The myth of mild coronary disease

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)



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?

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



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

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



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

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

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?

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?

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
Buy local, get a goiter

Buy local, get a goiter

The notion of buying food locally--"buy local"--i.e., food produced in your area, state, or region, is catching on.

And for good reason: Not only do you support your local economy, buying locally saves energy, since food doesn't have to be transported from South America or other faraway locations.

But what about those of us in the Midwest, particularly around the Great Lakes basin, i.e., the region previously known as the "goiter belt"? In the early 20th century, up to a third of the residents of this region had enlarged thyroid glands, or goiters, due to iodine deficiency. Lack of iodine causes the thyroid to enlarge, or "hypertrophy," in an effort to more efficiently extract any available iodine in the blood.

Well, there's been a resurgence of iodine deficiency nationwide with 11.3% of the population severely deficient, representing a four-fold increase since the 1970s.

Why an iodine deficiency? Because more people are avoiding iodized salt, the principal source of iodine for Americans since the FDA introduced its voluntary program for iodization of table salt back in 1924. Approximately 90% of the patients I ask now declare that they use very little iodized table salt. While a few take multimineral or multivitamin supplements that contain iodine, the majority do not. The globalization of the food supply--eat global--however, has softened the blow, since we eat tomatoes from Mexico, blueberries from Argentina, lettuce from the Salinas Valley of California.

Now, we have the growing trend to eat local. In the Midwest, it means that the vegetables, fruits, and meats grown locally will also be iodine depleted, since the soil is also iodine-poor, being so far from the sea.

Ironically, two healthy trends--avoiding salt and eating local--will be accounting for a surge in unsightly neck bulges in the Midwest, as well as an increase in thyroid disease.

The lesson: Avoid salt, eat local, but mind your iodine.

Comments (19) -

  • mike V

    4/3/2009 6:56:00 PM |

    Dr Davis:

    PREVENTION v PREVENTION!
    A curious thing but I wonder if you mid-westerners really need to be giving up iodized salt at all if you are taking care of your potassium and magnesium?
    When you get time, please let us know your patient findings on mineral status.
    "Lite" salt contains a % of potassium which may be  iodized. Of course one's ability to take potassium maybe compromised by some medications.

    Mike V

    *************************
    UK ARTICLE
    Is salt REALLY so bad for your blood pressure?
    By Jerome Burne
    30th March 2009

    It's been demonised for years. But suddenly experts are asking whether we're missing the bigger picture about salt...

    We're all eating too much salt and it's going to give us high blood pressure - that's the message we've heard for years, but now new research suggests salt is being wrongly demonised.
    A recent study suggests that by concentrating on the effects of salt we could be missing the bigger picture. That's because salt doesn't affect blood pressure on its own; it does so with another mineral we get in our diet - potassium.
    Blood pressure is constantly being raised and lowered - salt is involved in raising pressure by tightening arteries, while potassium is part of the relaxation system. So making sure you have enough potassium is vital.
    Salty snack: Research has found that eating more salt does not necessarily raise the risk of heart disease
    This was highlighted in the study from Loyola University in Chicago. Researchers measured the amount of salt in the urine, an accurate way of measuring how much had been consumed, and found no significant difference in the risk of heart disease whether patients had been eating a lot or a little. What did reduce the risk, however, was the ratio of salt to its balancing mineral potassium.
    The new study 'is a quantum leap in the quality of the data', says lead author Dr Paul Whelton, an epidemiologist and president of the university's health division. That's because it followed nearly 3,000 patients for between ten and 15 years.
    Whelton now believes many of us need to significantly increase our potassium intake to help our arteries.
    'To lower blood pressure and dampen the effects of salt, adults should consume 4.7grams of potassium per day,' he says.
    The British recommended daily dose of potassium is only 3.5g. Foods high in potassium include potatoes, sweet potatoes, yoghurt, tuna, lima beans and bananas.
    'To lower blood pressure and dampen the effects of salt, adults should consume 4.7grams of potassium per day'
    _______________________________________

    As for salt, Dr Whelton and colleagues from America's Institute of Medicine say we should stick to less than 6g (a teaspoon) a day, which is the same as the existing UK guidelines.
    But his study is not the only one to raise questions about conventional approaches to this problem.
    A review of the evidence published in the British Medical Journal (BMJ) seven years ago found that while cutting back on salt might help those taking medication for high blood pressure, the research showed no clear benefits for everyone doing it.

    Even more extraordinarily, in 2005, researchers at the Albert Einstein College of Medicine in New York published the results of a 13-year study that had followed 7,000 men and women - this showed that people who consumed less than 6g of salt a day actually had a ********'raised' risk of heart disease.*********

    The author of that study, Dr Hillel Cohen, says this was only an observation, and more work is needed to establish why this trend was found. 'But it does suggest a set limit of salt for everyone doesn't work,' he adds.

