diabetes epidemic.