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

Cureality | Real People Seeking Real Cures

Condition Afflicts Millions: Do you have “YBS”?

12. May 2014 Lisa G Nutrition (0)

After one of the harshest winters, spring has finally arrived. The welcomed warmer temperatures and longer daylight hours infuse us with a sense of renewal and new beginnings. Low and behold we begin to come out of hibernation and start the mad dash to engage in positive lifestyle changes such as eating better, exercising, proper sleep and taking appropriate nutritional supplements. But invariably, life happens.

Yep, just when you were about to get started, it happens. YBS sets in. I see this “condition” all too often with clients attempting to enter or re-enter into any number of behavior changes. I will go so far as to say we all have been afflicted at one point or another in our lives. I call this condition Yeah But Syndrome, or “YBS”. It is often paralyzing and prevents those afflicted from moving into action, instead remaining in a state of inertia.

There are many symptoms of YBS but the following are some of the most common.

• Yeah I planned to go to the gym today BUT, the kids needed a ride to practice.

• Yeah I really want to eat better BUT I don’t have the time.

• Yeah I didn’t plan to eat the cake BUT my husband wanted too, so I did also.

• Yeah I really meant to go to the grocery shopping BUT I was too tired, so I hit the drive- thru.

• Or this is a good one. Yeah I meant to start today BUT, I’ll start tomorrow.

But tomorrow never comes. You get the drift. We can all come up with a million yeah buts, in other words, excuses. The good news is the treatment for YBS is simple--just do it! Take action. The reality of today’s 24-7 planet is there will always be something. The kids, work commitments, family obligations and various projects that need your attention will perpetually be present in some shape or form. The difference to make the difference is to learn to dance in the rain, not wait for the rain to pass. When will all the stars align so that your world will be “just right” to start? If not NOW, WHEN will you begin?

The key word here is begin. Far too frequently, I coach clients that shoot themselves in the foot before they start. Instead of consuming yourself with all the barriers to entry, select reasonable, low-hanging fruit that is “doable.” The art of lifestyle change is to avoid all-or-nothing thinking and begin to appreciate what you CAN do, versus focusing energy on what you can’t do. What is one action you can do TODAY to move toward your wellness goal(s)? Start to focus on what you can do in the mist of your existing life demands. This mantra is a friendly reminder: BE-DO-HAVE. Be committed. Do what it takes. And you will have results.

Lastly, if you think removing cereal from your morning routine it is too difficult and you can’t do it. Guess what-- you’re likely right. What you think is what you get! But what if you think instead, “I can do this. There are many truly healthy options for breakfast to replace cereal such as eggs and veggies that will help me look and feel my best.” Then guess what--you will! This simple change in mind-set can start a tidal wave of change and prevent you from abandoning ship when life tosses you into rough waters. Ongoing support is hugely important to sustain lifestyle changes. Join the conversations in the Cureality Forum to engage the support of health coaches and Cureality Members to stay on track.

We Need More.....Kettlebell

8. May 2014 Amber B Exercise (0)

You either love them or you hate them.

When you are in love with kettlebells, like I am, you enjoy the multi-muscle group movements. Kettlebell workouts are fluid, like a dance, putting together a chain of movements that leave your heart pounding and sweat pouring. Yes, there’s some sneaky cardio component to a kettlebell workout. A great blend of aerobic and anaerobic conditioning.

If you hate kettlebells it’s because kettlebell exercises keep you honest with proper exercise execution. Form is imperative to moves like the kettlebell swing or the kettlebell snatch. Do it incorrectly and you’ll be either sore or have bruised wrists the next day. But this is no reason to shy away from the kettlebell. You have way too much to gain from this odd looking piece of exercise equipment.

You will get a mega -caloric burn. The American council on Exercise states that the average kettlebell workout burns 20 calories per minute. That’s 1200 calories in just one hour. Kettlebell workouts utilize many muscle groups to give you an efficient, total body conditioning workout.

If you’re looking for a toned back side get a kettlebell. The classic kettlebell swing works all the posterior muscles like your glutes, hamstrings, and lower back. But only if you use correct form. Otherwise you'll find yourself with nagging back pain, instead of a better butt.

Kettlebell exercises are functional movements that will allow you to play hard without getting injured. If you are an athlete, a nature enthusiast, or just want to keep up with the kids then you need to give kettlebells a try. During a workout, the exercises will target movements that will make getting up and down off the floor easier, as well as bending over to pick something up.

If you are interested in doing kettlebell workouts start with a coach or take class. You can’t fake form with kettlebell exercises or you could end up hurt. I’m not trying to scare anyone away because good form is easy to learn. Your body will memorize the correct movement pattern and you’ll be on your way to a successful kettlebell workout.

