Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Monday, January 4, 2010

Dr. William Davis' postprandial atherogenic particles hypothesis

 See the following comment and Dr. Davis' response.   What do you think?


Mark said...

Hey Stan.

Dr. Davis wrote:
"The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats."

We don't see triglycerides being converted to glucose. It's a one way street.

Would having increased carbohydrayte storage space in the body be preferable to storing triglyceride? We have an example of that in hyperglycemia. That's storage in the bloodstream. But the body works quickly to CORRECT that.

So it's not that the body lacks glucose storage and triglyceride is the bad alternative. Not that at all. The body works hard to push glucose out of blood storage and into triglyceride in fat cells. That's a good thing.

Postprandial high triglycerides from a high fat diet is a marker of fat intake. Postprandial low triglyceride on a high carb diet is a marker of carbohydrate metabolism. The later increase in triglyceride is the corrective process.

It's hard to make the case that triglyceride is itself bad when it's one of the body's innate responses to the bad hyperglycemia. If triglyceride is bad, then the body is stuck between a rock and a hard place. It's win-lose, so the low fat diet is worse than the low carb one.

Given my experience with dieting, I would favour low carb over anything balanced in the way of fat/carb. From dietary intervention trials, I'm unconvinced that high fat is worse (or much better) than a mixed blend of carb and fat from a mortality perspective. But from experience, I favour low carb for general sense of well-being.

Stan wrote:
"Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease. That I believe has nothing to do with dietary fat."

It's tough to isolate lipids as causal as opposed to effects of diet. Smoking and fructose lead to increased LDL. So in this case, high LDL is really a symptom smoking and fructose intake. The latter two likely being causal for anything related to your health. 8 egg yolks a day on a high fat diet and your LDL is a symptom of that. And some people have normal LDL on that even.

Did you see Peter's excession thread on hyperlipid? Something about genetic discontinuity in Europeans from 10k years ago to now. Relates to your last post.


Stan Bleszynski said...

Hi Mark,

My experience is similar and the motivation to stay on the low carb high animal fat nutrition is the same - well being.

Which of Peter's articles do you have in mind?

Mark said...

Hey Stan.

That's the article. I haven't looked through the full-text, though I downloaded it. It's:

I'll mail you the full-text.

A guy in my program lost 50 pounds in two months low carbing, although higher protein than JK would advise. My parents are both losing fat slowly on a paleo-like diet. I don't eat fruit myself, but I think that they would lose faster without it. I never had a problem with fat, although the first place I gain it is in the face so it's incentive never to gain any. But it's helped with body aches I get and with fallin asleep in the day and I am much more focused now. I also have much better memory and can think much more clearly. There's been no better improvement in my life than from low carbing and high fatting.

I question whether a JK diet does anything for mortality, but that's the least of my worries. Living to 70 instead of 80 is blah when your happiness is at stake.


LeenaS said...

Hi Stan

Is it not so, that the measured "triglyserides" i.e. the measured VLDL include also chylomicrons (should there be any in the blood stream) and not only their remnants?

If so, Gretchen's LCHF "triglyserides" shows the natural and harmeless effect of fat indigestion: in about one hour or so, most of the eaten fat, transported as chyhomicrons, has found its way out of the blood stream, to be used as fuel or into storages... which is exactly as it should be :)

And b.t.w., thanks for your blog from a freqauent visitor from Finland. We've been on LC since 2000, and the last three years on OD type diet.

With best regards,

Stan Bleszynski said...

Hi LeenaS,

Thanks for encouragement and welcome to the blog!

I am also on OD since 1999 and very happy about the way it keeps me energetic and healthy.

I agree, postprandial triglycerides from chylomicrons (dietary fat) are the totally different population than those manufactured in the liver out of glucose and fructose following a high carb meal. Nevertheless I also doubt if even the sugar-manufactured triglycerides would be harmful, I think it is the primary effect of sugar, excess carbohydrates (of any kind) and excess insulin that is the main cause of problems. In addition, direct and indirect effects of chronic and excessive load of carbohydrates upon the liver, pancreas, thyroid, adrenals, ovaries (in women) and kidneys are damaging.


Peter said...

