Throw away total cholesterol!

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

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

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

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

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

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

Smart Start not so smart




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

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

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

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

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

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

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

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

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

Does anybody have a normal vitamin D level?

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

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

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

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

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

Don't believe your LDL cholesterol!

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

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

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

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

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

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

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

Are you the exception?


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

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

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

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

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

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

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

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

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

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

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

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

Other evidence that self-empowerment in health is growing:

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

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

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

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

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

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

Vitamin D deficiency is rampant

Today alone I've seen several people with severe deficiencies of vitamin D.

We're now checking everyone's blood vitamin D level at the start of the program. The measure that most accurately reflects your vitamin D status is 25-OH-vitamin D3. This is very confusing to many physicians, who traditionally have thought of 1,25-di-Hydroxy vitamin D3 as the standard test to measure. What they're failing to recognize is that this second measure is a kidney product, not a reflection of vitamin D status.

Using 25-OH-vitamin D3, several people today alone had levels of <10 ng/ml, clearly in the category of severe deficiency (generally regarded as <20ng/ml).

The majority of people we see in the office are Wisconsin residents. It's no wonder they're deficient. Although it's mid-May, we've seen the sun only a handful of days this year. And most of the days have been too chilly to wear short sleeves and shorts to permit sufficient surface area for UV exposure.

Living in a sunny climate, however, is no guarantee that you have sufficient blood vitamin D levels. Two recent studies have shown that 30-50% of the residents of sunny southern Florida and Hawaii are also deficient. (Why, I'm not sure.)

Although our experience thus far is anecdotal in several hundred people, my impression is that people who have normal blood levels of vitamin D (we regard normal as 45-50 ng/ml) have a far easier time of halting or regressing coronary plaque.

Vitamin D is among the most exciting nutritional tools we've come across in a long time. The conversation is making the media, which impresses me tremendously, given the fact that nobody stands to profit financially to any significant degree through vitamin D supplementation.

For a wonderful collection of discussions on vitamin D, go to Dr. John Cannell's website, www.vitaminDcouncil.com. You'll find a huge quantity of scientific background and conversation on the whole idea. I believe you will be thoroughly impressed with just how powerful the argument in favor of vitamin D has become.

What if wheat products were illegal?

Imagine if anything made of wheat were illegal: bread, bagels, crackers, pasta, pretzels, donuts, Shredded Wheat cereal, Raisin Bran, pastry, cookies, cakes, cupcakes. . . Your grocery store would then be unable to carry any of these products.

How empty would the grocery store shelves be?

There would be very little. The stores would be filled instead with vegetables and fruits, meats, and dairy products. But aisle after aisle would be empty. There'd be no cereal aisle. There'd be no snack chip aisle. The ordinarily overcrowded bread shelves wouldn't be there.

Bakery? Nope, not there either. Pasta and noodles? Empty. How about cakes and pastries? Also gone.

Getting the picture? American groceries are dominated by wheat products. What would happen to your health and the health of your family if wheat were abruptly removed from your choices? Would you be less healthy?

No. In fact, your health would be hugely improved. You'd lose a significant quantity of weight. Extraordinary numbers of people would lose diabetic or pre-diabetic tendencies. Feelings of sluggishness, sleepiness, and moodiness would dissolve. Blood pressure would be reduced. The incidence of cancer, skin disease, and inflammatory diseases would plumet.

From a plaque control perspective, your HDL cholesterol would rise, triglycerides drop. Small LDL would improve dramatically.

The message: Slash wheat products from your diet. Yes, you'll miss the smell and taste of freshly baked bread. But you'll do it for many more healthy years. And you may do it without a 14 inch scar in your chest.

The sobering tale of small LDL

Every day, I learn to respect small LDL more and more.

Small LDL particles, and its evil partner, low HDL, is among the most common reasons why someone fails to fully gain control of coronary plaque and heart disease risk.

Just yesterday, I saw a slender businessman (6 feet 1 inch in height, 186 lb.) whose small pattern persisted despite niacin, fish oil, oat bran, and raw almonds. We generally think of small LDL as an overweight person's pattern, but in some people the genetics are quite powerful and it can be expressed even in slender people.

The solution: More physical activity and exercise; cut back on processed carbohydrates, particularly wheat products like breads, pasta, crackers, breakfast cereals; think about magnesium (see our two recent reports on magnesium on the www.cureality.com membership website, the latest report to be posted this week); be sure sleep is adequate (gauge this by whether you're energetic during the day and don't fall asleep watching TV or movies). Lack of sufficient physical activity in people with sedentary jobs is probably among the most common reason the small LDL pattern persists.

Ignore small LDL and it can be like a hidden cancer in your body, growing and metastasizing (not literally, of course), fueling coronary plaque growth. Be sure your doctor assesses whether you have small LDL if you hope to gain control of your coronary risk.

