las

Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Tuesday, November 1, 2011

Is Glycemia a Continuum?

Something has been "egging me" since I wrote my last two blog posts (Some Spiked Leptinade with My Science Krispies Please! and Keep the Leptinade flowing! I'm going to die from my glucose anyway ...) on two of the studies Dr. Rosedale cited in support of his starch-is-never-safe stance.  Put another way, in his own words
...there is really no totally safe level of blood sugar that will not cause non-enzymatic glycation or damage. The thresholds for diagnosing diabetes are arbitrary numbers. As such, I consider most everybody to have diabetes; just different degrees.
I'm a little confused over Rosedale's stance, but I can't really get bogged down because, frankly, he's not talking straight.  He seems to be saying hyperglycemia is not diabetes it's the underlying hormonal imbalance, insulin and leptin resistance specifically.  He seems to be under the mistaken notion that 
When one is relatively young or pre-diabetic, the secretion of insulin and leptin when one eats non fiber carbohydrates can compensate for the moderate intake of starch and other sugars, but it does so at the expense of greater and greater insulin and leptin resistance accumulated over months and years.
In other words using your insulin somehow accumulates some sort of damage or whatever resulting in insulin resistance.  Leaving aside that there is no evidence to support this, is there really some continuum of insulin resistance?   One need never read a scientific study to see just how ridiculous this is as diabetes, even though on the rise with obesity, is still relatively rare in the human race that just reached 7 billion in number alive today on this planet -- the vast majority of whom consume considerable carbohydrate if not carbohydrate-centric diets.  If we were all somewhere on the path to whatever it is that Rosedale considers to really be diabetes, many billions more would become IR at some point.  And yet diabetes rates are low in cultures eating traditional high carb low fat diets.  If anything, these populations seem to be especially sensitive to the introduction of fat to their diets, often becoming diabetic w/o going through the path of obesity.

Still,  as chaotic as blood glucose levels are in normal people, and while we may be able to delineate risks associated with some measures in this whole mess in same said normal people, it is clear that what we call diabetes is anything but some variability on some continuum.  Diabetes finally rears its ugly head when the beta cells fail.  Many folks can be "prediabetic" for most of their lives without ever becoming diabetic.  Indeed if memory serves, the five-year conversion rates are in the low single-digit percents.   And yet for all the issues with diagnostics and such, the cut-offs for a diabetes diagnosis hold up pretty well in most cases in identifying people who have a certain degree of beta cell dysfunction.  It's almost like a switch is thrown.  I've read numerous studies that compare obese non-diabetics and diabetics, or lean non-diabetics and diabetics, and although there will be some differences between the lean and the obese, these are almost invariably more  clearly distinguishable between diabetics and non.  In terms of 24 hour hormonal and metabolite level profiles, those with impaired glucose tolerance or slight hepatic IR resemble normal people more-so than diabetics, so while they may be on the road to diabetes, they are still more normal than diabetic.

This concept of a threshold "switch" is also supported by the rapid reversals of diabetes with certain interventions,  gastric bypass surgery being probably the most dramatic of these.  GBP is only approved for morbidly obese individuals and there is often an extended screening/approval process involved.  Also nobody becomes morbidly obese overnight so acquiring this state required years of chronic energy surplus (even if they are now in energy balance albeit at excessive weight) no doubt consisting of considerable carb-induced insulin spikes, not to mention considerable time exhibiting some degree of hyperinsulinemia.  If Rosedale's "accumulation nation" theory is correct, there should be no undoing the damage for these folks.  And yet even before significant weight loss, greater than 4 of 5 regain glycemic control within days or a few weeks.  We see the same for early insulin treatment (2-3 weeks) and that crash diet (8 weeks) as well.  Even more profound reversals are seen in animal studies (e.g. severing nerves, injecting hormones into brain, etc.).

The bottom line to me is that this notion that hyperglycemia is just some high end state on a glycemic continuum, or, in Rosedale's world, we're all just on the lower end of some hyperglycemic/diabetic continuum, does not seem to jive with observation.  Diabetics are a distinctly different population metabolically.  Unless intervention flips that switch back (I hate to use any reference to switches as I'm not talking Leptinmanese* here) diabetics are metabolically distinct from non-diabetics, even if their glycemic control is excellent through diet, exercise and/or medication.  As such, it seems the ultimate exercise (cycling) in futility to try to equate the glycemic state of a normal person to that of a diabetic.  Is glycation a continuum?  No, it is not either.  That there's no clear threshold in correlation with various risks is somewhat debatable.  I happen to think the shallow J curves that were the subject of the first blog post say otherwise, as does the moderate taking off of the risk of stroke only across a 20 percentile range from 75-95th (at most 27%) but clear increased risk (more than doubling) in diabetics in the second study/post.  As such, this whole part of the discussion on "safe starches" or carbohydrates and blood sugar levels in general is a needlessly fear-mongering diversion.

What happens when a non-medicated "classic" type-2 diabetic with fasting blood glucose over 150 eats 100, 200, 500g carb/day is nominally applicable, if at all, to what happens when a non-diabetic, even a mildly IR one, with fasting glucose in the 80's or 90's or even low 100's does the same.  And there's really no comparison between a post prandial spike to even 200 mg/dL and a fasting level of 200 mg/dL even in a diabetic.  We need to move the conversation back to comparing apples to apples, or I suppose coconut oil ball to coconut oil ball.

*We've been having some fun here with Dr. Jack "Leptin Reset" Kruse aka "The Quilt" and have dubbed him the superhero Leptin Man.  He's famous for discussing flipping his epigenetic switches and such, hence the reference here.

4 comments:

MM said...

Well, I have to say weight loss has had an almost magical effect on my blood sugar. I've managed to lose 20 pounds over the last year. It was very slow weight loss by most people's standards, but I don't think the speed of the weight loss has anything to do with the overall effect. I know that some people have postulated that the reason GBP surgery works is because the weight loss is so rapid, but I'm not sure that's really a factor. So, 20 pounds ago three slices of pizza would have sent my blood sugar up over 150, and I even had it go over 200 a few times. Now, it maybe tops out at 105, and I've had it often stay below 100. My blood sugar dropped slowly right along with my weight. I'm kind of shocked at how much starch I can eat now and it barely registers on my glucose meter. Type 2 diabetes runs in my family, and it could be that I've just postponed the inevitable, but I do not think I'm going to give myself diabetes by eating starch. It seems that at least for my body type weight is a big factor, maybe even the dominant factor.

Evelyn aka CarbSane said...

Congrats MM on 20 lbs gone! Woo hoo! Your experience would also add support to some sort of critical fat mass theory.

Frank said...

Not related but... did anyone saw that?

A higher-carbohydrate, lower-fat diet reduces fasting glucose concentration and improves β-cell function in individuals with impaired fasting glucose PMID: 21944267

Evelyn aka CarbSane said...

This is interesting because C/F for HC was 55/27 vs. LC at 43/39. Both 18% protein. So the low carbers would say that's not low carb, but that 43/39 is pretty darned close to the macro of the SAD. So Warshaw saying eat more carbs ... not so stupid after all, eh?

A lot of the stuff I've been reading this past week or so is making my head spin and having me question a lot of things I still presumed true wrt VLC.

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