Thyroid and the gut: Hidden health partners

8. May 2014 Chris K Thyroid (0)

Though I have personally dealt with both auto-immune thyroiditis (Hashomoto’s) and several gut issues (wheat sensitivity, gastritis, etc.), it was not until recently that I discovered how close the thyroid and gut work together to keep you healthy – and how problems with one can affect the other along with your overall health.

Most of us understand that the primary function of the gut, that 25 to 30 feet of “tubing” that includes everything from your stomach to your large intestines, is to process the food we eat and allow the “good stuff” (essential nutrients) to pass into our blood stream while keeping the “bad stuff” (harmful proteins) out. However, it may surprise some that the gut also holds as much as 70% of all the immune tissue in the body.

Now, imagine all the health havoc that could ensue if, suddenly, the gut stopped doing its job – particularly if it failed to stop toxic proteins from entering the blood stream and then mounted an overzealous immune response against them. Sometimes, those overzealous immune responses reach beyond their intended targets to attack otherwise healthy tissues and organs – like the thyroid gland.

Recent studies indicate that thyroid hormones play a significant role in maintaining gut integrity, preventing leaky gut that can, in some cases, lead to auto-immune attacks against the thyroid. A properly functioning gut also aids the production of thyroid hormones by converting some of the inactive “T4” thyroid hormone into the functional “T3” hormone. Failure to simultaneously maintain both a healthy gut and a healthy thyroid can create a vicious cycle leading to chronic health problems and declining vitality.

What it all means is that to enjoy optimal health, you must promote good thyroid health to promote good gut health and vice versa. Unfortunately, traditional medicine tends to focus on one issue to the exclusion of others. A typical endocrinologist may treat your under active thyroid without spending a moment to address underlying gut issues. A gastroenterologist will work alleviate a gut problem but will rarely address a potential thyroid problem.

This illustrates, once again, how our bodies work as a system and why it is necessary to bridge the “healthcare gaps” in traditional medicine by becoming personally responsible for your health. I encourage everyone to consult the Cureality Program Guide and online Cureality Diet and Thyroid Health Tracks to learn more about how to optimize both your gut and thyroid health on your journey to realizing complete, whole-body health.

Omega-3 fatty acids likely NOT associated with prostate cancer

18. July 2013 William Davis Omega-3 fatty acids (6)

A weakly constructed study was reported recently that purportedly associated higher levels of omega-3 fatty acid blood levels and prostate cancer. See this CBS News report, for instance.

Lipid and omega-3 fat expert, Dr. William Harris, posted this concise critique of the study, exposing some fundamental problems:

First, the reported EPA+DHA level in the plasma phospholipids in this study was 3.62% in the no-cancer control group, 3.66% in the total cancer group, 3.67% in the low grade cancer group, and 3.74% in the high-grade group. These differences between cases and controls are very small and would have no meaning clinically as they are within the normal variation. Based on experiments in our lab, the lowest quartile would correspond to an HS-Omega-3 Index of <3.16% and the highest to an Index of >4.77%). These values are obviously low, and virtually none of the subjects was in “danger” of having an HS-Omega-3 Index of >8%. So to conclude that regular consumption of 2 oily fish meals a week or taking fish oil supplements (both of which would result in an Index above the observed range) would increase risk for prostate cancer is extrapolating beyond the data.

This study did not test the question of whether giving fish oil supplements (or eating more oily fish) increased PC risk; it looked only a blood levels of omega-3 which are determined by intake, other dietary factors, metabolism and genetics.

The authors also failed to present the fuller story taught by the literature. The same team reported in 2010 that the use of fish oil supplements was not associated with any increased risk for prostate cancer. A 2010 meta-analysis of fish consumption and prostate cancer reported a reduction in late stage or fatal cancer among cohort studies, but no overall relationship between prostate cancer and fish intake. Terry et al. in 2001 reported higher fish intake was associated with lower risk for prostate cancer incidence and death, and Leitzmann et al. in 2004 reported similar findings. Higher intakes of canned, preserved fish were reported to be associated with reduced risk for prostate cancer. Epstein et al found that a higher omega-3 fatty acid intake predicted better survival for men who already had prostate cancer, and increased fish intake was associated with a 63% reduction in risk for aggressive prostate cancer in a case-control study by Fradet et al). So there is considerable evidence actually FAVORING an increase in fish intake for prostate cancer risk reduction.

Another piece of the picture is to compare prostate cancer rates in Japan vs the US. Here is a quote from the World Foundation of Urology:

"[Prostate cancer] incidence is really high in North America and Northern Europe (e.g., 63 X 100,000 white men and 102 X 100,000 Afro-Americans in the United States), but very low in Asia (e.g., 10 X 100,000 men in Japan).”

