Blood Sugar 140: Context is Everything I - Diabetic vs. Non

In Blood Sugar 140: Where did the 140 mg/dL threshold come from?, I laid some groundwork as to the source of the concern over postprandial blood glucose levels over 140.  Before moving on, I thought I'd share an additional example of the 140 mg/dL threshold being evoked.  Here is a thread on Dr. Dansinger's WebMD diabetes forums:  glycation damage.

I ask this question because the consensus is that blood sugars over 140 cause the sugar to stick to vessels and organs. Dr. Gabe Mirkin writes of this on his web site. Others like John McDougall do not seem to worry about sugars over 140.

I can understand that you don't want fasting sugars over 140 but apparently even postprandials over 140 cause damage. I am wondering how long it would take for damage to be recognizable if post prandials are above 140. And does it matter how long they remain over 140 after eating?

... A corollary to this would be the question --if you can keep your blood sugars at all times below 140 does this guarantee that you will not get complications--whether by means of diet, exercise, meds or any combination of treatments?

... I never worried about this until reading on this group that sugars shouldn't go above 140.

Now I looked for the Dr. Mirkin reference and found a lot of info, but not specifically referring to postprandial levels other than that the current guidelines use a cut-off of 140 mg/dL at the 2 hour mark of an OGTT for a diagnosis of impaired glucose tolerance, IGT.   Others in that discussion pointed out that it wasn't all pp levels, but the 2 hr level for an OGTT.  Jenny Ruhl's site is also brought up.  (As an aside, one Mirkin hit was a blog curation site that directed me to this post by Wheat Belly, pre-book bonanza.  Seems back in 2008, a bowl of Cheerios only surged BG to 140, in 2011, a bowl of oatmeal would typically cause a surge to around 180!).

I want to make a few things clear before moving on with this series.  This is not an anti-Jenny, anti-Paul or anything of the sort.   It is intended to dispel some of what I see as anywhere between unnecessary concern to downright paranoia over the "toxic" effects of glucose cultivated in the low carb community.  In some cases I see this taken out of context, but it is fair to say that Jenny's writing (on the website anyway, I haven't read her book) can tend towards unwarranted hyperbole at times (e.g. calling the crash diet dangerous and idiotic), but many take her advice to diabetics out of context as well, to apply to their non-diabetic existences.  Paul seems to go out of his way not to offend or to take every possible objection to including starch in his diet into consideration, and I think this is "to a fault" at times.   It is very easy to get sucked into this glucose is toxic, we're all diabetic mindset, especially if one gets under the influence of someone like Wheat Belly who believes one's blood sugar should be at pre-prandial levels within an hour of eating any meal.   I was pretty convinced in 2009 that I must be IR at least and boy was I shocked to discover I had dead nuts normal glycemic control eating high or low carb.  If anything I think I have some minor insufficiency for gluconeogenesis -- AM hypos, especially exercising in the morning when VLC, were likely my issue several years back.

I tend to agree with those who view the targets given to diabetics as being too permissive, and can understand the desire of diabetics to seek out a safe glucose level -- the "corollary" question in that WebMD exchange.  In that light, the 140 pp target is a far preferable goal compared with than the current recommendations:

Less than 180 but high enough that hypoglycemia won't result from any "onboard" insulin if testing at only 1-2 hours.

The recommendations are skewed towards insulin-dependent diabetics for whom hypoglycemia is a very real possibility and more immediately life-threatening than for non-insulin using type 2's.  What really bothers me, however, is the derision for using insulin at all in the community.  If someone is insulin deficient -- and a T2 can be both hyperinsulinemic at baseline and GSIS-impaired -- low carbers should not be so hostile towards those who use it.  By that I mean since practically day one of finding this online community I was hearing diabetics derided for not wanting to see the light and insisting on eating carbs and just covering it with insulin.   It's like "I care about my health", "my stupid fill-in-the-blank just wants to eat crap and take medications" and all my doctor wants to do force carbs on me and hand me prescriptions.  

This is where I think Gary Taubes has been most damaging to the discussion in demonizing a hormone required for life!  Insulin does more than just act on fat cells, it prevents catabolism of and promotes growth of lean tissues like muscle and bone.  Many of the reduced diabetic complications seen in patients with better glycemic control may well be due to the fact that better glycemic control often involves proper insulin dosing.  Advances in insulin therapies -- injection methods, pumps, long-acting, etc.etc. -- have dramatically improved the ability of diabetics to not only meet ADA targets, but obtain truly "normal" glycemia.  I will address this point in a later post in this series, but I can think of nothing more harmful to health than the insulin phobia rampant in the LC community.  While the frank type 2 diabetic is baseline hyperinsulinemic, they don't produce the appropriate acute insulin response.  Given the health issues accompanying improper insulin/signaling, it seems a no-brainer that establishing  as normal a level of both insulin and glucose as possible.

So anyway,  after my exchange with Karen (a diabetic) on the first post, I split this Context post in two in order to address the relevance of the 140 mg/dL level for diabetics vs. non-diabetics, and in the next part I'll address the context of that level in terms of the OGTT to which it applies.  Back to topic at hand.

