Type 2 Diabetes: The Last Phase of Insulin Resistance

 I've covered insulin resistance (IR) and mentioned its relationship to type 2 diabetes, but I need to discuss diabetes in a bit more depth, if only to establish a background for future posts.

A central and controversial thesis behind this blog and many of the ideas behind low-carb diets is that tissues become insulin resistant after prolonged exposure to elevated insulin levels, caused by a diet high in carbohydrates.  That's a bit of an oversimplification, but that's the gist.  I'll go into greater depth shortly to back up that assertion.  Central to this post in particular is the idea that type 2 diabetes is nothing more than the final (insert pregnant question mark here, and anticipate a future post) phase of IR, in which all major tissue groups have become insulin resistant.

Both conditions are well-known to correlate with metabolic syndrome or syndrome X, and as seen here and elsewhere it's all been long thought to be caused by obesity.  As far as I can tell from currently available research, that assumption is still the state of the art, though some research is finally beginning to stumble on a more sensible explanation.  That is, that diet is the root cause of this cluster of diseases, including obesity.

Unfortunately, most studies don't isolate the component of diet that's to blame, because they combine high fat (which we like around here) with refined carbohydrates (which we assert are the enemy) and (correctly) blame the diet for IR.  Other studies start with IR and find it to be the cause of metabolic syndrome. All that's left is to test high fat and refined carbohydrate diets separately to (inevitably) arrive at carbohydrates as the root cause, and for someone to connect the dots from dietary carbohydrates (especially refined carbohydrates) all the way to the endpoints of metabolic syndrome, and today's topic, type 2 diabetes.

As for that final step, establishing type 2 diabetes as a manifestation of insulin resistance, we're getting so close!  But still a bit backward, it seems, no matter how consistently we witness the order in which they occur, even in a controlled study (the only one I could find even making the attempt, and the full text is not freely available, which may be contributing to its failure to make a significant impact on the field.)

The complete (if somewhat simplified) picture goes like this.  Your skeletal muscle is your body's main consumer of insulin and glucose, and your adipose (fat) tissue is #2.  So it's usually (but not always) in that order that the tissues become insulin resistant, given the high-carbohydrate diet and perhaps a genetic predisposition to IR.  Once the two major consumers of glucose and insulin begin failing to respond, and perhaps the third, your liver, your capacity to manage your blood sugar levels by secreting ever-increasing amounts of insulin is greatly impaired, and you are diabetic.  In other words, your adipose tissue can't pick up the slack from your insulin-resistant muscles (making you fat in the process) because it too has become resistant, and either your liver can't handle the load on it's met the same fate, and you now have diabetes.

The hypothesis I'm proposing in this blog, the one so ably elucidated in the book I keep mentioning, the one partially described and defended in this post, predicts that type 2 diabetes is treatable without insulin, and likely even reversible using the same treatment: you guessed it, the low-carb diet.  Without carbohydrates in the diet, your ability to produce or make use of insulin is largely irrelevant, because it's not necessary for your new mode of metabolism.  Thus depriving your tissues of both glucose and insulin over time via diet, insulin sensitivity should eventually be restored to normal or near-normal levels, and by definition you will no longer have type 2 diabetes.