Since the Japanese typically eat about 8x more omega-3 fatty acids than Americans do and their
blood levels are twice as high, you’d think their prostate cancer risk would be much higher...
but the opposite is the case.

Omega-3 fatty acids are physiologically necessary, normalizing multiple metabolic phenomena including augmentation of parasympathetic tone, reductions of postprandial (after-meal) lipoprotein excursions, and endothelial function. It would indeed make no sense that nutrients that are necessary for life and health exert an adverse effect such as prostate cancer at such low blood levels. (Recall that an omega-3 RBC index of 6.0% or greater is associated with reduced potential for sudden cardiac death.)

I personally take 3600 mg per day of EPA + DHA in highly-purified, non-oxidized triglyceride form (Ascenta Nutrasea liquid) that yields an RBC omega-3 index of just over 10%, the level that I believe the overwhelming bulk of data suggest is the ideal level for humans.

Are statins and omega-3s incompatible?

18. June 2013 William Davis (4)

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)
--Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)
--Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.

DHA: the crucial omega-3

22. May 2013 William Davis (5)

Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:

□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam's Club Triple-Strength, Costco, Nature Made, Nature's Bounty, as well as prescription Lovaza. (That's right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.

Krill oil: Do the math

21. May 2013 William Davis (0)

The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:

Here are some representative krill oil preparations available on the market:

MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

What tests are MORE important than cholesterol?

12. May 2013 William Davis (8)

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.

All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

21. November 2012 William Davis (3)

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.

Apple Cranberry Crumble

18. November 2012 William Davis (0)

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)

Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.

All posts by william-davis

Honey: More fructose than high-fructose corn syrup

11. August 2009 William Davis (21)

Honey: It’s natural. Mom probably gave it to you, either straight or in tea for a sore throat when you were a kid. Even today, honey is touted as possessing almost supernatural qualities for promoting health.

Honey contains B vitamins, minerals, and a handful of antioxidants. It also contains . . . fructose. 60% of honey, in fact, is fructose.

While the average per capita intake of honey is only a modest 1.29 lb per year (National Honey Board; 2008) and therefore contributes only 0.77 lb of fructose per year, there are people who, believing honey to be healthy, use it to excess and use far more than 1.29 lb per year.

How does that compare to table sugar, or sucrose?

Sucrose is 50:50 glucose to fructose. How about high-fructose corn syrup, the sweetener found in virtually all processed foods that has replaced sucrose as the most common sweetener? Depending on the variety, high-fructose corn syrup is generally 42-55% fructose. Many of us (including me) believe that the proliferation of high-fructose corn syrup in processed foods is a big part of the reason Americans are fat and diabetic.

Yes: Judged by its fructose content, honey is worse than high-fructose corn syrup. It is also worse than sucrose.

It means that honey can also contribute to the adverse health effects of fructose, as detailed in this prior Heart Scan Blog post.

Sun, fish, and seaweed

8. August 2009 William Davis (9)

Extraordinary heart health springs from three basic sources in our environment:

Sun, fish, and seaweed.

Sun: Sunlight exposure is nature's intended source of vitamin D. Humans were meant to run naked, or at least scantily clad, in tropical or sub-tropical climates. The large surface area of skin ensured plenty of skin activation of vitamin D, along with long days of intense sun (unlike the seasonal variation of day length and less intense sun further north).

Fish: Fish are the principal source of omega-3 fatty acids, as are, to a lesser degree, wild land animals. Humans as hunter-gatherers tracked, captured, and slaughtered fish and wild game, eaten immediately, since there was no means of storage. Omega-3-rich game was the principal source of fat for primitive cultures.

Seaweed: Seaweed is the world’s most concentrated source of iodine. While seafood like fish and shellfish also contain iodine, seaweed contains, on average, a thousand-fold greater quantity. Seaweed, like plants found on land, are also rich in phytonutrients.

The healthiest cultures on earth follow this simple recipe for health. The unhealthiest population on earth-meaning Americans (i.e., without benefit of bail-out medications and procedures that keep us alive, or vaccinations that protect us from infectious diseases)--neglect all three. Witness the Okinawans, whose daily meals nearly always contain some form of fish and seaweed, and whose sub-tropical climate provides greater sun exposure. It is not unusual for Okinawans to live to 100 years of age, not as an exception, but the rule. Heart disease was virtually unknown except in 90-year olds and older-that is, until the recent adoption of Western practices like fast food and snacks.

It's pretty incredible when you think about it: Simple practices can markedly reduce your likelihood of heart attack and developing heart disease.

Perhaps you’d rather not run naked along a semi-tropical beach, spear fish, and gather seaweed. You could always do the modern equivalents and achieve similar benefits.

