Dysregulation of Glucose Handling: Underlying Defect, Permanent Damage or Fixable Milieu?

How many times have you heard some version of the following?

• Sure starches are OK for 20-something CrossFitters
• My body just can't tolerate carbohydrates
• If I hadn't damaged my metabolism, maybe I could eat carbs now, but I can't
• I used up my carb allotment as a kid so I can't eat them now (I blew out my pancreas)
• Type II diabetes is a disease of carbohydrate intolerance

The list could go on.

When the topic of "safe starches" comes up on LC blogs or discussion forums, there's only betting on how many comments of the "I couldn't eat a half a potato, my BG would go through the roof" variety will be generated, not whether or not such comments will be made at all.  What is disturbing about this is the proportion of these comments that comes from NON-diabetics, many of whom seem to have been convinced that a normal glucose spike is abnormal, and that it is going to turn them diabetic any day now.  Many of the pre-diabetic or diabetics remain convinced that they've exhausted their pancreas with all that carb eating throughout their lives.  While there is a lot of confusion (I would perhaps call it controversy, but not contention) about this in the scientific community, but even those (researchers in the field)  who seem to favor carbohydrate restriction for the treatment of diabetes do not seem to blame carbs for the development of the disease.

Type 2 diabetes is clearly a progressive in nature, and yet there almost seems to be a regulatory switch that flips when someone goes from a little outta-whack to frank diabetic.  And yet, it remains unclear that it is necessarily a degenerative disease.  That current treatments generally do not seem to forestall the deterioration of pancreatic function is largely responsible for the "conventional wisdom" that T2 is an irreversible condition only to be managed to slow progression to insulin dependence.  For all the knocking of science and scientists going on out there, some rather amazing progress is being made elucidating the causes of diabetes.  Part of the problem as I see it, is there's more than one underlying cause for the collection of syndromes involving hyperglycemia.   You often have misdiagnosed 1.5's in the mix of study subjects  For the rest of this post realize I'm talking about the classic T2 -- that associated with obesity.

As I've blogged on here quite a few times before, there are these nagging "isolated" cases in the scientific literature where some even rather long-standing cases of diabetes have been rapidly reversed.  These include that crash diet study,  several studies on gastric bypass surgery in diabetics, and early insulin therapy (there are also cases of vagus nerve severance I've not addressed here).  In each of these cases, normal pancreatic function and response to the endogenously produced insulin has been restored in relatively short order -- from days to several weeks.  And here we are talking some of the most "metabolically deranged" on the glucose tolerance spectrum.

Now one could argue that there is recidivism -- many do relapse to diabetic -- though I think the rates of long term diabetes remission are rather impressive in many of these cases.   But here's the thing:

A Type 1 diabetic never has a single day of normal glucose homeostasis ... no matter the diet.  They have a permanent inherent defect (e.g. islets that don't produce insulin).

Just one single day of normal glucose homeostasis in a T2 diabetic is the proverbial black swan.  

Especially when we're talking such short time periods to achieve it.  This black swan argues against many of the theories as to what causes diabetes or what's going on metabolically in those who have it.   This is not to say there's not some predisposing genetic/physiologic make-up -- there are too many familial-linked inherent differences in various metabolic functions to discount this.  But whatever these mechanisms are, they just seem to work to flip the switch sooner towards dysregulation ... but there's a lot of evidence that the switch can be flipped back.  

Therefore looking at T2 as a progressive disease involving permanent degeneration is probably one of the more misguided general opinion in medicine.  Here is where the Vernons (LC, animal-based diet) and Fuhrmans (HC, plant-based diet) of the world seem to be on the same side but they aren't really.  The LC diabetes folks seem to collectively believe in a permanent glucose intolerance -- one that can be treated/managed by severely limiting dietary glucose, but that remains inherent in one's constitution.  Dr. Wheat Belly Davis describes his own diabetes only as in remission.  But folks like Fuhrman openly express their belief that diabetes can be reversed, not simply managed.   Unless one questions the success stories of Fuhrman (and they are subject to the same scrutiny as all success story reports, so may well be exaggerated), he has had patients reverse their diabetes.  And how do they know?  Well, they eat carbs and have NGT (normal glucose tolerance).

In both the crash diet study, blogged on here, here and here, and the early insulin therapy study, the subjects were given nutritional counseling and returned to a "normal" diet, albeit probably more aligned with the current wisdom in the EIT study.  Indeed in the crash diet study many participants even regained weight yet remained diabetes free by OGTT.  If memory serves, one participant in that crash study interviewed in the press remained diabetes free a year after the study, and his diabetes diagnosis had been several years prior.

So, Dysregulation of Glucose Handling:

• Underlying Defect?   Sure, in T1's and 1.5's there is a manifest defect in pancreatic function.  In T2's?  Clearly there are some underlying predispositions, but also, clearly, these predispositions do not necessarily manifest in diabetes, nor are they irreversible.  If there was some sort of pre-existing glucose intolerance, then perhaps 1 in 100 might be able to see reversal, however temporary, from any of the aforementioned interventioned.  That we see significant, often majority responses argues heavily against the defect being an underlying one.  
• Permanent Damage?  Again, that we can see rapid reversals in so many argues strongly against this being the case either from overuse of the pancreas or from glucotoxicity.  Which is not to say that some physiological damage/deterioration may not have already occurred that may impact health, but whatever causes the impaired glucose metabolism appears to not be permanent absent beta-cell destruction.
•  or Fixable Milieu?  I'll go a step further than fixable milieu for those who have never been diabetic.  For these people, it is far more likely than not that there is nothing wrong with their metabolisms at all other than mistaking normalcy for "everybody is a diabetic" memes.   Even for many diabetics, it most certainly seems fixable.   There certainly seems to be more evidence to support reversibility than not.  More, rather than fewer, can probably not only handle, but likely even thrive on diets with moderate and even high carbohydrate content (context dependent) once they have fixed their metabolisms.

In coming weeks I plan to address blood glucose levels, glycation and other things that I feel have often been misrepresented in the low carb community.