The myth of mild coronary disease

19. January 2008 William Davis (27)

I hear this comment from patients all the time:

"They told me that I had only mild blockages and so I had nothing to worry about."

That's one big lie.

I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?

"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild."

The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result.

So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture.

One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage.

Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up.

The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions.

Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)

17. January 2008 William Davis (24)

Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.

Vytorin study explodes--But what's the real story?

15. January 2008 William Davis (28)

The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Dr. Arthur Agatston in the news

15. January 2008 William Davis (7)

The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:
The South Beach Diet doctor takes on cardio care

Agatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III).

The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:

• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

• Do aerobic exercise, along with stretching and strengthening workouts.

• Ask your doctor about taking statins and other cholesterol-lowering drugs.

We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others.

But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this.

As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)

Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program.

That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.

Take this survey: I DOUBLE-DARE YOU

14. January 2008 William Davis (10)

In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed.

Here's what I said:

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.

But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible.

What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?

No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease.

But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries.

Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially.

I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am.

Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism

13. January 2008 William Davis (8)

The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book.

The new book is In Defense of Food: An eater's manifesto.

As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store.

In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."

In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:

"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters."

Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.

With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"

Cholesterol follies

11. January 2008 William Davis (5)

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.

So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.

If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

9. January 2008 William Davis (15)

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:

VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl

HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl

Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.

What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

6. January 2008 William Davis (19)

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.

But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.

Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

4. January 2008 William Davis (11)

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.

In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.

Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.

Copyright 2008 William Davis,MD

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Are you hungry?

6. December 2011 William Davis (43)

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

Chocolate . . . for adults only

30. November 2011 William Davis (22)

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.

I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

19. November 2011 William Davis (29)

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

14. November 2011 William Davis (73)

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

2. November 2011 William Davis (0)

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

30. October 2011 William Davis (53)

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

21. October 2011 William Davis (39)

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

19. October 2011 William Davis (33)

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

14. October 2011 William Davis (21)

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

14. October 2011 William Davis (6)

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI."

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

All posts by william-davis

Genetic vs. lifestyle small LDL

19. February 2010 William Davis (59)

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)

Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)

Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)

Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)

Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

17. February 2010 William Davis (15)

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

16. February 2010 William Davis (44)

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles

For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?

14. February 2010 William Davis (20)

University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

What Mr. Clinton did NOT do

12. February 2010 William Davis (36)

You've likely already heard that former President Bill Clinton underwent a heart catheterization today during which one of the bypass grafts to his coronary arteries was found to be occluded. The original coronary artery was therefore stented.

Dr. Alan Schwartz, Mr. Clinton's cardiologist, announced to the gathered press that Mr. Clinton had followed a good diet, had adopted a regular exercise program, but that his condition is a "chronic disease" like hypertension that is not cured by these efforts.

Needing a stent just 6 years after four bypass grafts are inserted is awfully soon. I would propose that it has less to do with having a "chronic disease" and more to do with all the things that Mr. Clinton likely is NOT doing. (In addition to all the other things that Mr. Clinton did not do.) In other words, in the Track Your Plaque world, procedures are a rarity, heart attacks virtually unheard of. I would wager that Mr. Clinton has been doing none of the following:

--Taking fish oil. Or, if his doctor was "advanced" enough to have advised him to take fish oil, not taking enough.
--Vitamin D--Followers of the Heart Scan Blog already know that vitamin D is the most incredible health find of the last 50 years, including its effects on reducing heart disease risk. Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. A typical dose for a man his size is 8000 units per day (gelcap only!).
--Eating a true heart healthy diet. I'll bet Mr. Clinton's doctor, trying to do the "right" thing, follows the prudent course of advising a "balanced diet" that is low in fat--you know, the diet that causes heart disease. Judging by Mr. Clinton's body shape (central body fat), it is a virtual certainty that he conceals a severe small LDL pattern, the sort that is worsened by grains, improved with their elimination.
--Making sure that hidden causes are addressed--In addition to the "hidden" small LDL, lipoprotein(a) is another biggie. Lp(a) tends to be the province of people with greater than average intelligence. I believe Mr. Clinton qualifies in this regard. I would not be at all surprised if Mr. Clinton conceals a substantial lipoprotein(a) pattern, worsened in the presence of small LDL.
--Controlling after-meal blood sugars--Postprandial (after-eating) blood sugars are a major trigger for atherosclerotic plaque growth. There are easy-to-follow methods to blunt the after-meal rise of blood sugar. (This will be the subject of an in-depth upcoming Track Your Plaque Special Report.)
--Thyroid normalization--It might be as simple as taking iodine; it might involve a little more effort, such as supplemental T3. Regardless, thyroid normalization is an easy means to substantially reduce coronary risk and slow or stop coronary plaque growth.

It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.

Magnesium and arrhythmia

11. February 2010 William Davis (35)

Because magnesium is removed during municipal water treatment and is absent from most bottled water, deficiency of this crucial mineral is a growing problem.

Magnesium deficiency can manifest itself in a wide variety of ways, from muscle cramps (usually calves, toes, and fingers), erratic blood sugars, higher blood pressure, to heart rhythm problems. The abnormal heart rhythms that can arise due to magnesium deficiency include premature atrial contractions, premature ventricular contractions, multifocal atrial tachycardia, atrial fibrillation, and even ventricular tachycardia, fibrillation, and Torsade de Pointes (all potentially fatal). Magnesium is important!