Glycemic index: A flawed concept

7. August 2009 William Davis (0)

Kallio P et al Am J Clin Nutr 2008

Squares = rye bread, circles = oat bread

Fructose is a coronary risk factor

4. August 2009 William Davis (21)

As discussed in a previous Heart Scan Blog post, Say Goodbye to Fructose, a carefully-conducted University of California study demonstrated that, compared to glucose, fructose induces:

1) Four-fold greater intra-abdominal fat accumulation

2) 13.9% increase in LDL cholesterol, doubled Apoprotein B

3) 44.9% increase in small LDL, 3-fold more than glucose

4) Increased postprandial triglycerides 99.2%.

Other studies have shown that fructose:

--Increases uric acid--No longer is red meat the cause for increased uric acid; fructose has taken its place. Uric acid may act as an independent coronary risk factor and increases high blood pressure and kidney disease.

--Induces insulin resistance, the situation that creates diabetes

--Increases glycation (fructose linked to proteins) and protein cross-linking, processes that underlie atherosclerosis, liver disease, and cataracts.

Make no mistake: Fructose is a powerful coronary risk factor.
There is no doubt whatsoever that a diet rich in fructose from fruit drinks, honey, raisins and other dried fruit like cranberries, sucrose (table sugar), and high-fructose corn syrup is a high-risk path to heart disease.

Also note that many foods labeled "heart healthy" because of low-fat, low saturated fat, addition of sterol esters, or fiber, also contain fructose sources, especially high-fructose corn syrup.

Who lost weight?

1. August 2009 William Davis (30)

The results of the latest Heart Scan Blog poll are in.

I went wheat-free and I . . .

Gained weight 6 (3%)

Lost no weight 41 (21%)

Lost less than 10 lbs 28 (14%)

Lost more than 10 lbs 34 (17%)

Lost more than 20 lbs 22 (11%)

Lost more than 30 lbs 28 (14%)

I'm still losing weight! 30 (15%)

(189 respondents)

This means that, by eliminating wheat:

24% had no success

31% had moderate success (less than 10 lbs or more than 10 lbs)

25% had extravagant results with 20 lbs or more lost

It would be interesting to know where along the weight-loss spectrum the last category, "I'm still losing weight," group falls. (Anyone with a good story please speak up!)

I believe we can conclude from this casual exercise that, as a simple strategy, wheat elimination is surprisingly effective.

Why would 3% gain weight? Well, without knowing the details, there are several possible explanations:

1) Weight gain developed through other foods. For instance, I've had people eliminate wheat only to replace it with fattening gluten-free alternatives. Remember: wheat-free is not gluten-free. Others load up on the wrong foods, e.g., Craisins and other dried fruit; overdo dairy; or snack on wheat-free but unhealthy foods like ice cream and chips.

2) Too much alcohol

3) Hypothyroidism--A lot more common than you'd think. In fact, this has been the case with a majority of people who have done everything right, yet either failed to lose weight or gained weight.

Those are the biggies.

I'd like to hear your personal stories of wheat elimination--the ups and downs, your success or failure, how you felt during the process, how easy or difficult, your eventual results. Just post them as a response to this blog post.

A niacin primer

29. July 2009 William Davis (19)

A reader of Life Extension reminded me of a piece I wrote about niacin a couple of years back.

Anyone desiring a primer on how and why to use niacin to correct lipid and lipoprotein patterns might find this useful.

While some people, no matter what they do, cannot tolerate niacin (about 10% of people), many others enjoy spectacular benefits.

Q: I recently had a cholesterol profile blood test and learned that I may be at risk of heart disease because my levels of beneficial HDL (high-density lipoprotein) are too low. I read that niacin could help increase my HDL, but my doctor said niacin is dangerous. Whom should I believe?

A: Your doctor would be right—if we were still living in 1985. Since then, however, we have learned how to use niacin (vitamin B3) safely and effectively. Unfortunately, many physicians have not yet caught up, or are still trapped by the idea that cholesterol-lowering statin drugs are the only way to decrease cardiovascular disease risk. I have personally prescribed niacin for thousands of patients as part of our program to reverse coronary disease. In fact, niacin is the closest thing we have available to a perfect treatment that corrects most of the causes of coronary heart disease.

Continued here.

What would life be like . . . ?

29. July 2009 William Davis (16)

What if coronary heart disease could be prevented--no eliminated--applying methods that were accessible, easy, and cheap?

What if coronary heart disease and, thereby, angina, heart attack, sudden cardiac death, ventricular tachycardia, heart failure, and the cerebrovascular equivalent, stroke, could be eliminated using readily available tools available to virtually everyone in the U.S.? And, over a year, it cost less than a once-a-week latte at Starbucks?