Burn off the fat

If you've ever wondered just how many calories you're burning with various activities like yard work, driving, climbing stairs, etc. go to this great website that will calculate it for you: http://www.caloriecontrol.org/exercalc.html.

Here are some examples:


Dancing for 30 minutes(fast, e.g., tango): 193 calories
Yoga for 30 minutes: 204 calories
Washing the car for 30 minutes: 173 calories
Vacuuming for 30 minutes: 88 calories

(All are for a 170 lb person.)

As you see, physical activity does not necessarily have to consist of exercise. It doesn't require fancy equipment or expensive outfits. But it does require you to keep moving. Sedentary work is among the most common reasons I see in my patients for failing to control weight and its associated lipoprotein patterns, like low HDL and small LDL.

If your work is sedentary, then a minimum of 60 minutes of physical activity per day is necessary to begin to correct weight-related patterns. If you gauge by calories burned, then a useful goal is 500 calories per day in physical activity--at a minimum.
All posts by william-davis

Take a niacin "vacation"

I've been seeing a curious niacin phenomenon that has not, to my knowledge, been reported anywhere in the medical literature.

People with lipoprotein(a), or Lp(a), are best treated with niacin, particularly given the relative lack of other effective therapies. I now have seen approximately 10 people with great initial responses to niacin, only to observe Lp(a) levels slowly drift back up to the starting level over a period of 2-3 years.

In other words, if starting Lp(a) is 200 nmol/l (approximately 80 mg/dl), drops to 70 nmol/l on niacin. Then, over 2-3 years of treatment, it drifts back to 200 nmol/l. Very frustrating.

Somehow, your body's Lp(a) manufacturing mechanism circumvents the niacin, sort of like antibiotic resistance (without the bacteria, of course).

My response to this, though untested, is to have people take an occasional "niacin vacation". I don't mean take a trip to the Bahamas while on niacin. I mean take 2 weeks off from niacin every three months or so. My hope is that the occasional vacation from niacin will allow the body to continue to respond and suppress "resistance". When resuming niacin, you may have to escalate the dose gradually to avoid re-provoking the "flush".

The same "resistance" seems to develop to testosterone in males: an initial drop followed by a gradual increase. Curiously, I've not seen this in females with estrogens, which seems to generate a durable Lp(a) suppressing effect. For this reason, an occasional testosterone "vacation" might also be considered.

So far, I've advised several people to try this. The long-term success or failure, however, is uncertain. I know of no other solutions, however.

If you have Lp(a) and are on long-term niacin, you should consider talking about this issue with your physician. Like many aspects of Lp(a), while fascinating in its complexity, much remains uncertain. Stay tuned.

When LDL is more than meets the eye

Jerry wanted to know what to do with his LDL cholesterol of 112 mg/dl. "My doctor said that it's not high but it could be better."

So I asked him what the other numbers on his lipid panel showed. He pulled out the results:

LDL cholesterol 112 mg/dl

HDL 32 mg/dl

Triglycerides 159 mg/dl


I pointed out to Jerry that, given the low HDL and high triglycerides, his calculated LDL of 112 was likely inaccurate. In fact, if measured, LDL was probably more like 140-180 mg/dl. LDL particles were also virtually guaranteed to be small, since low HDL and small LDL usually go hand-in-hand (though small LDL can still occur with a good HDL).

So Jerry's LDL is really much higher than it appears. To prove it, Jerry will require an additional test, preferably one in which LDL is measured, such as LDL particle number (NMR), apoprotein B, or "direct" LDL.

It's really quite simple. Jerry likely has a high number of LDL particles that are too small. This pattern confers a three- to six-fold increased risk for heart disease.

Treatment requires more than just reducing LDL. Small LDL--an important component of this pattern, responds, for instance, to a reduction in processed carbohydrates like wheat products (breads, breakfast cereals, pretzels, etc.), NOT to a low-fat diet. Weight loss to ideal weight, especially loss of abdominal fat, will yield huge improvements in these numbers. Niacin may be a necessary component of Jerry's treatment program, since it increases LDL size and raises HDL.

For more discussion on measures superior to LDL cholesterol, see my upcoming editorial, Let Dr. Friedewald Lie in Peace (an expansion of a previous Heart Scan Blog). It will be posted on the Cardiologist on Call column on the Track Your Plaque website within the next week.)

Oil-based vitamin D


As time passes, I gain greater and greater respect for the power of restoring vitamin D blood levels to normal, i.e. 50-70 ng/ml. Just yesterday, I saw several people with blood levels of <10 ng/ml--severe deficiency.