Hi Stan,

I absolutely agree, the two pictures in Dr D's graphs are utter opposites. I too would also doubt that the apoB100 on the VLDLs is any more "toxic" than the apoB45 on the chylomicrons. What matters to me is the blood glucose, spiking to 200 is killing endothelial cells, and the blood insulin (not shown but certainly spiking with the glucose) which drives the repair process beyond what is appropriate for the amount of damage done by the hyperglycaemia... And if we must include lipids we can always suggest the hyperglycaemia glycoxidises either apoB100 or apoB45 to give persistent remnants which cannot be taken up by the LDL receptors, only by RAGEs. In the latest lipid hypothesis these are the problem ones. Of course, to lipophiles these persistent remnants are markers of previous damaging hyperglycaemia, not necessarily the problem in its own right.

Dr D does good things, and looks for feedback from CACS, but he still seems deeply entrenched in the lipid hypothesis. TYP does a lot to address glucose and insulin issues while worrying about lipids!

All the best, have a great year as the nights draw out, fantastic clear winter weather over here.

Peter (just starting to resurface!)

Carlos Monteiro said...

Hi Stan, I think you are mostly right in your view regarding high carbs.
Follows some highlights from the acidity theory of atherosclerosis (1, 2), where stress and glucose metabolism are the main factors according our view:
1. The heart is an organ of high metabolic activity, susceptible to drops in pH during ischemia and hypoxia. The chronic or acute elevated catecholamine release may accelerate the myocardial anaerobic glycolysis leading to significant increase in lactate production.
2. Either in essential or renal hypertension the concentration of lactic acid in both venous and arterial blood may be significantly elevated.
3. Lactic acid in the blood plasma is significantly elevated during stress situations and serving as indicative of stress levels;
4. Ingestion of glucose, fructose and other sugars may have the effect to raise blood lactic acid with this increase being most marked and lasting longest after fructose, that is largely used as sweetener in soft drinks, fruit punches, pastries and processed foods. Dietary fructose has also resulted in increases in blood pressure;
5. High carbohydrate diet may increase significantly the activity of serum lactate dehydrogenase
7. The autonomic nervous system is influenced by high-carbohydrate dietary, with greater sympathetic nervous activity.

Carlos Monteiro
Infarct Combat Project

1) Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at
2) Blog with new evidences about the acidity theory of atherosclerosis at

Stan Bleszynski said...


Welcome to the blog. I came across lactate hypothesis some time ago reading an article where the author argued that the only difference between arteries that get plaque especially in the locations that are stressed, and veins that never get it, is production of lactic acid in the smooth arterial muscles under mechanical stress.

On the other hand there is also Dr. Kwasniewski's hypothesis that atherosclerotic disease is caused by aerobic+anaerobic glucose metabolism through pentose phosphate pathway (PPP). Incidentally PPP leads to production of cholesterol and lipids in the affected tissues. Presence of cholesterol and lipids in atherosclerotic placque has baffled researchers so much that they blamed (and some still do) dietary cholesterol.

It is also possible that lactic acid - a byproduct of anaerobic glucose metabolism under hypoxia is just a secondary marker of the primary damage done - again - by the excessive glucose metabolism.

I think we can probably pinpoint the real sweet culprit...


Stan Bleszynski said...

Hi Peter,

I hope you are coping well with the sudden onset of Global Warming - oops - "Climate Change" . 8-:)

It is indeed pretty clear what the culprit is although there must be more than one way the disease progresses in details, otherwise it would be automatic and would affect everyone who consumes excessive sugar and starch in the same way and at the same speed.

I always like to remind myself that if everything seems too obvious and everyone agrees - then something has to be wrong.


Carlos Monteiro said...

Stan, I’m sorry if I didn’t make clear the basic mechanism in my first post. The acidity theory of atherosclerosis is inside the response to injury concept. It has the following sequence of events:
I. Sympathetic dominance by continuous stress plus
II. Deficiency in production of endogenous digitalis-like compounds with alterations of Na(+), K(+)-ATPase activity results in:
III. Lowered pH (acidity) that increases perfusion pressure and provokes effects on contractility of coronary arteries leading to changes in hemodynamic shear stress and atherosclerosis as consequence.
There are many and many evidences and supportive studies as you can see at the paper.

