"You've got 10 minutes"

20. mayo 2009 William Davis (0)
There's a new trend in office healthcare in Milwaukee: Time-restricted office visits.



I'm told by several physicians who are employed by a major healthcare system here in town that they are peridically watched--physically watched by an administrator--to make sure that they do not exceed the allotted 10 minutes of time. My cardiologist colleagues, I gather, were at first incredulous at such intrusions into their practices, but apparently had no choice: They were employees.



Goiter, goiter everywhere

20. mayo 2009 William Davis (25)
The results of the recent Heart Scan Blog poll are in.

The question:

Do you used iodized salt?

The responses:

Yes, I use iodized salt every day
94 (28%)

Yes, I use iodized salt occasionally
56 (16%)

No, I do not use any iodized salt
41 (12%)

No, I use a non-iodized salt (sea salt, Kosher)
126 (37%)

No, I use a non- or low-sodium substitute
15 (4%)


Thanks for your responses.

If only 28% of people are regular users of iodized salt, that means that the remainder--72%--are at risk for iodine deficiency if they are not getting iodine from an alternative source, such as a multivitamin or multimineral.

Even the occasional users of salt can be at risk. The common perception is that occasional use is probably sufficient to provide iodine. This is probably not true and not just because of the lower quantity of ingestion. Occasional users of salt tend to have their salt canister on the shelf for extended periods. The iodine is then lost, since iodine is volatile. In fact, iodine is virtually undetectable four weeks after a package is opened.

In my office, now that I'm looking for them much more systematically and carefully, I am finding about 2 people with goiters every day. They are not the obvious grotesque goiters of the early 20th century (when quack therapies like the last post, the Golden Medical Discovery, were popular). The goiters I am detecting are small and spongy. Yesterday alone I found 5 people with goiters, one of them visible to the eye and very distressing to the patient.

It seems to me that iodine deficiency is more prevalent than I ever thought. It is also something that is so simple to remedy, though not by increasing salt intake. Kelp tablets--cheap, available--have been working quite well in the office population. My sense is that the Recommended Daily Allowance of 150 mcg per day for adults is low and that many benefit from greater quantities, e.g., 500 mcg. What is is the ideal dose? To my knowledge, nobody has yet generated that data.

Thyroid issues being relatively new to my thinking, I now find it incredible that endocrinologists and the American Thyroid Association are not broadcasting this problem at the top of their lungs. This issue needs to be brought to the top of everyone's attention, or else we'll have history repeating itself and have goiters and thyroid dysfunction galore.

For more on this topic, see the previous Heart Scan Blog post, "Help keep your family goiter free."

Goiter and the Golden Medical Discovery

17. mayo 2009 William Davis (19)

Thick neck, or goitre . . . consists of an enlargement of the thyroid gland, which lies over and on each side of the trachea, or windpipe, between the prominence known as "Adam's apple" and the breast bone. The tumor gradually increases in front and laterally, until it produces great deformity, and often interferes with respiration and the act of swallowing. From its pressure on the great blood vessels running to and from the head, there is a constant liability to engorgement of blood in the brain, and to apoplexy, epilepsy, etc.

The causes of the affection are not well understood. The use of snow water, or water impregnated with some particular saline or calcareous matter, has been assigned as a cause. It has also been attributed to the use of water in which there is not a trace of iron, iodine, or bromine. . . The disease is often due to an impeded circulation in the large veins of the neck, from pressure of the clothing, or from the head being bent forward, a position which is often seen in school children.


Treatment

We have obtained excellent results in many cases, not too far advanced, by a method of treatment which consists in the employment of electrolysis. . . Many cases at the present time are operated upon with entire success.

Those who are afflicted with this disease and unable to avail themselves of special treatment cannot do better than to take Doctor Pierce's Alterative Extract, or Golden Medical Discovery, and apply over the skin around the tumor, night and morning, the following, which may be prepared at any drug store:

Resublimed Iodine--One dram
Iodide of Potassium--Four drams
Soft Water--Three ounces 


Apply to the tumor, twice daily, with feather or camel hair pencil.


From The People's Common Sense Medical Adviser by R.V. Pierce, MD; 1918.

Magnesium and you-Part I

15. mayo 2009 William Davis (11)
If this were 10,000 B.C., you'd get your drinking water from streams, rivers, and lakes, all rich in mineral content. Humans became reliant on obtaining a considerable proportion of daily mineral needs from natural water sources.

21st century: We obtain drinking water from a spigot or plastic bottle. Pesticides and other chemicals seep into the water supply. Municipal water purification facilities have intensified water purification in most communities to remove contaminants like lead, pesticide residues, and nitrates. (For a really neat listing of the water quality of various cities, the University of Cincinnati makes this data available.)

But intensive water treatment also removes minerals like calcium and magnesium.

Many people have added water filters or purifiers to their homes,, like reverse osmosis and distillation, that are efficient at extracting any remaining minerals, converting “hard” into “soft” water. In fact, manufacturers of such devices boast of their power to yield pure water free of any “contaminant,” minerals like magnesium included. The magnesium content of water after passing through most commercial filters is zero.

Modern enthusiasm for bottled water has compounded the problem. Americans consumed a lot of bottled water, nearly 8 billion gallons last year. In the U.S., nearly all bottled water has little or no magnesium.

The result is that we can no longer rely on drinking water to provide magnesium. The Recommended Daily Allowance (RDA)—the amount required to prevent severe deficiency—for magnesium is 420 mg per day for men, 320 mg/day for women. In cities with the highest magnesium water content, only 30% of the RDA can be obtained by drinking two liters of tap water per day. In most cities, only a meager 10–20% of the daily requirement can be obtained. That leaves between 70–90% that needs to come from other sources. As a result, the average American ingests substantially less than the RDA.

Blast triglycerides

15. mayo 2009 William Davis (0)
The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

13. mayo 2009 William Davis (15)
Followers of The Heart Scan Blog know my feelings about Cheerios:


Can you say "sugar"?

Cheerios and heart health


There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

12. mayo 2009 William Davis (1)
The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.


From Heart Disease Diagnosis and Treatment
Emanuel Goldberger, MD
1951

Iodine is not salt

12. mayo 2009 William Davis (3)
I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:


Sodium = iodine


Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

10. mayo 2009 William Davis (9)
"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

8. mayo 2009 William Davis (15)
There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself


This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.
All posts by william-davis

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

Risks for coronary disease 2008

31. December 2007 William Davis (27)
According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2

27. December 2007 William Davis (46)


Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.











Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?

24. December 2007 William Davis (6)


Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

21. December 2007 William Davis (44)
Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

20. December 2007 William Davis (17)
Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

18. December 2007 William Davis (25)
Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.