How would the healthcare landscape change? What would become of hospitals, manufacturers of the billions of dollars of hospital equipment necessary to supply the cardiovascular hospital industry (e.g., stent manufacturers, catheter manufacturers, defibrillator and pacemaker manufacturers, pharmaceutical manufacturers who no longer have to produce the volume of antiplatelet agents, inotropic drugs, antiarrhythmic agents, etc.)?

How would our lives change? What would the end of life look like if people stopped dying of heart attack, sudden cardiac death, congestive heart failure at age 55, 65, or 75, but lived out their lives to die of something unrelated?

What if the solution had little or nothing to do with drugs but evolved from simple nutritional strategies, supplements meant to correct the deficiencies that accompany modern lifestyles, and a few unique strategies targeted towards the genetic predispositions that lead to heart disease?

What if all this were possible at a cost of a few hundred dollars per year?

It would certainly be a cataclysmic change. Hospitals would shrink to a small remnant of their current gargantuan, dozens-per-city presence. The need for hospital staff would be slashed by over half. The rare cardiologist would tend to congenital heart disease sufferers and other unusual forms of heart disease and he or she might have a colleague or two in all of a major city.

Healthcare costs would plummet, no longer having to sustain the enormous cardiovascular healthcare machine of hospitals, staff, industry, and long-term care. Health insurance, private or public, would drop by 50%.

It would free up nearly a trillion dollars that could be redirected towards other pursuits, like schools and research. Extraordinary leaps forward in quality of life and science would emerge, given that magnitude of funding.

It's not as grand a thought experiment as Alan Weisman's The World Without Us, in which he imagines what the world would be like without humans altogether.

How long would it take to recover lost ground and restore Eden to the way it must have gleamed and smelled the day before Adam, or Homo habilis, appeared? Could nature ever obliterate all our traces? How would it undo our monumental cities and public works, and reduce our myriad plastics and toxic synthetics back to benign, basic elements?

But I believe this thought experiment--what would life be like without heart disease because it was eliminated using inexpensive tools-- is more plausible, more likely to occur. In fact, it has already begun to occur.

See those vines growing up the side of the hospital?

Are jelly beans heart healthy?

27. July 2009 William Davis (0)

Total Fat

3 g or less

Less than 6.5 g

Saturated Fat

1 g or less

1 g or less

Cholesterol

20 mg or less

20 mg or less

Sodium

480 mg or less per RACC* & labeled serving

480 mg or less per RACC* & labeled serving

Nutrients

Contain 10 percent or more of the daily value of 1 of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber

Contain 10 percent or more of the daily value of 1of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber

Trans fat

Less than 0.5 g per RACC* and labeled serving

Less than 0.5 g per RACC* and labeled serving

Whole Grain

N/A

51 percent by weight/RACC*

Minimum Dietary Fiber

N/A

1.7 g/RACC of 30 g

2.5 g/RACC of 45 g

2.8 g/RACC of 50 g

3.0 g/RACC of 55 g

(RACC=Reference Amount Customarily Consumed)

Thyroid correction: The woeful prevailing standard

27. July 2009 William Davis (16)

Rich has been taking Synthroid or levothyroxine for many years.

When Rich came to my office for continuing management 10 years after his bypass surgery, I checked his thyroid panel:

TSH 7.44 uIU/L

Free T4 1.88 ng/dl (Ref range 0.80-1.90 ng/dl)

Free T3 2.0 pg/ml (Ref range 2.3-4.2 pg/ml)

Rich's thyroid hormone distortions--high TSH, low T3--are sufficient to account for a tripling of heart attack risk long-term.

As Richs' thyroid was being managed by his primary care physician, I notified this doctor of Rich's panel. He therefore increased Rich's levothyroxine from 75 mcg per day to 100 mcg per day. Another thyroid panel several months later showed:

TSH 0.98 uIU/L

Free T4 2.38 ng/dl

Free T3 2.0 pg/ml

As you would expect, increasing the intake of the T4 hormone (levothyroxine) increased free T4 and suppressed TSH.

But what about T3? It's unchanged.

Indeed, Rich says that he feels no better and, in fact, wakes up in the morning foggy and requires a nap in the afternoon.

In my experience, the majority (approximately 70%, but not 100%) experience subjective improvement when T3 is added in some form and the free T3 level is increased. While the data (summarized here) are conflicted on whether there is objective benefit to T3 management and supplementation, there seems to be a poorly-quantified subjective improvement.

Rich's increased levothyroxine dose decreased (calculated) LDL cholesterol by 10 mg/dl. Based on my experience, I'll bet that his lipid panel would likely be further improved with T3 correction.

What I find incredible is the absolutely rabid resistance waged by primary care physicians and endocrinologists against this notion of T3, mostly due to fears of the remote likelihood of inducing atrial fibrillation and osteoporosis, while they are ready to prescribe lifelong statin drugs without a moment's hesitation.