    Effective or not, cutting back on salt makes up only a small part of the regime recommended for anyone with raised blood pressure, which is also known as hypertension.
    The first step is usually a version of the Dash (Dietary Approaches to Stop Hypertension) diet that recommends fruits, vegetables, and low-fat dairy foods, and which has been shown to be effective in bringing blood pressure down. But this can be hard to follow if you've been eating less healthily for years.
      Eating a healthy amount of potassium in your diet can offset the impact salt has on raising blood pressure
    Dr Peter Berkin is a GP in Milton Keynes who favours treating chronic disorders with diet where possible.
    'Doctors always recommend weight loss and improving your diet but they rarely have the time or facilities to help patients to make and stick with the changes,' he says.
    The result is that after six weeks or so, most patients are prescribed drugs to lower their blood pressure.
    An estimated ten million people in the UK have high blood pressure, and in England alone millions of prescriptions are written for drugs to treat them every year. But are drugs the best way to treat the problem?

    What patients are often not told is the numbers of people who have to be treated with a drug in order for just one person to benefit.
    In the case of elderly patients with mild hypertension, of every 76 patients who take the drug, one will avoid a stroke, according to Michael Oliver, professor emeritus of cardiology at the University of Edinburgh, writing in the BMJ.
    Professor Oliver was also concerned about the side-effects of these drugs that benefit so few. 'Reduction of mild hypertension can lead to vertigo, particularly in elderly people,' he wrote.

    The drugs have a range of other effects. Diuretics, which make you go to the loo more often, reducing the volume of water in the blood and in turn lowering blood pressure, can cause gout.

    Calcium channel blockers, which relax the arteries, can bring on headaches, while ACE inhibitors, which work by stopping the blood vessels from narrowing, often cause a nasty cough.

    More seriously, several of these drugs are now linked, ironically, with a raised risk of heart disease.
    One study of 1,860 men followed over 17 years found that ^^^^^^those treated with diuretics were 23 per cent more likely to have a heart attack********* than those who weren't.
    Another widely used class of drug is the beta-blocker. These work by blocking a natural substance that causes the arteries to narrow and the heart to beat faster, enabling the arteries to widen again.
    However, using these actually raises heart problems, according to a review by doctors at St Luke's Roosevelt Hospital in New York. They found that patients given beta-blockers had more heart attacks and more strokes.
    'A study found that people who consumed less than 6g of salt a day had a *****raised risk of heart disease'******
    _______________________________________

    The reason could be that most of the studies involved a widely used beta-blocker, atenolol. Worryingly, even though the problems with atenolol have been known for years, 14 million prescriptions for it were written in England and Wales in 2007.

    'Atenolol should not be given to anybody,' says Dr John Cockcroft of the Wales Heart Institute in Cardiff. 'Nobody disagrees atenolol is guilty, yet we are still using it.'
    Drugs certainly bring dangerously high blood pressure down, and for those with high blood pressure they are a lifesaver. But do people with only slightly elevated blood pressure really need them? Research shows that 167 patients need to take the drugs for a single person to benefit.
    A number of GPs believe that more could be done to help people simply with diet and lifestyle.

    'Around 33 per cent of people aged 25 to 55 have borderline hypertension,' says Dr Adam Carey, a nutrition expert who runs a corporate health programme helping employees to get fit, as well as advising the Welsh rugby union team on nutrition.

    'We can get that down to 9 per cent without using drugs, but by giving them a structured programme of diet and exercise.
    'The key is to cut out refined carbohydrates such as white flour and sugar. These foods push up your blood sugar level, and the body stores the extra sugar as fat.
      
    Foods high in potassium include potatoes, sweet potatoes, yoghurt, tuna, lima beans and bananas
    'Eating carbohydrates that haven't been refined, such as brown rice and wholegrains, smoothes out the sudden spikes and troughs of blood sugar that come with sweets and pastries.'

    The American study showed, raising your potassium is important. But there is another pair of minerals involved in controlling blood pressure in the same way as the sodium in salt and potassium do - calcium and magnesium.

    While calcium tightens the blood vessels, magnesium relaxes them. The recommended daily allowance for magnesium is 300 to 400mg and it is found, together with potassium, in green leafy vegetables, nuts and seeds. One of the effects of diuretics can be to flush magnesium and potassium out of the body.

    Relaxation techniques such as meditation can help, too. Anxiety pushes up your blood pressure by raising levels of hormones such as adrenaline and cortisol.

