Insulin Resistance: The Root of All Evil

 Central to the theme of this blog is the concept of insulin resistance, which along with insulin itself, I'll identify as the cause of a great many problems.  I'll start with the basics.

As I mentioned before, insulin is secreted by cells in your pancreas in response to elevated blood glucose levels, which in turn are caused by dietary carbohydrates.  Your body converts digestible carbohydrates into glucose, which is what stimulates the release of insulin, and that insulin is necessary for your body to make use of the glucose and manage your blood sugar levels.  When tissues become insulin resistant, their ability to make use of blood glucose is impaired, leading to a whole range of problems.

There appears to be a very influential genetic component to the risk of developing insulin resistance (IR), but no specific cause has yet been identified to everyone's satisfaction.  A great deal of evidence exists to support the (intuitive) hypothesis that it's caused by chronically elevated blood insulin levels, which in turn can only be caused by a high-carbohydrate diet.  This hypothesis stipulates that many conditions, including obesity, type 2 diabetes, and even heart disease are symptoms of the problem.

This idea is also consistent with the etiology of these conditions, and their correlations with each other.  We know that IR is tissue-specific, and that different tissue types become insulin resistant at different rates and in different orders, apparently determined by genetic factors.  One common scenario described by the hypothesis (and frequently observed) is as follows.  After some years of chronically elevated insulin levels, skeletal muscle tissues become insulin resistant.  This has negative effects of its own, but for our purposes it largely removes the main consumer of glucose from the glucose "economy" in the body.  The second-biggest consumer is your adipose (fat) tissue.

When your adipose tissue becomes the main consumer of glucose, because your muscles have begun to fail to make use of it, you start putting on weight rather quickly, because that's how fat tissue responds to glucose and insulin.  At some point, even your adipose tissue will probably become insulin resistant.  At this point, you'll stop gaining weight, or at least slow down, and if your muscle tissues are already resistant, you are now diabetic.

The last two paragraphs do not represent current medical thought.  It's currently believed that IR is caused by obesity, and that it correlates with diabetes for unknown reasons.  So what I'm trying to present is a bit of logic that puts the high-carbohydrate diet squarely at the beginning of the cause-and-effect chain.  This diet leads to chronically elevated blood glucose levels, which necessarily lead to high insulin levels.  Prolonged exposure to elevated insulin levels causes insulin resistance (in one tissue type after another) and, once the major consumers of insulin have become resistant, the result is diabetes.  The hypothesis that proposes this chain of events successfully and simply explains a great many observations and answers many outstanding questions.

For example, obesity is strongly correlated with type 2 diabetes, but why aren't all diabetics obese?  Our answer is that in some individuals, adipose tissue becomes insulin resistant (making weight gain effectively impossible) before the skeletal muscles do.  Why do diets high in fiber, a carbohydrate, seem to be beneficial with regard to obesity, IR and diabetes?  Fiber can't be digested (converted into glucose, like other carbohydrates) by humans, so it doesn't raise blood sugar levels or stimulate an insulin response.  Some kinds of dietary fiber may also trap otherwise digestible carbohydrates in the digestive tract and prevent their metabolism.