Launch of new Track Your Plaque newsletter: Cardiac Confidential

27. July 2009 William Davis (3)

Track Your Plaque has just launched a new version of our newsletter. We call it Cardiac Confidential.

Cardiac Confidential is meant to be a no-holds-barred, go-for-the-throat exposé of the world of heart disease. We will expose the dishonest, reveal what we view as the underlying truth. We'll even have an occasional "undercover" report of what goes on in hospitals and the go-for-the-money world of heart procedures.

Read the first issue here (open to everyone) in which "Laurie" describes her encounter with a sleazy, profiteering cardiologist. She survives, but not without paying a dear price.

All posts by william-davis

Take a walking vacation

20. May 2006 William Davis (1)

If you're planning a vacation, why not consider a walking vacation?

The concept is really taking off. All you need is a pair of comfortable shoes and an interesting locale. More and more services are popping up to help you plan fun and interesting destinations and itineraries. One such catalog can be found at http://walking.about.com/od/tours/a/walkingvacation_3.htm

Lengthier walks may require some advance planning and toting some supplies. Don't forget the water!

From a health viewpoint, a walking vacation sure beats the heck out of a cruise that packs on 12 pounds of extra weight from the 24-hour a day buffet. If you're in the midst of a weight loss effort, several hours of walking through interesting locales and scenery can make it effortless.

There's loads of neat places to visit from a walker's perspective. One interesting website is www.waterfallwalks.com that lists trails that provide spectacular views of waterfalls.

Another variation on this theme is biking vacations. My wife and I are trying to set the time aside for a biking tour of wineries in the French countryside. That's our kind of multi-tasking!

"Expanded indications for implantable defibrillators"

19. May 2006 William Davis (0)

So reads the headline on a magazine I received recently (along with thousands of my colleagues) from a major hospital system.

It goes on to say: "In January 2005, indications for implantable cardioverter-defibrillators (ICDs) were substantially broadened [emphasis ours] to include most patients with a left ventricular ejection fraction (EF) of 35% or less. This change translates into a 2- to 3-fold increase in the number of Medicare beneficiariries eligible for ICDs."

Ka-ching!!! Hear the money piling up in the bank?

The device manufacturers are constantly churning data and lobbying for reimbursement to expand the use of their devices to more and more people. Defibrillators in particularly are generally a $25,000 to $50,000 opportunity for the device manufacturer alone, not counting the costs incurred at the hospital for implantation.

Beware. As reimbursement for stents and other procedures diminishes, expect a sudden "demand" for more and more people to get implantable defibrillators. Better yet, stay away from the whole issue by preventing your heart attack.

Get a heart scan--but then don't delay taking action!

19. May 2006 William Davis (2)

I just came from one of the local hospitals after having performed a heart catheterization on a patient I met earlier this week.

Jack had gotten a heart scan a year ago with a score of 246, placing him in the 76th percentile. The "event" rate with this percentile rank is around 3% per year--not very high but enough to pose risk over a long period.

Jack chose to ignore his score. After all, the pressures of work at the University, maintaining his home and yard, etc. consumed all his energies. He came to my office--now one year after his scan--and told me about the chest pressure he was getting. Initially, his chest pains occurred with extended walking. In the past week, however, Jack was experiencing chest pressure with just walking 30 feet.

This pattern of increasing symptoms is called "accelerated angina", meaning that Jack was rapidly heading towards a heart attack. So I advised a heart catheterization in near future.

Jack's catheterization showed extensive plaque including a 50% blockage in the mainstem artery and 90% in the artery to the front of the heart (left anterior descending artery). Jack is going to have a bypass operation tomorrow.

What if Jack hadn't ignored his heart scan from a year ago? Well, I'd be very confident in saying that he would not be undergoing bypass surgery tomorrow.

The lesson: Don't dilly-dally on taking action to keep your plaque from growing. While it's not an emergency, it can easily become one if you choose to ignore your scan.

Feel that nudge in your back?

17. May 2006 William Davis (0)

You feel that nudge in your back? That's your local hospitals competing for your bypass surgery business.

Just this morning while watching a morning news show, I saw three advertisements for hospital bypass surgery programs. One ad featured a man in his 50s telling his story:"The cardiologist determined immediately that I needed a triple bypass operation. My family and I are very grateful to _____ hospital!"

In what other field is failure celebrated so prominently? When I see these ads, I hear "My doctors failed to provide early detection and then prevent what became a life-threatening condition, even though heart disease is a chronic process that requires decades to develop." What if our man said instead,"I had a heart scan and my score was high. So I was shown why I had so much plaque. They then showed me how to control and even reduce the amount of plaque I had. I'm living safely and symptom-free without need for surgery or procedures."

