Reactive Hypoglycemia, Insulin Resistance, and Carbohydrates: What Is The Connection?
Reactive hypoglycemia impacts millions and seems to be correlated with other underlying metabolic problems, such as insulin resistance, type 2 diabetes, and obesity. Why do all of these various diseases cluster together? And what can this observation tell us about the fundamental reasons why we suffer from chronic diseases and why we get fat?
Traditional thinking about the relationship between overweight and disease tells us that any solutions for obesity must be compatible with the Caloric Balance Hypothesis. This, again, is the idea that the calories we eat and burn regulate our fat tissue.
Caloric Balance does not give us a plausible biological mechanism by which accumulating a positive caloric balance puts us at risk for conditions like insulin resistance and reactive hypoglycemia. And this is a crucial point. Unless you suggest a way that calories themselves -- units of energy -- somehow can cause disease, the theory is an incomplete theory, at best.
On the other hand, the Lipophilia Hypothesis gives us a very specific explanation. It tells us that too many carbs in the diet and too much insulin cause insulin resistance, reactive hypoglycemia and overweight. These problems associate because they're essentially different heads of the same hydra.
Okay, so two theories. Two explanations. What does the evidence tell us? Is there evidence, for instance, that over secretion of insulin can cause insulin resistance? Is there evidence that hyperinsulinemia can in turn lead to reactive hypoglycemia?
In fact, such evidence appears to abound:
1. Please read chapter 11 in Good Calories, Bad Calories (pages 186-194).
2. Also see chapter 4 in Life Without Bread (pages 33-53).
3. In addition, here are some randomly selected studies and articles about IR and reactive hypoglycemia. Here's one entitled: "Carbohydrate nutrition, insulin resistance, and the metabolic syndrome in the Framingham offspring cohort."
From the summary:
"The higher the insulin level in the blood, the more insulin resistant is a person and the more likely they are to develop the metabolic syndrome (which includes obesity). Diet affects blood insulin level and may play a role in the development of the metabolic syndrome. One aspect of diet that may control insulin levels is the source and quality of dietary carbohydrates."
The authors go on to argue that our diets make us sick because they lack fiber and contain fats. But in trying to justify what appears to be a theoretical perspective derived from Caloric Balance, the authors inadvertently appear to have given Lipophilia defenders yet more support.
4. Here's another example of the same kind of happy accident: "The role of carbohydrates in insulin resistance."
In the abstract, the authors actually argue that:
"The available data support the idea that consumption of diets high in total carbohydrate does not adversely affect insulin sensitivity compared with high fat diets."
This piece of news, if correct, would actually support Caloric Balance! However, the authors then admit that:
"Animal data suggests that simple sugars, in particular fructose, had adverse effects on insulin action."
Wait a minute. In animals, sugars and fructose and simple carbs can have "adverse effects on insulin," but not in humans? Amazingly, that's exactly what the authors seem to suggest:
"But adverse affects have not been shown conclusively in humans."
Okay, precisely what do these authors mean by "conclusively"? Because other studies seem to be pretty close to conclusive when it comes to showing that carbohydrates can impact blood insulin levels negatively.
5. To wit, here is a study from Gerald M. Reaven, a researcher whom Gary Taubes and other low carb diet proponents often quote: "Role of insulin resistance in human disease (syndrome X): an expanded definition."
From the abstract:
"It seems likely that the cluster of changes associated with resistance to insulin mediated glucose uptake comprise a syndrome, which plays an important role in the etiology and clinical course of patients with non-insulin dependent diabetes, high blood pressure, and coronary heart disease."
6. Here's another study from a 2005 issue of the journal Nutrition and Metabolism, "Fructose, insulin resistance, and metabolic dyslipidemia."
"Emerging evidence from recent epidemiological and biochemical studies clearly suggest that the high dietary intake of fructose has rapidly become an important causative factor in the development of metabolic syndrome... An important but not well appreciated dietary change has been the substantially increased amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup."
The authors then describe specifically how these simple carbs and sugars drive the creation of new fat, the synthesis of triglycerides, and other problems. And then they conclude:
"These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models."
So we apparently do have abundant data that show that carbs -- or at least refined carbs -- can drive insulin resistance and reactive hypoglycemia. This again would support the Lipophilia Hypothesis. And once again, the Caloric Balance Hypothesis is hung out to dry.