Stan Bleszynski said...

Hi Carlos,

It is an interesting hypothesis, thank you for mentioning it because (at least) it stimulates me to learn more about the subject.

I understand what you are trying to say, but (my humble opinion) I do not think that modification of sympathetic response and lower pH is the primary stimulus.

I suspect that those are secondary symptoms of excessive or abnormal glucose metabolism.

That in turns modifies the sympathetic response and causes other effects such as abnormal lipoprotein profile, abnormal insulin response to dietary carbs, elevates inflammatory markers, coincides with poor thyroid autoregulation, triggers abnormal adrenal response and other documented effects.

For example, consuming carbs does energise sympathetic system (S) while eating lots of fat boosts parasympathetic (PS) system.

Over-energized S does alter our reaction to stress. For instance, people on the high carbohydrate low fat diets are extremely prone to suffer panic attacks and feel often paralyzed under stress, have to be very careful about it. See Dr. Ornish program...

OTOH, the high fat low carb diet stimulates PS and is inherently stress-protective! Stress produces very different effects in us low carbers - it simply energizes us to action rather that having a paralyzing effect as for most people on the "normal" low fat diets! Dr. Kwasniewski wrote about that in his books. Through my experience I found that to be correct!

Best regards,

Carlos Monteiro said...

Stan, it is interesting your citation about high carbohydrate/ low fat diets are extremely prone to suffer panic attacks and feel often paralyzed under stress panic attack. Related to this follows a study showing some possible mechanisms that may contribute to the exaggerated lactate response to alkalosis observed in panic disorder:
“A variety of physiological or pathophysiological mechanisms may contribute to the exaggerated lactate response to alkalosis observed in panic disorder. Identifying the specific mechanism of this abnormal response may increase our understanding of the underlying pathophysiology of panic disorder. Three possible mechanisms suggested by investigators demonstrating this effect are 1) hypoxia secondary to cerebral vasoconstriction; 2) a disturbance in the regulation of intracellular pH; and 3) increased adrenergic activity”
1) The Lactic Acid Response to Alkalosis in Panic Disorder: An Integrative Review Richard J. Maddock, M.D.J Neuropsychiatry Clin Neurosci 13:1, Winter 2001. Full free paper at
2) Maddock RJ, Mateo-Bermudez J: Elevated serum lactate following hyperventilation during glucose infusion in panic disorder. Biol Psychiatry 1990; 27:411–418. -- Related to items 2 and 3.

Stan Bleszynski said...


Thanks for the links, I read the first paper. I am interested in this topic because I used to have tachycardia episodes, about once every couple of months, prior to 1999, that fit descriptions of a typical panic disorder (PD). Then 9 years ago it went completely away never to re-occur.

I still am not sure if lactate is primary factor or secondary by-product in PD. I suspect the latter. My favored theory involves adrenal-thyroid hormonal run-away effect triggered by hypoglycemia. That would go like this:

1. Hypoglycemia triggers adrenal hormones production to boost production of glucose out of glycogen in the liver. If glycogen is depleted, not enough glucose would be produced resulting in more (excessive) adrenal secretion.

2. Adrenal hormones boost also thyroid hormones, causing accelerated heart beat adding to the panic and stress feeling, that in turn may further stimulate adrenal hormones, and so on.

I have no idea how likely is the above scenario but that's best I could think of. No doctor I ever spoke to was able to come up with anything logical about PD that would explain the mechanism, other than the banalities such as "needing to relax" etc.


Carlos Monteiro said...

Stan, my father in law Dr. Quintiliano de Mesquita (his memorial is at had a theory to fight panic attack based in mind power. You can see his thoughts about it at, that is unfortunately in Portuguese language. Dr. Mesquita has also developed the myogenic theory of myocardial infarction which I have a section at the Infarct Combat Project dedicated to the subject at Please see in it the link to the article What Causes Heart Attacks?, by Dr. Thomas Cowan discussing the myogenic theory. It was published in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2007.
The acidity theory complements the myogenic theory in the coronary side.
Best regards