Whenever talking normal glucose levels, I'm always reminded of Ned Koch's post from which the graphic at right comes. These are glucose levels in non-diabetics taken over the course of two normal days.  Now, granted not all seemed to even exceed the 140 threshold, but many.  If it were true that nerve damage occurs at glucose levels over 140, certainly cumulatively over time, we'd be seeing neuropathy more in the general population.

This is a very important point.  Normal individuals eating a "normal" diet will regularly exceed 140 mg/dL, though not necessarily by much, to no apparent detriment.  Neuropathy would simply be far more common in occur in younger populations if BG's over 140 damaged nerves to any significant level.

In a diabetic, however, not only do postprandial glucose levels climb higher, they tend to stay elevated for longer periods of time, thus if the hyperglycemia is toxic per se, the exposure is greater.  The glucose levels also may never fall below, say, 100 or even far higher depending on the degree of glycemic control.  Therefore it is not surprising that IGT or diabetes was diagnosed by OGTT in 2/3rds of subjects presenting with neuropathy in this study.    I shall discuss the implications of that finding in a separate post as well.

In someone with impaired insulin secretion (T1 = none/insignificant, T1.5 = insufficient, T2 = varying depending) if blood glucose goes over 140, it likely climbs considerably over that and takes longer to clear (and/or is added to by inappropriate endogenous glucose production).  The more carbs ingested the higher the glucose spike in somewhat proportional fashion.  This is because insulin is not secreted properly and the glucose will be cleared by non-insulin dependent mechanisms.  A person with normal insulin secretion will almost never get a glucose spike over around 180 because their glucose stimulated insulin secretion (GSIS) is proportional to the glucose ingested.  So a diabetic consumes 50g carb or 100g carb and their BG level climbs quite a lot higher after the 100g load, but a non-diabetic consumes 50g or 100g or 200g, and their BG level may climb 10 or 20 points higher at the high dose, but their GSIS will just increase proportionally to handle the load to avoid runaway glucose levels.  

This is why Wheat Belly comes across (well one of the reasons anyway) so disingenuously to me.  It is not readily apparent to a casual reader that he, himself, is a diabetic.  Sometimes he mentions it, sometimes not.  He'll make statements such as a typical glucose response to a bowl of oatmeal is in the 170's, but he doesn't always clarify, and is often less specific than the example I'm about to give.  This post is typical of Davis' glucophobic hyperbole:  Oatmeal: Good or bad? 

If you are not diabetic and have a fasting blood sugar in the “normal” range (< 100 mg/dl) , you will typically have a 1-hour blood glucose of 150-180 mg/dl–very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Even if the spike is as high as he says, it won't stay up there very long in a non-diabetic, but he's likely wrong that the spike would go much higher in the non-diabetic with other stuff added, because these people will simply secrete more insulin to keep that from happening.  

There is NO evidence in the scientific literature, physiology texts or any similar source that I've come across to support the exhausted pancreas theories espoused in low carb circles.  It matters not how many repeat this meme, it doesn't make it so, and the onus is on those making the claims to back them up.  Eating sugar or carbohydrates in general does not cause diabetes.  The pancreas has more than enough insulin making capacity to last more than a lifetime.  It's not like eggs in your ovaries as I've seen the analogy drawn.  Yes, with aging comes some declining function, just as sarcopenia can become an issue, but that decline is not due to having used up some insulin reservoir.   Eating a low carb diet to avoid getting diabetes on this basis is, frankly, downright foolish.  Equally foolish, IMO, is looking at thresholds and studies in diabetics and applying those same measures to the non-diabetic.    A non-diabetic will simply rarely if ever exceed around 180 mg/dL no matter what, and this includes "compensators" -- those with IR for whom an exaggerated GSIS compensates for impaired transport to achieve normoglycemia.   So long as one is not continually adding to whatever has caused the IR, there's little indication the pancreas can't keep on keeping on.  Remember, the LIRKO mouse is hyperglycemic throughout most of its shortened life, but hyperinsulinemic to the bitter end.   We can argue over the glucose and/or insulin being toxic in this mouse, but it's pretty clear that at least in the mouse, raging chronic hyperglycemia didn't kill off its beta cells.

In summary, then, application of thresholds and targets aimed at diabetics to non-diabetics should be qualified and are often so out of context as to be irrelevant.  I would agree that maintaining more truly normal glycemic control in the diabetic -- keeping glucose spikes under 200 and 2 hr readings below 140 -- may well be a more effective means to prevent diabetic complications.  I'd sure as heck aim for that myself were I diabetic.  But I don't see any reason for a non-diabetic to worry or obsess over postprandial spikes exceeding that magic 140 mg/dL number.    If your low carb diet has rendered your formerly non-diabetic metabolism into a functionally diabetic one, it may be time to rethink things a bit.  Insulin does more than stimulate glucose transport into your cells.

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Next:  Blood Sugar 140: Context is Everything II: The OGTT