Glucose Assessments, Safe Starches and Interpretations

Before I serve up any more leptinade here at the Asylum, I wanted to share some broader thoughts on the analyses and implications of various measures of blood glucose levels as relates to normal and non-T1 diabetics.

The Common Measures:

1.  Fasting Blood Glucose (FBG):  Usually after at least a 10 hr or 12 hr fast.  The implication of this is that it is a measure of basal glucose levels.   Probably more than any other parameter, this one is subject to any manner of fluctuations and can vary 10-20 points mg/dL or more from just one aberration in eating the day before.  Also the degree of activity and length of time since awakening can dramatically alter FBG as can one's stress levels, medications (even an aspirin) and sleep patterns.  This is not going to make as much of a difference with an untreated frank diabetic as their overactive glucose production by the liver likely dominates.  But for the non-diabetic, it is easy to have a "bad day" exceeding prediabetic thresholds.  

2.  Oral Glucose Tolerance Test (OGTT):  After a fasted period, the subject drinks a glucose drink of 75 g (sometimes 50 or 100 g) and the blood glucose levels are measured periodically for 2-3 hours after.  The type of  information reported for this test is
a.  2-hour Glucose:  Compared to a threshold to which the BG level should have returned to in this timeframe is established for the dose of glucose.  
b.  Peak Glucose Response: The "spike" level from baseline
c.  Glucose AUC:  The "area under the curve" quantifying the total glucose exposure over 2-3 hours
The results of this test can also vary depending on length of fast and even be impacted by a large meal the night before.  Excessive spiking or delayed glucose clearance garner an impaired glucose tolerance (IGT) diagnosis.  Chronic low carbers generally know to "carb up" for several days or more before testing this.

3.  Glycated Hemoglobin - HbA1c:  Since this is a proxy for average blood glucose levels over a period of 2-3 months, this is considered a better measure of overall glycemia.  If one had to pick only one measure, this would be it.   However there's a lot of misinformation out there regarding this parameter that, at the very least, deserves honest discussion.  

Interpretation of the Results ~ Diet v. Pathology:

1.  FBG:  Elevated FBG is indicative of hepatic (liver) insulin resistance.  One role of insulin in the body is to suppress endogenous glucose production by the liver through gluconeogenesis and/or glycogen breakdown.  This parameter is NOT influenced by the content of the diet directly except perhaps in extreme conditions (massive overfeeding).  Rather a diet that promotes hepatic IR may indirectly influence FBG.  No matter how poor your insulin response to carbs, this diet-derived glucose is long gone before the requisite fasting period ends.  

2.  OGTT:  None of these can distinguish between pancreatic insufficiency vs. peripheral IR independently.  A time course of insulin levels is required.  
a.  Generally 2-hr glucose is the best measure of peripheral IR, and/or in conjunction with peak or AUC data.  A shallow slope on the tail end of the peak is more indicative of IR.
b.  Peak data generally helps identify those who are not truly on the path to garden variety T2 and likely exaggerated spikes are due to insufficient insulin response.  
c.   AUC also generally more effective in indicating IR.  
As with FBG, this is only influenced by one's habitual diet inasmuch as that diet impacts one's insulin resistance/sensitivity.

3.  HbA1c:  Depending on the eating habits of the person (especially hypercaloric states vs. weight stable or reducing) this parameter may well miss those non-true-T2's or even the mildly IGT.  There are subsets of "pre-diabetics" who are IGT without having elevated FBG and vice-versa.  A slightly elevated HbA1c could be due to either or both.   Underlying IR combined with a SAD style diet (high in carbs and fats) will almost inevitably increase this parameter.

Consistency Please!!

If you've heard it once, you've probably heard it a thousand times:  correlation does not equal causation.  And yet it seems that this only applies in LLVLClue-land and related terroirs* to metabolic abnormalities they wish to explain away, and not to those that "prove" hypotheses held dear.  Let us look at the analogy of LDL/cholesterol.  Let me state upfront that I do not believe cholesterol "causes" heart disease, that it clogs the arteries or anything of the sort.  LDL is a symptom of the underlying pathology (or pathologies) that actually causes the detriment to the cardiovascular system.  However, in the context of "usual diets", almost every study shows some correlation with good old-fashioned LDL-C and CVD-risk/incidence.  For all the special tests looking at particle sizes and particle numbers, these correlations persist.  It turns out other lipoproteins tend to be even better predictors, but, sorry, the data shows what it shows.**

