"I have a 'cheat' day once per week--Is that okay"

If you are trying to eradicate one of the REAL causes of risk for heart disease, small dense LDL particles, is a once-per-week "cheat" day allowable? Can you get away with it by exercising more the following day, or being extra strict? 

No. Unfortunately, small dense LDL particles are unforgiving and persist for an unusually long period in the bloodstream, thereby adding to risk for cardiovascular disease. 

Transcript

Small Dense LDL Versus LDL Cholesterol

William Davis, MD 0:00

What I'm referring to is people who are following my programs to eradicate the production of small dense LDL particles, the real, among the real causes of coronary disease, played out in nearly 60 human clinical trials now, but swamped by this overwhelming obsession with LDL cholesterol, this crude, indirect surrogate marker for the lipoproteins, the fat-carrying protein in the bloodstream that actually do cause heart disease, especially in the company of other factors like insulin resistance and inflammation and vitamin D deficiency, omega-three fatty acid deficiency, endotoxinia, a bunch of other factors. But the driver of a lot of this is small LDL particles. So one of the things we do in my programs is we eliminate the foods that trigger formation of small LDL particles.

Foods That Create Small LDL

William Davis, MD 0:54

Very simply. Now, what are those foods? Well, it's a very limited list. It's very simple, actually. Wheat, grains, and sugars, not bacon, not pork fat, not saturated fat, not butter. It's wheat, grains, and sugars. Wheat and grains, because they have a specific carbohydrate called emylopectin A, which is highly digestible. Which is ironic because most of the compounds that cause problems in humans from grains are indigestible or only partially digestible, such as the gliden protein and wheat germagglutinin, either indigestible or only partly digestible, and that's why they exert such toxic effects on humans. But the amylopectin A carbohydrate is the exception. It's highly digestible. That's why it raises blood glucose, blood sugar, so high, higher than table sugar ounce for ounce. But what I'm talking about is the capacity for amylopectin A in wheat and grains and sugars, fructose, sucrose, glucose, to trigger the formation of small LD. Now, it's not a direct process, it's an indirect process.

How Carbs Become Triglycerides And VLDL

William Davis, MD 2:00

In that, those carbohydrates, amylopectin A and those sugars, are converted by your liver by a very vigorous process. The liver is very good at this, converting those carbs and sugars to triglycerides. Recall that triglycerides are fats. So that process is called liver de novolipogenesis, the creation of new fats, because it takes those carbs and sugars and makes them into fats. Now, triglycerides sometimes accumulate in the liver. That's the origin of fatty liver. But triglycerides can also be released into the bloodstream by the liver. Now, they can't release them directly into the liver because triglycerides are fats, and fats, if they floated freely in your bloodstream, would coalesce and thereby plug up the capillaries of your organs and you would die. So the liver knows to package your triglycerides, these new fats, de novalipogenesis, into a water-soluble protein-containing particle called very low density lipoprotein. It is rich in triglycerides, but it also has factors that solubilize that particle, the VLDL particle, in the aqueous or water-based bloodstream. So it doesn't plunk up your organs. Well, that VLDL is itself able to contribute to the formation of atherosclerotic plaque in places like the coronary arteries, the heart's arteries. But there's a very complex interaction that's been worked out by scientists over the decast few decades, and that is the VLDL particle that floats in the bloodstream now, interacts with LDL particles. And not LDL cholesterol. Cholesterol is just a marker. The actual particles themselves, the lipoprotein particles themselves. So VLDL particles interact with LDL particles. It contributes triglycerides to those LDL particles, then there's a series of enzymatic reactions performed by enzymes such as lipoprotein lipase, hepatic lipase, cholesterol estrotransfer protein, and a number of other that convert that triglyceride-enriched LDL particle into something smaller.

Why Small LDL Is So Dangerous

William Davis, MD 4:16

Now it's not just about size. Yes, smaller LDL particles are better able to infiltrate into the walls of arteries and contribute to atherosclerosis, but there's more to it than that. That smaller LDL particle is much more prone to glycation, glucose modification. So you can see that consumption of carbs and sugars is a double whammy, right? Raises blood glucose that in turn glycates those small LDL particles, making them more atherogenic. That is more likely to cause atherosclerotic coronary disease and disease in other arteries. The small LDL particles are also more prone to oxidation. The cholesterol residues are much more prone to oxidation, which makes them even more aggressive in causing coronary atherosclerosis. Small LDL particles have a different surface conformation because of the loss of all those triglycerides. That means the apoprotein B, one of the primary proteins in that LDL particle, that's supposed to be exposed on the surface so that the liver can recognize it and then grab it, clear it from the bloodstream, which it does if it's a very large LDL particle, as would be caused by consumption, say of bacon fat or butter or other or other fat. When the LDL particle is small, the apoprotein B, its surface exposures change, its conformation has changed, and the liver can no longer recognize that apoprotein B well. And so that small LDL particle with its partially concealed apoprotein B circulates in the bloodstream, not cleared by the liver, and it persists for five days, perhaps longer, in certain genetic variations. It persists for a long time. Meaning, you know, your blood circulates over and over and over and over, every minute, every hour, every day. If there's a persistent small LDL particle that is lasting about a week, it's given huge, prolonged opportunity to enter the arterial wall and trigger the formation of atherosclerotic plaque. It gets even worse. When that small LDL particle is able to infiltrate into the walls of arteries, it's more likely to provoke inflammation, it's more likely to attract the deposition of monocytes and macrophages, those are the white blood cells, inflammatory white blood cells, that contribute to the inflammation and the expansion of atherosclerotic plaque. So small LDL particles, very perfectly crafted to cause atherosclerosis.

