Jimmy Moore asked an array of people in LC circles for their thoughts HERE
The subject of this installment is Dr. William Davis of Heart Scan Blog.
The focus cannot be only on insulin. Glucose itself is harmful via the process of endogenous glycation, i.e., glucose-driven modification of proteins. The higher the blood glucose, the greater the glycation, with the process beginning at blood glucose levels of 100 mg/dl or more. Blood glucose after a 3-egg omelet is typically 95 mg/dl. Blood glucose after a bowl of slow-cooked, stone-ground oatmeal is typically 150-200 mg/dl in non-diabetics.
Firstly, kudos to Dr. Davis for saying the focus cannot be only on insulin ... but ... then what does the rest of this have to do with James' series on the demonization of insulin??
That aside, I would like to address these numbers he throws out there. I have far from an ideal metabolism and after a bowl of oatmeal my BG peaks around 120 on a bad day. An omelet? My BG might go up 10 pts if my glucose is in the low-mid 70's before hand, but not at all if it's in the 80's. Of course that's anecdotal but I'm not seeing where a *normal* person goes much higher. (Oh, and BTW, since Zoe Harcombe has a bowl of plain oat porridge for breakfast every day ........)
The difference is striking. Higher blood glucose means glycation of lens proteins (cataracts), small LDL particles (atherosclerosis), kidney tissue (kidney disease), skin (wrinkles).I would like to see some studies on glycation for acute blood glucose levels. Granted, longer lived biological molecules may sustain accumulated damage over time, but once the glucose level goes back down, there's no reason for glycation to not reverse itself. Glycation is governed by equilibrium kinetics. Higher concentration of two compounds, more attachment ... lower concentration, detachment!
And, of course, fats do not trigger insulin nor glucose to any substantial degree (unless filled with heat-generated exogenous glycation/lipoxidation products as in deep-fried oils).
True, but Dr. Davis totally ignores the fact that VLCHF meals, as we've discussed before, fail to properly suppress the release of free fatty acids leading to elevated postprandial NEFA. These have consequences that can be as deleterious as glycation if not more. So here we have a whole goose-gander thing going on. Both elevated NEFA and BG can be blamed for various maladies associated with diabetes, MetS, etc. So:
- Focusing on just one of the culprits is short sighted
- If postprandial transient elevated glucose levels are an issue with respect to chronically elevated levels, then so too are postprandial elevated NEFA levels.
As I pointed out in a study cited by Dr. Feinman, there IS a "hangover" effect for the elevated NEFA with low carb leading to elevated fasting and increased 24-hr exposures. This is not seen for "normal" or even diabetic individuals from eating a bowl of oatmeal! As pointed out by James Krieger in his series, elevated fasting BG is due to insulin failing to properly suppress gluconeogenesis. Yeah, if I'm messed up metabolically and I have a huge bowl of sugar sweetened oatmeal before going beddie bye my BG may remain a few or even several points higher by morning, but if I have a reasonable serving and have not turned myself into a "carb cripple" with chronic VLCHF eating, it's not going to last more than a couple of hours.