So, too, we must view interpretations of glycemic data with equal skepticism.  IS it the glucose causing all ills?  I would contend that since lipotoxicity (at least a low grade, perhaps better termed lipidisruptivity) precedes hyperglycemia that we do not see glucotoxicity absent lipotoxicity.  I've presented a lot of evidence that hyperglycemia is the "endgame" symptom in this cascade and I'll be glad to provide those cites to new readers who request them in comments (or you could use labels or search the blog there on the right).  So yes, glucose and lipids (NEFA specifically) do directly damage cells.  But do they exert these actions at just slightly high-normal levels?  Put another way, is ANY degree of glycation necessarily detrimental?  Rosedale and Davis seem to believe so.  I'm not seeing the evidence in the studies these two put forth in their respective blogs and books.   Insulin resistance in and of itself may be the problem and what "causes" increased risk w/o frank diabetes.  I'm even willing to bet it is the channel through which all metabolic risks of this nature flow.

I'll go a step further as regards blood sugar levels and say that it should absolutely NOT be Paul Jaminet on any sort of "hot seat" needing to defend that starches are "safe" to consume.  It is Rosedale, Davis and the rest of the Science Krispies, as I call them, who must substantiate their own wild claims and defend their assertions, not the other way around.  Human beings, all but an infinitesimally small percentage of them, have been consuming far more than 100-150g starches -- "safe" according to Paul (free/limited toxins) or otherwise -- to no ill effect, and, indeed thriving.  

Do I think a SAD-eating pre-diabetic should eat more carbs to rectify their situation?  Of course not.  But I challenge any of them to eat Paul's excellent PHD and not see improvement.  More importantly, this improvement should last, and, if anything at some point a few more carbs and less fat might be in order for some.  Something that is not vilified in PHD terroir. 

As for Jimmy Moore?  Paul Jaminet is not a medical doctor, but his diet could be just what the doctor ordered.  Pity that he punted here.

*Terroir - From the French meaning "land", an "ism" from Leptin Man.  Plural is terroirs via Wiktionary.
**Yes, I'm aware these correlations are sometimes positive in nature, something I consider a good thing in my "woman of a certain age" condition and aging fast!


Christopher said…
Wow. This deserves a wider audience...
Harry said…
Thank you very much for this post, excellent account of the complexities that attend using proxy markers for glucose metabolism (and indeed, for health in general).
You are doing some excellent and valuable work here.

CarbSane said…
WOW ... Thanks Guys!
Galina L. said…
Thank you very much. Your post definitely helps with whole confusion about BS issues. I sometimes wonder, how the number of 140 mg/dL was determined to be the max appropriate level of raised BS.
@ Evelyn your Leptin Man rendering never fails to crack me up. The "Q" on his chest is an especially nice touch. :) "Leptin to leap puffy quilts in a single bound!
Lerner said…
Galina, the choice of 140 is explained in the study cited yesterday: in short, that is the threshold where retinopathy occurs-->

I'll also point out the final sentence there: "These results [on mortality] do not challenge
the existing diagnostic criteria for diabetes
of 7.0 mmol/l for fasting and 11.1 mmol/l
for 2-h glucose concentrations, which were
based on data that showed a sharp increase
in retinopathy incidence and prevalence."
CarbSane said…
Thanks Lerner -- And I would point out that a "spike" to or even above 140 following a meal is nowhere near analogous to a fasting level. Nowhere near!

@FTD: You mean able to leap tall levees in a single bound right? LOL. Look! Up in the sky! It's a BAB*, it's a Quilt ... No! It's Leptin Man!

*BAB is his acronym for big ass breakfast
David Pier said…
Regarding HbA1c, there is quite a bit of individual variation in the half-life of hemoglobin that can cloud interpretation a little bit. An additional useful measure is fructosamine, especially when corrected for total blood protein level. Fructosamine is a reaction product of glucose and various blood proteins, and measures a shorter time range of blood glucose than HbA1c, but is unaffected by red blood cell turnover.
Galina L. said…
The study doesn't prove at all that BS level of 140 is a threshold for a retinopathy. Also, two hours after a meal is very different than one hour. Once I registered 245 after a bowl of pasta in one hour after my meal. In 2 hours it fell to between 120 and 130 . Can't blame Jimmy if he wants to be on a safe side. I don't know what kind of reaction he has now. Retinopathy is not a joke. It would be nice to know when and how it starts.
CarbSane said…
@Galina: " Retinopathy is not a joke."

Well of course it's not. Scaring people into thinking that pp glucose levels in the mid 100's is going to destroy their bodies is not a joke either.