  • P

    4/3/2009 7:28:00 PM |

    Dr. Davis, can you suggest a good omega-3 capsule? I know you have previously mentioned that one can use any omega-3 we get at Costco. I used Naturemade (or Nature's own, I do not remember the name right now) omega-3 capsules. HOWEVER, they have started smelling fishy these last few days! Obviously the oil in them has gone rancid! The capsules are not supposed to expire till 2011, so its really bothering me that they turned bad so soon. I store them in my pantry which is cool and dark, so the capsules were not exposed to harsh sunlight.

  • Anonymous

    4/3/2009 7:56:00 PM |

    Dr.Davis

    This is very informative.
    What is the best base level of Iodine daily to promote thyroid health?

    Thanks for you great blog!

    Aaron

  • David

    4/3/2009 8:10:00 PM |

    So iodine aside, I'm curious as to your take about the whole salt issue. Taubes touches on it in Good Calories, Bad Calories, and essentially looks to insulin --not salt-- as the villain in blood pressure problems. NHANES III seems to help things along in that direction as well: http://www.ncbi.nlm.nih.gov/pubmed/18465175

    I would grant that high salt intake might be a problem for a certain percentage of sensitive individuals, but I kind of doubt that percentage is all that high. I also wonder if sodium sensitivity in some people has more to do with other factors, such as magnesium deficiency (since magnesium regulates sodium) than with sodium actually being malicious in and of itself. *shrugs*

    Some say that the chemically processed, straight sodium chloride is what causes the problems, and that a good full-spectrum sea salt is the way to go, as it contains all the original trace minerals to balance things out. I use Redmond RealSalt (I love the taste). I've known three people now who have gotten on the RealSalt (in large quantities) only to have their blood pressure go down. With no other changes. I don't really understand it, but it's interesting, and helps to further my skepticism about the supposedly universal salt/BP connection.

  • Sabio

    4/4/2009 2:55:00 AM |

    Loved this entry (a fellow paleo) -- thank you for your blog. I added my own libertarian take on it.

  • xenolith_pm

    4/4/2009 3:38:00 AM |

    Eat two Egglands Best eggs a day and you'll get your daily allowance of iodine.

    Or, just a pinch of dry sea kelp in your tea will do the same.

    Or, just a single daily serving of seafood (any of the wild finfishes, roe [fish eggs], crustaceans, or mollusks) should do the trick too.

    Unfortunately, sea salt (unless it's been purposely iodized) has only a small, insignificant trace amount of iodine.

  • Braesikalla

    4/4/2009 8:52:00 AM |

    Iodine seems to upregulate the sensitivity of steroid receptors. There is anecdotal evidence that in the case of diabetes the amount of injected insulin (which is a steroid hormone) has to be drastically reduced to avoid severe side effects like hypoglycaemia ( http://www.healthy-eating-politics.com/diabetes-iodine.html ).
    Since vitamin d is actually a steroid hormone, too, could it be that the recommended range of sufficiency (60-80 ng/dl) has to be adjusted for someone who is on iodine supplementation and therefore likely has increased steroid receptor sensitivity?
    Any thoughts?

  • Dr. William Davis

    4/4/2009 12:42:00 PM |

    Mike V--

    Admittedly, "avoid salt" is a generalization.

    There are genetic types who gain little by minimizing salt. Then there are people at the other end of the spectrum who gain visibly and dramatically with salt restriction, e.g., drops in systolic BP 30+ mmHg, weight (water) reductions of many lbs, even changes in blood electrolytes.

    Salt is one of those things that is handled in dramatically different ways among different humans.

  • Kismet

    4/5/2009 11:18:00 AM |

    David, I believe there's also increased stomach cancer risk with salt...

  • Anna

    4/5/2009 8:25:00 PM |

    It's easy to avoid salt imbalances if one avoids processed foods, as processed foods contain lots of sodium, very little potassium and magnesium.

    Eating real foods one prepares at home may be salted with sea salt with little worry of taking in too much salt.  I tend to think that the association of disease with salt is a marker for malnutrition and poor nutrition from a crappy SAD diet, too high in carbs, too low in protein and natural fats, and deficient in multiple micronutrients.  

    Taubes wrote a great article in Science a few years back on the soft (political) science behind the salt restriction advice.  That's eventually what moved him to investigate the fat/cholesterol hypothesis, because the most influential salt restriction theorist was such a "bad" scientist and bragged so much about his influence that Taubes' skepticism went on high alert.

  • David

    4/5/2009 10:29:00 PM |

    Kismet,

    I won't argue that point, but I would question it, just because I think more information would be helpful. A lot of the studies on salt and stomach cancer that I've seen are observational in nature. Observational studies are useful as far as they go, but they're not good at proving causality. In other words, perhaps it's true that people who get stomach cancer eat a lot of salt. But is the salt actually causing the cancer? People who eat a lot of salt also eat a lot of nitrates-- in fact the two often go together. So which is it that causes the cancer? Salt or nitrates? We can't tell from the observational studies, because there are still too many variables to narrow down the relationship.

