The Condemnation of Carbohydrates: A Food Manufacturers Guide to Understanding Diabetes

July 30, 2013
The commonly held notion that sugar intake equals diabetes is a kind of unofficial dogma. But like many dogmas, this one falls apart upon closer examination.

From the near-daily news reports about the diabetes epidemic, the sum of the problem always seems to add up to carbohydrates + overeating = diabetes. After all, the modern diet is awash in sugar, and of course, diabetes is defined by high blood sugar.

It's a no-brainer: Ban the "Big Gulps," and diabetes will vanish along with obesity. We all just have to give up our addiction to sugar.

The role of carbohydrates in diabetes is complex, even when, on the surface, it appears simple. In diabetes, blood sugar is elevated because glucose can't enter the cells efficiently. This is due to one of two mechanisms that define the type of diabetes. In type 1 diabetes, the cells of the pancreas that produce insulin - the pancreatic hormone that coaxes cells to take up glucose - are destroyed by the immune system early in life. Type 1 diabetics must take insulin and coordinate the dose with their intake of food, particularly carbohydrates. The American Diabetes Association recommends a balanced diet that includes carbohydrates, emphasizing carbs that are unrefined.

In type 2 diabetes, cells fail to respond properly to the insulin that is available, a condition referred to as insulin resistance. In an attempt to overcome insulin resistance, the pancreas increases insulin production. This can result in stress to the pancreas and eventual failure to produce sufficient insulin. Type 2 diabetes accounts for 95 percent of new diabetic cases and is on the rise along with obesity. In fact, obesity is a primary risk factor for type 2 diabetes.

Here is where the real condemnation of carbohydrates begins.

The Holy Grail of avoiding or reversing type 2 diabetes is solving insulin resistance. The easy answer is to blame carbohydrates. After all, carbohydrates stimulate insulin production, and insulin allows fat cells to take up glucose and make fat. However, there's a problem with this popular narrative: The primary destination of glucose is not fat cells, but muscle cells that turn glucose into muscle glycogen, a critical energy storage form of glucose.

Type 2 diabetics have low muscle glycogen stores, something we generally ignore because studies tend to focus more on adipose tissue when it comes to insulin resistance. That's why we label insulin the "fat-storage hormone" instead of the "strengthening" or "endurance" hormone, which are more accurate descriptions. Fat cells make fat from glucose only when we overeat, not merely because we have an increase in blood sugar.

The other problem with blaming carbohydrates for insulin resistance is generally hidden from the public: To study the mechanism of insulin resistance, researchers need to produce it in animals. A high-fat diet is a common tool of research when it comes to inducing insulin resistance. Insulin resistance can be induced by a high-sugar diet that also is high in fat. For sugar to induce insulin resistance, the diet must greatly exceed energy needs or and be physiologically unrealistic with respect to sugar intake, particularly fructose intake.

The attempt to link sugar with type 2 diabetes is so exuberant it sometimes trips over itself with contradictions, especially concerning fructose and HFCS (high-fructose corn syrup - something of a misnomer, in that sucrose and fructose are chemically nearly identical). Products containing fructose are preferred by consumers and food manufacturers over those containing only glucose, due to the intrinsically greater sweetness of fructose and its ability to improve the texture and appearance of baked goods. As a result, fructose and HFCS are present in many beverages and foods.

Ignored in the indictment of fructose is the fact that it's an extremely low glycemic index food. The Glycemic Index is a measure of glucose in a food or beverage compared to a baseline of the amount in a slice of white bread. It was developed as a comparison for persons with diabetes, not in order to be used as a weight-loss tool. Moreover, while HFCS has replaced about half of the sucrose in the modern diet, that doesn't mean we're drowning in fructose or even in sugar.

USDA food consumption data, adjusted for loss from 1970 before the current epidemic of obesity and type 2 diabetes, tells an interesting story. The average per-capita calorie (kcal) intake in 1970 was 2,076. By 2010, it had risen to 2,534-a difference of 458 kcals per person per day. But how those calorie are distributed bears investigation. Per-capita intake of added caloric sweeteners in 1970 was 333 kcals per day. In 2010, it was 367, an increase of only 34 kcals, down from peak added sugar consumption of 422 kcals in 1999.

In other words, sugar consumption has actually been decreasing for the past 14 years, during which time type 2 diabetes has continued its rise.

So what accounts for the increase in calories? In 1970, calories from added fats and oils (including dairy fats) equaled 346. By 2010, it rose to a peak of 588. That's an increase of 242 kcals from fat, a fact always ignored in the blaming of carbohydrates for obesity and type 2 diabetes. And, during that same period, intake of flour and cereal products rose by 167 kcals, from 429 to 596 kcals. Flour and cereal products contain no inherent fructose. When we mix that flour with fat, we generally get a low glycemic index food, because fat slows digestion.

Americans eat more sugar than is recommended, about 14 percent of total kcals, down from 16 percent in 1970. But we also eat more fat than is recommended and do less exercise than is recommended - and turn more of our staple starches into desserts than is recommended.

There still is a need to define the mechanism of insulin resistance. However, it will be harder to do so if we insist on going down the route of predetermined conclusions, á la, "We all know carbs are bad; now let's find the evidence to support it."

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