Vitamin D deficiency this severe poses long-term risk for osteoporosis, arthritis, colon cancer, prostate cancer, inflammatory diseases, diabetes, and heart disease. Vitamin D appears to make coronary plaque reversal--reduction of your heart scan score--easier and faster.

But it is important that you take the right kind of vitamin D. Several of the people I saw yesterday with vitamin D levels of somebody living in total darkness were taking vitamin D, but they were taking tablets. Tablets are the wrong form. Powder-based tablets, in my experience, yield little or no rise in blood levels. Some preparations generate a small rise but the dose required is huge.

If you're going to take vitamin D, take a preparation that yields genuine and substantial rises in blood levels. This requires an oil-based capsule. I commonly see blood levels of 25-OH-vitamin D3 rise from, say, 10 ng/dl to 60 ng/ml when oil-based capsules are taken.

The most common dose I prescribe to patients is 2000 units per day to females, 3000-4000 units per day to males in non-sun exposed months. Ideally, your dose is adjusted to blood levels.

The Vitamin Shoppe preparation pictured here is one I've used successfully and generates bona fide rises in blood levels. And it costs around $5. Just be sure the preparation you buy is oil-based.

For rapid success, try the "fast" track

Have you tried fasting?

Before your eyes glaze over, let me tell you what I mean. I don't mean a water-only fast for two weeks while you drool over all the temptations around you and you feel sorry for yourself.

I also don't mean the juice fasts that some people use that turn into fruit juice fasts of pure sugar.

Here's another way to do it. Usually, 48 hours of doing this will yield several benefits:

--Weight loss of 1 lb. You will likely experience an even greater weight loss of 2-4 lbs, but much of this will be water loss.

--If you're like me and share a heightened sensitivity to sugars and carbohydrates (like wheat), you may find out just how awful you feel when you eat certain foods. Many people tell me they feel absolutely wonderful when they fast--clearer thinking, increased energy, improved mood. Not the constant gnawing urge to eat they expected.

--After your fast is over, you look back and realize just what large portions of food you were eating. You'll be content with smaller quantities--and enjoy it more.


The "fast" I've used successfully includes two foods:

1) Vegetable juices--that you either juice yourself or purchase. V8 or its equivalent works pretty well. Though purchased V8 is not the best, it's better than nothing and does work reasonably well. If you juice your own vegetable juices, watch out for the diarrhea if you're unaccustomed to vegetable juices. Four 8 oz glasses per day works well.

2) Soy milk--for a source of protein and modest quantity of sugar and fat. I like the Light Silk Soymilk (Vanilla) which contains 80 calories, 2 g fat (0.5 g monounsaturated), 7 g sugar, 6 g protein per 8 oz glass. Four 8 oz glasses of soymilk also work well. In my neighborhood, 8th Continent is another good choice.


Sip both of these throughout the day. Of course, drink water in unrestricted amounts.

What can you expect in your coronary plaque control/heart scan score reversal program? When the fast is over, a rise in HDL, reduction in small LDL, reduction in triglycerides, reduction in blood sugar and insulin, and a smaller tummy. This strategy can be useful to kick-start weight loss efforts or as a periodic way to maintain control over weight and lipid/lipoprotein patterns.


Nutritional Composition Silk Soymilk--Vanilla

Nutrition Facts
Serving Size 1 cup (240mL)
Servings per container 8 H/G OR 4 QT

Amount per Serving

Calories 70
Calories from Fat 20

% Daily Value
Total Fat 2g 3%
Saturated Fat 0g 0%
Trans Fat 0g
Polyunsaturated Fat 1g
Monounsaturated Fat 0.5g

Cholesterol 0mg 0%
Sodium 120mg 5%
Potassium 300mg 8%
Total Carbohydrates 8g 3%
Dietary Fiber 1g 4%
Sugars 6g
Protein 6g
Vitamin A 10%
Vitamin C 0%
Calcium 30%
Iron 6%
Vitamin D 30%
Riboflavin 30%
Folate 6%
Vitamin B12 50%
Magnesium 10%
Zinc 4%
Selenium 8%

No flush = No effect



"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."


That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.

"Black holes" on heart scan


Lots of smokers, especially younger smokers, rationalize their habit by telling themselves that they'll stop if and when any hint of adverse health effects develop.

The problem is that, even in the first decade of smoking, dramatic and profound effects can develop--but you won't know it.

One of the most graphic examples of this I see every day in people who have heart scans. While CT heart scans are, of course, for identification of coronary plaque/coronary disease, they're also great for visualizing the lungs.

This man is a light smoker. The lungs are the black tissues (that's normal) on either side of the (white) heart in the center. Now, note the holes in the lung tissue. That's what they literally are: holes left by the destrucive, tissue-eating effects of cigarette smoking.