    Maybe lots of salt does cause stomach cancer. I honestly don't know what to think. But I do think that caution is needed when evaluating observational studies for the purpose of establishing causality, especially when they are so often contradictory (see another study on salt and stomach cancer here that shows an opposite conclusion from the mainstream: http://cebp.aacrjournals.org/cgi/reprint/1/7/607.pdf)

    David

  • freecicero

    4/7/2009 12:37:00 PM |

    Dr. Davis:

    What do you think of the ideas of those who advocate drastically increasing iodine intake to Japanese levels?

    Examples:

    http://www.optimox.com/pics/Iodine/opt_Research_I.shtml

    Radio inteviews Dr. Stan, Dr. Blaylock, Dr. Flechas:

    http://curezone.com/ig/f.asp?f=1723

  • Anonymous

    4/8/2009 4:56:00 PM |

    Lack of iodized salt may not be as big an issue as lack of iodine in store bought baked goods. We absorb only 10% of the iodine in salt but 90% of the iodine in baked goods. Bakeries used to condition doughs with iodine but now use bromine which competes with iodine. We are now under-Iodiniated and over-Brominated.

  • Anonymous

    4/8/2009 4:58:00 PM |

    Braesikalla, insulin is not a steriod hormone, it is a peptide.

  • Trinkwasser

    4/12/2009 2:13:00 PM |

    I've seen localised clusters of goiters in Europe but hadn't realised you had such a large zone of iodine depletion.

    Here (UK) we have localised areas of other mineral shortages, animal farmers have to put out salt licks or add magnesium, manganese etc. to the feed, and some arable and vegetable farmers need to mineralise their soil. There are large areas deficient in selenium (and I believe in some parts of China it is at near toxic levels) your local farmer may be someone to ask about your local conditions.

    They told me to eat less salt and my BP kept going up, plus I started getting leg cramps. I ate less carbs and it came back down, they didn't tell me that one! I believe the population of salt sensitive hypertensives is quite low, yet they tell the rest of us to avoid it as well.

    Strangely when I was chomping sodium bicarbonate (acid reflux) I started getting leg cramps again, that time adding magnesium sorted them (and my electrolytes came back spot on) the interrelationship can be complex.

  • Dane Miller

    4/16/2009 2:27:00 PM |

    Who avoids salt?  That seems ridiculous.  Especially if you exercise, you need even more salt.

  • fierce4nations

    5/24/2009 3:50:01 AM |

    High salt levels can build up in your body and chlorine (chloride from the sodium chloride aka table salt) can displace the nessesary iodine in your body especially from thyroid. This can cause health problems including goiters. Iodine can be relaced by consuming it in small amounts. One very effective way is by adding small amounts of Lugol's solution of iodine in your drinking water. A couple of drops per liter is enough. Pure iodine itself will not dissolve in water therefore you must have some type of iodine solution in order to properly intake it.
    You can easily make your own Lugol's Iodine. Here is the formula: (adjust it to your desired amount by multiplying or dividing the factors)
    10 grams of potassium iodide
    5 grams of pure iodine (crystals, prills, or flakes)
    85 mL of distilled water or drinkable (spring) water
    Mix the potassium iodide with the water first then add and stir the iodine until all is dissolves. This usually takes some time but can be speed up by heating the water a little.
    You can purchase iodine and potassium iodide at www.ushalogen.com

  • Dana Seilhan

    9/27/2010 3:02:43 AM |

    It might be better to think of the buy-local movement in terms of, "It's silly to buy foods from elsewhere that we're perfectly capable of growing here," while still importing foods that contain nutrients that are deficient locally.  That's the whole point of trade, after all:  acquiring things you wouldn't have otherwise.

    Expecting foods grown in the ground to provide us with iodine when we've got perfectly good seafood in the oceans that give us the same thing is kind of silly.  Rather on the order of using tofu or seitan as meat substitutes when there are perfectly good cows and chickens running around out there.

    An alternative, too, is to completely avoid goitrogenic foods if you live far from the sea.  It's believed that this is why cruciferous vegetables taste bitter to some people but not others:  the genes responsible seem to have evolved in people who lived far inland.  They needed to maximize thyroid function, so a mutation that allowed them to detect foods that were most likely to mess with thyroid function came in very handy.  No reason we can't make conscious choices in that direction now--it's not like we can't live without any of the foods in question.

    Dealing with environmental pollution and avoiding chemical stressors is important too, as you know.  But every little bit that we ourselves can control right now, counts for something.

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