Of course, the hospital is out $60,000-100,000 for the surgery. How else could they afford ad campaigns costing several million dollars a year? See these advertisements for what they are: Marketing generated by profit-seeking businesses competing for your dollars--lots of them.

Throw away total cholesterol!

17. May 2006 William Davis (1)

Richard's total cholesterol without treatment was 186 mg/dl. "That's great!" his doctor declared, referring to the conventional dictum that total cholesterols less than 200 carry low risk. Several fingersticks in a mall kiosk set up by a local hospital to check total cholesterols confirmed Richard's low number.

But after Richard's unexpected hospitalization and two stents for severe coronary blockages, he demanded better answers.

Tragically, the answer was there all along: Despite a "favorable" total cholesterol, his HDL ("good") cholesterol was a miserable 32 mg (ideal >60 mg).

Total cholesterol is actually the sum total of HDL cholesterol, LDL cholesterol, with a contribution from triglycerides. That's why a low total cholesterol can conceal a low HDL.

This situation is quite common. And low HDL is accompanied by a constellation of other undesirable causes of heart disease, most notably small LDL.

Don't accept total cholesterol as your sole measure of risk. It's nearly worthless. If you live in Bangladesh or a third world country, well perhaps that's the best you can get. But if you live in the U.S. or developed world, it's absurd to rely on total cholesterol.

Smart Start not so smart

15. May 2006 William Davis (2)

Kellogg's has crafted a campaign to support the American Heart Association featuring acress Sela Ward. Her attractive face, familiar to many TV and movie viewers, does add a comforting face to their efforts.

What's in this cereal made by the manufacturers of Pop-Tarts, Cheez-It, Rice Krispies, and Chips Deluxe cookies?

There are, indeed, some healthy ingredients: oat bran, potassium; you can even get a version made with soy protein. But there's sugar listed as the second ingredient. High-fructose corn syrup is also listed prominently. (Remember this issue? High-fructose corn syrup causes overwhelming sugar cravings, causes your triglycerides to skyrocket, and is probably among the principal food ingredients that make you obese.)

Upon detailed questioning of my patients struggling to lose weight, this and products like it are often among the "healthy" foods they've gravitated towards. We spend a great deal of time dissuading them of this idea.

A one-cup serving of Smart Start is low in fat (1 gram) but contains 43 grams of carbohydates, of which there are 14 grams of sugar. There are a meager 3 grams of fiber. To me, this sounds like a cupcake.

The Kellogg's people are exceptionally clever marketers. Partner with the American Heart Association and movie stars? Brilliant!

You should trust food manufacturer advertising about as much as you trust drug manufacturer advertising, which is to say not at all.

Kellogg's sold $10 billion dollars of food products last year. They are the world's leading producer of breakfast cereals. They are a leading producer of convenience foods: cookies, crackers, cereal bars, and frozen waffles under the brands Keebler, Pop-Tarts, Eggo, Cheez-It, Nutri-Grain, Rice Krispies, Famous Amos, and Kashi.

Can they cash in on healthy trends? They'll certainly try.

Does anybody have a normal vitamin D level?

15. May 2006 William Davis (0)

We now routinely check everyone's vitamin D blood level at the start of the program. (The measure to obtain is 25-OH-Vitamin D3. This is not to be confused with 1,25-OH2-vitamin D3, which is a kidney function measure.)

Of the 10 people with levels drawn today, none were even close to normal levels (which we define as 50 ng/ml)--not a single one.

The majority were in the range of severe deficiency (<20 ng/ml). Only two had levels in the 30s. None had higher. (Remember: I'm talking about people in Wisconsin, a terribly sunlight-deprived area much of the year. This might not apply quite as vigorously to Florida residents or others in sun-exposed regions.)

Curiously, I've also seen several people this week who had extraordinary quantities of coronary plaque on their heart scans (scores >1000), all of whom had extremely low vitamin D levels. One of these people had fairly unimpressive lipoproteins, with very minimal abnormalities identified. (This is quite unusual, by the way.) It makes you wonder if a profound deficiency of vitamin D is sufficient to act on its own as an instigator of coronary plaque.

The more we examine the issue of vitamin D deficiency, the more fascinating it gets. I suspect we've just scratched the surface and there's a lot more to learn about this tremendously interesting nutrient. Nonetheless, with what we're seeing in our experience, I'm urging everyone to get a blood vitamin D level.

Don't believe your LDL cholesterol!

14. May 2006 William Davis (0)

Harry's case is typical. For years, his doctor told him his LDL cholesterol of 123 mg was okay. But a heart scan score of 490 (90th percentile at age 52) made him question just where his coronary plaque came from.

