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!)

Monday, December 20, 2010

Insulin Wars VI: Dr. William Davis of Heart Scan Blog

I thought I would share some thoughts on some of the responses of LC "experts" to James Krieger's excellent series on insulin.  For any who missed them, here are the links  “Insulin…an Undeserved Bad Reputation”, Part 2,Part 3, Part 4Part 5.

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.  


Frank said...

I can't remember the post, but I clearly recall Dr. Davis writting a post on the negative effect of elevated post-prandial NEFA, where he was saying that it might be even worse than glucose, and was telling his reader not to overdo the fat. It had cause quite a stir on his blog in the comments section.

Funny that he does not say anything about it here.

Now, if elevated NEFA are bad, elvated glucose is bad, and high-protein diet are probably not optimal as far as longevity is concern, what is left, again? Controlling calories... and if calories are so much not important, i'm wondering why only calorie restriction has been shown so far to increase lifespan, not protein restriction nor glucose restriction. Certainly calories are irrevelant when it comes to metabolism!

Sanjeev said...

how does one "focus on" insulin anyway?

Since it's not easily measureable most folk measure glucose.

it's been a while since I read him; he could have changed his approach which used to focus hugely on insulin.

CarbSane said...

He's pretty obsessed with wheat these days and not so much for the toxic/addictive aspects but because it's highly insulinogenic. He caused quite a stir a while back when he pegged butter as fattening because it does provoke an insulin response. So in way he's probably as obsessed as ever. But he seems to really obsess over glucose levels to an extreme with no apparent evidence for it while ignoring NEFA's. Surely as a cardiologist "know it all" he's aware of the issues surrounding them and CVD?

CarbSane said...

Hit post too soon. Wanted to add that it's one of the bigger pet peeves of mine when I see folks post about their insulin levels when they are measuring glucose. A T2 diabetic has an impaired phase 2 spike which is why carbs elevate BG and in the first place.

Sanjeev said...

I might get on the anti-wheat bandwagon too.

One thing I note about the Masterjohn/Minger critiques of the China study: this is fine for critiqueing Campbell:

"the study had x number of variables, and just by coincidence you could expect to find y number of correlations to disease"

Yet I've not (yet) heard this applied to Ms Minger's work (quite an impressive corpus, but that doesn't justify a double standard)

MM said...


You wrote: "Glycation is governed by equilibrium kinetics. Higher concentration of two compounds, more attachment ... lower concentration, detachment!"

Glycation is reversible?! Wow, this is news to me. Is there a study about it, or is this just basic biochem that I would know if I had bothered to take it in college? :)

Thanks for the great info.

Nigel Kinbrum said...

There are three steps in the formation of an AGE. The first two steps are reversible but the third isn't. See Amadori product

CarbSane said...

Thanks Nige, sometimes wikipedia can boil things down nicely. I should have been more specific that there was a progression. The first one is governed by equilibrium kinetics, there's no reason to believe that glycation occurs any more rapidly while BG is elevated for an hour or so than in it reverses once BG subsides. I don't have data, but it's not a rapid reaction from what I can gather (if I'm wrong on that please correct me folks). The problem for diabetics is constantly elevated glucose levels so that whatever small amount of first-phase glycation might occur during a sugar spike can't subside. I think Davis is being a bit over the top with his 100 cut-off.

CarbSane said...

I don't eat much wheat myself, but until I can make my own wheat free tortillas, the LC ones will have to do. I don't seem to have any reaction to it. I've not looked at the China study stuff as of yet, but yeah, I've noticed a bit of a double standard where correlations are concerned ;)

Davis seems to be obsessed with belly fat and love handles all caused by wheat.

CPM said...

Re: Minger/Campbell

I don’t really see the double standard myself. Minger constantly emphasizes that correlation is not causation and all that she is doing is developing a hypothesis to be tested, while Campbell argues that cherry-picked correlations are hard evidence that his “plausible biological model” is correct.

Campbell’s theme you see in The China Study, his blog posts, his articles, and his letters to the editors is that we need to move past “reductionist” science and embrace a “holistic” science (that he bemoans is not currently allowed in his peer-reviewed material). In Campbell’s new holistic science, hypotheses need not be tested. In fact, as long as you have a “plausible biological model” (i.e. hypothesis) you are encouraged to pick and choose whatever spare correlation you want and use this as hard evidence that your model is correct (sort of like Creationists do – you have a model that the Earth is 6000 years old, and you throw out dinosaurs because they are “uncorrected” correlations.) He says this point blank:

“In summary, I agree that using univariate correlations of population databases should not be used to infer causality, when one adheres to the reductionist philosophy of nutritional biology and/or when one ignores or does not have prior evidence of biological plausibility beforehand. In this case these correlations can only be used to generate hypotheses for further investigation, that is, to establish biological plausibility. If in contrast, we start with explanatory models that represent the inherent complexity of nutrition and is accompanied by biological plausibility, then it is fair to look for supportive evidence among a collection of correlations,…”

Sanjeev said...

I'm sure Denise Minger would be the first to repeat "x number of variables, so expect y correlations purely by chance. I was just noting I had not read it applied to her work YET

> when one adheres to the reductionist
> philosophy of nutritional biology and/or


His reductionism stuff sounds identical to Bruce Lipton's, for whom vibrations (not substrates) activate enzymes and ESP is plausible, and "quantum pixie dust" spread over all your problems explains how all woo-woo works (even absent proof that it works at all)

CarbSane said...

@CPM: I should have been a bit better with my wording because I haven't read enough about the China Study to comment on Campbell or Minger. I was referring to the tendency of folks "picking up the ball and running with it" at times. Many who are quick to dismiss correlation = causality for things that don't confirm their beliefs seem oblivious to the hypocrisy of touting correlations as causations for things that confirm their beliefs.

LOL, if you really want to make your head spin Google proving causality and find some of the statistics discussion forums. Wowzers!

CPM said...

"picking up the ball and running with it"

Oh, I can see that. That’s kind of what the diet industry is all about. I tend to avoid the people that get too dogmatic about it, though I might find myself joining in at times - as soon as Chris Masterjohn posted his blog about choline deficiency and fatty liver disease, I started eating eggs every day. But I do realize a lot of nutrition (like Paleo) is just a hypothesis, and I try to remain pretty open-minded and agnostic to it all.

I just thought there was a striking contrast between someone constantly emphasizing the point that correlation is not causation while an emeritus professor at Cornell was going all mumbo-jumbo holistic pseudoscience.

CarbSane said...

Oh, I can see that. That’s kind of what the diet industry is all about

It's what media is all about :( Every day we get that this study or that showed this or that. I ignore anything where "not statistically significant" is demonstrated, because even statistical significance doesn't always translate, therefor I'm not going to worry about those studies that don't even reach that measure.

I've had rows of sorts with folks who post the emails of researchers in their "debunkings". I will point out that the actual conclusions of the study were solid, it was the media report that distorted them. I've been told it should be incumbent upon the researchers to set the record straight. Yeah, maybe, but do they have to answer to every quack who distorts their results to meet some purpose?

Regarding obesity, I think the focus needs to be separated:
1. How do we help those who are currently of normal weight prevent becoming obese. versus
2. How do we help those who are obese reverse their situation.

I propose that (1) and (2) may share some similar approaches, but that what's good for (1) may not have much impact on (2) and vice versa for all factors.

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