The Cheat Day Problem

William Davis, MD 7:00

So back to this question. Can you have a cheat day? Well, you may have gathered if one exposure, so let's say you had one exposure, something that contains the amylopectin A of wheat or grains, or perhaps some sugars in a snack or a dessert, where you're gonna have small LDL for about a week, five to seven days. So that one exposure gives you a week's worth of cardiovascular risk. And if you have a cheat day once a week, you've got essentially 52 weeks a year of a markedly, markedly increased exposure to cardiovascular risk and expansion of atherosclerotic

Real Patient Lab Results

William Davis, MD 7:44

plaque. I learned this a long time ago. When I had people, I would put them on the diet. So we do an NMR lipoprotein panel, for instance, right? And their starting panel showed, and these are people with coronary disease, they suffered sudden cardiac death, they suffered a heart attack, got a stent of the right coronary artery, or their LAD, left anterior descending, or they survived bypass surgery, or whatever. They had known coronary disease, they wanted to get rid of it, put a stop to it, stop its progression. And of course, conventional methods don't work, they hardly do anything. Statin drugs, low saturated fat, all the garbage advice people are given. So we do an NMR lipoprotein panel, and among the findings is small LDL particle number of, let's say, 1800 nanomoles per liter particle count per volume, which is very common. It's almost the virtually the rule in people with coronary disease. So maybe their total LDL particle number, big and small and medium, is maybe 2400. But the small LDL particle number within that 2400 is 1800. So the majority, 1800 over 2400, are the small particles. That person goes wheat, grain, sugar-free. We do all the other things to influence insulin resistance and inflammation, vitamin D, omega-3 fatty acids, magnesium, iodine, address the microbiome, right? Gastroentastal microbiome. Small LDA drops from 1800 to maybe 700. So much better. Not perfect. We're aiming for 200 or close to zero as possible. So I asked my patient, are you sure you're doing the diet? Oh yes, I am. I'm doing everything. Are you sure? Well, every Friday I have a bed, I have a cheat day, and I have one slice of pizza. And so I figure that can't hurt, right? On Saturday, I'll exercise an extra 20 or 30 minutes. I'll go for an extra long walk. I'll eat extra clean. It doesn't work that way, right? So I learned this the hard way, and the evidence bears this out. And this is not just based on my experience in thousands of patients. It's been borne out by the evidence also, that small LDL particles have an extended, we say half-life, how long it endures in the bloodstream. So that one slice of pizza on a cheat day on Friday was enough to cause residual, substantial residual persistence of the small LDL particles. It was better, yes, but it was still persistent at a level sufficient to allow the further expansion of carnal athertic plaque and thereby risk for such things as heart attack, sudden cardiac death, and development of symptoms that justify more procedures.

Building A Sustainable Grain-Free Plan

William Davis, MD 10:27

And so it really helps. So when I say try to limit your net carbs in my programs to 15 grams or less, net carbs, not total carbs, net carbs, and we address all those factors in insulin resistance and inflammation, and we restrict ourselves to no grains, no sugars, but unrestricted fats and calories, right? We stick to it because going off program is not just a matter of a few hours or a few days, and you cannot undo it with exercise or a better diet to compensate the next day. Because once you provoke the small LDL particle, it's persistent. It's sobering. Having done this in thousands of patients over the years, I learned that it was painfully easy to provoke a flood of small LDL, it was very sobering. But it also told you that strict adherence to this approach was extremely effective. Now it doesn't mean the diet is restrictive, right? Because you can still have all the olive oil you want, butter, you can eat the fat on your steak, uh, you can eat the skin on your salmon or your chicken. We're not going to restrict calories. If you want to have a pizza or muffins or a birthday cake, you can have it, but we're going to make it using alternative ingredients, right? So if you don't know what I'm talking about, see my cookbooks, my wheat belly cookbooks, almost all my books have some recipes in there. So, bottom line the diet is not restrictive, but it's selective.

Final Warning About Cheat Days

William Davis, MD 11:55

We avoid the foods that cause the provocation, the formation of small LDL particles, and that's how you gain control over cardiovascular risk. But don't give yourself that one cheat day, it's just not worth it.