Lipoprotein analysis told a very different story: His LDL particle number was 2400 nmol, meaning his trueLDL was more like 240 mg, nearly double the value of LDL obtained through his doctor. Harry had other sources of risk, too, but the LDL particle number was a clear stand-out.

Why does this happen? How can LDL cholesterol be so terribly inaccurate?

LDL cholesterols obtained in virtually all labs are not measured, they're calculated. The calculation was developed in the 1960s by Dr. Friedewald at the National Institutes of Health and therefore goes by his name (the Friedewald calculation). Dr. Friedewald derived this simple calculation to permit doctors across the U.S. to obtain LDL cholesterols, which were technically difficult to measure in those days by using measured HDL, total cholesterol and triglycerides.

Doctors were told that the only time that the Friedewald calculated LDL was inaccurate was when triglycerides exceeded 400 mg. So most family practitioners and internists still believe that calculated LDL's are, for the most part, quite accurate.

Nothing could be further from the truth. When LDL's are actually meaured, you find that LDL is rarely accurate. In fact, in our experience, inaccuracy of 30-50% is the rule, sometimes 100%. The one telltale hint that calculated LDL is wrong is when HDL is <50 mg--that's nearly everybody.

So what's your LDL? You won't really know unless it's measured. Our preferred method is NMR (LipoScience) LDL particle number, probably the most accurate of all. Second best: apoprotein B, direct measured LDL, and non-HDL. (We'll cover this issue much more extensively in an upcoming report on the www.cureality.com website in an extensive Special Report.)

Are you the exception?

14. May 2006 William Davis (0)

I read about 40 heart scans this morning. In the stack was a 41-year old man with a heart scan score of 841.

That's terribly high for anyone, let alone a 41-year old person. He's lucky to find out about this before catastrophe strikes.

People like this worry me. In general, we advise men to consider a heart scan age 40 and older; women 50 and older. If there's anything exceptional about your family history or your own history, then you might notch these numbers down another 5-10 years. For instance, if your Dad had a heart attack at age 43, you might consider a scan at age 35. Or, if you've had diabetes for several years and you're a 42-year old woman, you might think about a scan. (Men tend to develop measurable plaque by heart scans 10 years before women.)

There are no hard and fast rules. It's unusual for a male to have a score >0 before age 40. Likewise, it's very uncommon for a woman to have a score >0 before age 50. But there are occasional exceptions--but they can be very important exceptions.

Our 41-year old man with the score of 841, for instance, probably had a high score since his mid-30s. I've seen several women without any obvious risk factors with scores in the several hundred range in their early 40s.

My rule: When in doubt, opt for safety. Every day, I still read about people in their 30s, 40s, and 50s dying of heart attacks. It shouldn't happen.

When in doubt, get the heart scan. The most you'll lose is the cost of the scan and a modest exposure to radiation. If your score is zero, you know you're safe for the next 5 or more years. But if you have an exceptional score at a young age, take preventive action.

Self-empowerment in health: The new wave in health care

12. May 2006 William Davis (0)

Track Your Plaque is just one facet of the broad and powerful emerging wave of self-empowerment in health.

Hospitals, drug and device manufacturers, and the medical establishment don't like this idea. People managing their own health? That's ridiculous! Dangerous! But mostly unprofitable.

Self-empowerment means having easy access to simple, safe, and inexpensive diagnostic tests like heart scans, carotid scans, bone densitometry (for osteoporosis), cholesterol tests, abdominal ultrasound, even brain scans (e.g., CT or MRI) for people with a family history of brain aneurysm.

Opponents of this idea worry about the "false-positives" that come about with broad testing, i.e, detection of abnormalities that are artifactual. Our experience is that false-positives are only an occasional problem with any test. Instead, we find that most people have many true-positives. In CT heart scanning, for example, we find many unsuspected enlarged aortas (potential future aneurysms), valve disorders, and aortic calcium. These are all important in a preventive program. Unfortunately, your doctor's definition of false-positive often means that no corrective procedure or operation is required.

Other evidence that self-empowerment in health is growing:

--The nutritional supplement movement. What better example of power in managing your own health is there than the fabulous array of nutritional supplements available?

--Medications moving to over-the-counter status. Gradually, more and more medications are trickling into availability for you to obtain without a doctor's prescription.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The rapidity and depth of information available on the Internet today is mind-boggling. It will fuel the self-empowerment movement by providing sophisticated information to the health care consumer previously available only through your physician.

--High-deductible health insurance plans. If health care consumers will bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention to minimize long-term costs.

There are more. But the movement is powerful and broad--and unstoppable. Let the establishment with vested interests in preserving the status quo fuss and complain, just like horse and buggy manufacturers did in the early 1900's when the autmobile came along.