Magnesium supplementation is therefore necessary for just about everybody to maintain normal tissue levels. (The exception is people with kidney disorders, who should not take magnesium without supervision, since they retain magnesium.)

Here is a Heart Scan Blog reader's dramatic rhythm-correcting response to magnesium supplementation:

Dr. Davis,

A few months ago, I contacted you inquiring if you had written any articles on arrhythmia. You were generous enough to answer and guide me to an LEF article you'd written in which you stressed fish oil and magnesium. I had been suffering with bad PVCs [premature ventricular contractions] for over 20 years, and they had gotten so bad recently that I was told my next options were ablation or pacemaker!

I was already on fish oil and had not seen any difference, and so I researched the magnesium you suggested more thoroughly and found a huge body of studies supportng its effect on arrhythmia. I also read many posts on heart forums with people having success with it. After getting advice from various bloggers, I tried magnesium taurate in the morning and Natural Calm (an ionized form of mag citrate) in the afternoon and evening. Within three days the PVCs were quite diminished and by 2 weeks totally gone! As long as I keep taking it, they never return---not even one irregular blip---even when I drink strong coffee! The magnesium also cleared up my restless leg syndrome, my eye twitching, and insomnia. (Apparently, I was the poster-girl for magnesium deficiency.)

I am so angry that after all these years of suffering, trying various medications, and seeing at least 4 different cardiologists that NOT ONE ever even mentioned trying magnesium. The generosity of the few minutes you took to answer my email and steer me in a helpful direction brought me total relief.

Thank you SO MUCH!

Warmly,
Catherine C.

Video teleconference with Dr. Davis

10. February 2010 William Davis (4)

Dr. Davis is available for personal

one-on-one video teleconferencing

to discuss your heart health issues.

You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil

Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.

The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Thinner by Thursday

10. February 2010 William Davis (0)

You want to lose a few pounds . . . Okay, maybe 50 or 75.

Should you exercise? Lengthen you workout? Push the plate away, deny yourself seconds, use a smaller plate?

Of all the weight loss strategies I've tried in patients, there's only one that stands out as a means of obtaining immediate--meaning within 3 days--weight reduction.

Wheat elimination.

Omega-3 Index: 10% or greater?

9. February 2010 William Davis (19)

We've previously considered the question:

What is an ideal level of omega-3 fatty acids in the blood?

Recall that omega-3 levels in red blood cells (RBCs), a measure called the "omega-3 index," have been associated with risk for sudden cardiac death:

In a recent analysis, 265 people experiencing sudden death during a heart attack (ventricular fibrillation, successfully resuscitated) showed an omega-3 index of 4.88%, while 185 people not experiencing sudden death during a heart attack showed an omega-3 index of 6.08%.

We have more ambitious goals than just avoiding sudden death, of course! How about the omega-3 index associated with reduced risk for heart attack? A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks, suggesting that even higher levels are necessary to prevent non-fatal events.

Most recently, another study comparing 50 people after heart attack with 50 controls showed that people with heart attack had an omega-3 index of 9.57% vs 11.81% in controls--even higher. (This study was in a Korean population with higher fish consumption. There was also a powerful contribution to risk from trans fat RBC levels.) The investigators concluded: "The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors."

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

I believe the emerging data are becoming increasingly clear: If you desire maximal control over heart health, know your omega-3 index and keep it 10% or higher.

Let's soak 'em with fish oil

8. February 2010 William Davis (12)

If you don't think that charging drug prices for fish oil is wrong, take a look at a letter from an angry Heart Scan Blog reader:

Hello Dr. Davis,

My 44 year old brother had an MI [myocardial infarction, or heart attack] in June. He got pushed around due to "bad government insurance," a state-run program for the "uninsured": government pays 1/3, job pays 1/3, and individual pays 1/3.

What they didn't tell him is that there is no major medical coverage and little to no prescription coverage. We fought for 4 months to get him open heart surgery that the insurance was not going to pay for.

Now, with no assistance, terrible insurance, and no disability he has little to no income. He is a heavy equipment mechanic and is trying to be the "good American"-- take care of his bills, not file bankruptcy, etc.

Anyway, the doctors never seem to pay attention to what they prescribe. Lipitor was not working for him, due to side effects. Now they want to give him Zetia and Lovaza....Zetia at $114, and Lovoza is $169.85! Wow! For dead fish???? I think this is a little fishy! I looked up Lovaza, gee how nice, they will give you a $20 coupon....

Forget it, he can't afford this stuff. So I am enrolling in the Zetia program for him. And trying to get him OTC [over-the-counter] fish oil. The most prevalent fish oil around here (that I take myself is) Omega 3 Fish Oil that has EPA 410mg, DHA 274.

Thanks for your blog. It made me feel better that I wasn't the only one outraged by this stuff. I 've been a nurse for 20 years and it just never seems to get better. Thank you for your wisdom.

Sincerely JP, Tennessee

Had this reader not been aware that her brother could take fish oil as a nutritional supplement, he likely would have been denied the benefit of omega-3 fatty acids in slashing the risk for recurrent cardiovascular events. You and I can buy wonderfully safe and effective fish oil as a nutritional supplement, but there won't be a sexy drug representative to sell it, nor an expensive dinner and payment for a trip to Orlando to hear about it.