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.
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.
**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!