Is Rosedale's rhetoric helping to answer when and how retinopathy starts? I don't think so.
CarbSane said…
@David: Good point. I came across some studies comparing mean blood glucose with HbA1c and showing considerable differences between individuals. There appears to be a "glycating phenotype" out there.
Diana said…

May I ask, how big was that bowl of pasta? Do you guesstimate that it was a cup of cooked pasta? The average US portion size is double that. (My guesstimate, not a scientific survey). Then there is always seconds.

If you ate half the portion, would your BG have spiked to 245?

Does anyone here see what I'm after?

Portion size.

When Jimmy says that pasta is an unsafe starch, maybe what he's really saying is, "Two cups of cooked pasta, with a cup of meat sauce topped by 2 ounces of parmesan is unsafe." In which case I'd agree with him. That's a shitload of calories, a lot of carbohydrate and a lot of fat. Give your poor liver a break and cut the portion in half!

American portion sizes are un-f*ckingbelievable. They don't eat portion sizes of pasta in S. Italy the way they do here. What they call a portion we call a nibble.

However, if eating a reasonable sized portion of pasta is still sending your BG to 245 then don't eat it.

It's like me with gluten and lactose. I don't have celiac disease. I'm lactose tolerant. But I'm not gonna eat a loaf of bread and chase that with a bottle of FF milk because it's gonna make me fat.
Galina L. said…
Of course, it is a scaring rhetoric by sound of it. There is no proof the BS of 140 of short duration is dangerous. It is what nobody knows much about it for sure. Honestly, I don't think I am in a danger. No one in my family had such problem. Looking on my 92 yo grandma with Alzheimer gives me more creeps. Probably ,the best way to avoid it - escaping an old age by smoking or something similar.

I was served that pasta by the lady of the house, she prepared it with the pesto she made herself - it was the rare situation when I didn't have a choice. Probably , it was 1.5 - 2 cups. I would choose differently.I avoid wheat in general because of the possibility it may contribute to the progression of my Hashimodo thyroid decease. Anyway, I think people can do almost anything as an exception. Everyday choices are way more important.If I eat small potato with my meal, BS after one hour is usually 165. Which is not horrible for short period ones a day, on my opinion.I tried to experiment out of curiosity after more than 3 years of VLC what effect carb eating would have on me now. Actually, some old problems like abnormal hunger and desire to do grazing didn't return, but I experienced noticeable drop in energy after meals with starches, especially if combined with fruits. Pounds also started to creep back, migraines got slightly worse... I will repeat my experiment in a future as an Atkins-style reintroduction. Usually I am reasonable with my portions, I spend just a little more than 10 years in America, and local portions are not the norm for me.
Diana said…

It's difficult to communicate on the Internet. Things come out more abruptly than they would with words, in person.

Just to be clear - I'm not dumping on you or criticizing you, just pointing out that Jimmy Moore's crusade against "unsafe starches" without talking about portion size and exercise levels is ludicrous.

In Jimmy's world, eating a slice of bread with fried apples and a pecan log, after which you stagger to your car and drive home, is the same as eating a bowl of rice and bicycling home.

CarbSane said…
@Galina: Just curious -- was the 245 pp glucose when you were habitually doing VLC-ketogenic diet? that seems high no matter how big the bowl of pasta. So this does emphasize what Kurt was saying in comments on another recent post. Chronic VLC can make us have a "diabetic" response to a normal glucose challenge. I understand you're not one who does this often, and there's little to no chance any one incidence of this nature is even remotely harmful, but what of those who do. There are many low carbers who struggle week in and week out and "fall off the wagon" in the form of binging on carbs.

I find the rhetoric to be harmful in this regard. It's scaring people needlessly on a level far worse than the fat phobia ever imagined.
Galina L. said…
Of course, I had that abnormal BS reading because I ate the pasta while VLC eating and my body reacted in a such way because right now I am physiologically IR. All according to Dr.Kurt Harris. I am sure, if I start eating at least 1 cup of pasta a day, I would reverse it. I am glad we are having that discussion and you are posting recently a lot about blood glucose levels. Right now my diet is solving my health problems and I don't want to change it because some numbers look scary. I was thinking - should I try to dial with BS numbers? More understanding brings more realistic outlook. Thank you again. Sorry, I couldn't answer more quickly due to family obligations.

Diana, I understand. I didn't take anything you wanted to say as a criticism. I am not following Jimmy's ordeal very closely, but I read all posts about "safe carbs". My opinion about it - if somebody is in a ketosis a lot and decided to reintroduce starches, start slowly together with increasing exercise. Evelin is right to remind us that BS could rise due to several reasons.