How common are the holes (or emphysematous "blebs", as they're called in medical lingo)? Very common. You'll even see them in 30-somethings who've smoked only a few years.

These are holes that have nothing in them. The lung tissue that was destroyed to create the hole will never grow back, even when smoking stops. The holes in this example are actually small to average in size. I've seen much bigger. And this only represents the early stages of lung tissue destruction. A long-time heavy smoker shows all other sorts of abnormalities.

Whenever I show these "black holes" to people who smoke, they are horrified and I've actually gotten many people to quit. Take the opportunity to quit as soon as you can if you smoke.

Small LDL--a persistent bugger

Sometimes, small LDL is easy to get rid of. Take niacin, for instance, and it can simply disappear from your body.

But other times, it can be aggravatingly persistent. Several times every day, in fact, I need to run through the checklist of strategies to reduce small LDL with patients.

How important is small LDL? In my experience, it is among the most potent causes behind coronary plaque known. It's a big part of the explanation why some people at an LDL of cholesterol of X mg/dl will have heart disease, while others with the same X mg/dl of LDL will not. When present, small LDL particles are much more likely to trigger atherosclerotic plaque formation. Small LDL particles magnify Lp(a)'s ill-effects tremendously. The data vary but small LDL probably increases heart attack risk at least three-fold.



Here's a checklist of strategies that I advise patients to consider to minimize the small LDL pattern:


--Lose weight to ideal weight--This is very important and effective.


--Fish oil--A relatively small effect unless triglycerides are high to begin with.




--Reduction of wheat products--This can provide a BIG effect. More precisely, a reduction in high-glycemic index foods is effective. But the biggest day-to-day high-glycemic food culprits are wheat products like breads, pasta, crackers, chips, pretzels, and breakfast cereals. "You mean whole wheat bread makes small LDL?!" Yup.


--Reduction of sweets--For the same reasons as reducing wheat products.


--Add raw almonds and walnuts--1/4 to 1/2 cup per day.




--Replace wheat products with OAT products, especially oat bran. This does NOT mean oat-containing breakfast cereals with added sugar and wheat, e.g., Honey Nut Cheerios, Cracklin' Oat Bran Cereal, etc. You might as well eat candy. Buy oat bran as plain oat bran--nothing added. Use it as a hot cereal or added to yogurt, "breading" for chicken, etc.




--Vitamin D--A variable effect, likely resulting from its beneficial effects on "insulin resistance".


--Exercise


--Niacin--Very effective but not always enough.


Among the choices, my favorites are weight loss, niacin, and reduction of wheat products. Those will give you the biggest bang for your buck.

Red badge of courage

A group of 60- and 70-somethings were standing in the anteroom to the cardiac rehabilitation center. All (males) had their T-shirts pulled up, comparing their coronary bypass scars.

It reminds me of war veterans comparing their war wounds. The scars of suffering, of having "conquered" and won a war with a common enemy, a badge of courage.

This is part of the broad social acceptance of bypass surgery and other major procedures for heart disease. Hospitals support it. They do it for the psychological support for patients enduring a difficult process. Often, talking about a shared experience can be a helpful purge for the fears and frustrations of a traumatic event.

Curious thing, though. I've actually had people request bypass surgery simply because all their friends have had one. No kidding. "I just figure my time is coming. I might as well get it over with."

Get the picture? We've had a battle with heart disease and the hospitals have won. The enormous success of hospitals over the last 20 years is not because of delivering babies, it's not from psychiatric hospitalization, it's not from cancer treatment. It's from heart disease. The largest floors in the hospital are usually the cardiac floors. The bulk of revenues and profit are from heart disease.

If I manufacture widgets and each widget I sell makes me scads of money, guess what? I want to sell more and more widgets. I'll persuade people they need my widgets even if they don't. Perhaps I'll even persuade them that buying one is a noble cause. Maybe I'll subtly suggest that I am a charitable operation and I only sell my products for the public good. I could even name my company after a saint. Personal profit--absolutely not!

Ignore the hype. See hospitals and their "products" for what they are: A necessary service--some of the time; profitable products that they hope to sell to more and more people most of the time.

"We don't believe in heart scans"

Tim's CT heart scan score was an earth-shattering 3,447, clearly in the upper stratosphere of percentile rank. Risk of heart attack: 25% per year. At age 58, it was a wonder that nothing had happened yet.

Tim went to the Cleveland Clinic for an opinion, long a powerful bastion of heart procedures. The consulting cardiologist told Tim, "We don't believe in heart scans. They're wrong too often."

An opinion from a widely-respected cardiovascular center. If they don't "believe" in heart scans, does that mean they "believe" in stents and bypass surgery? Does it mean that the thousands of research studies that have now been published on the value of heart scanning are pure fiction? Is there a choice to believe or not believe?

I continue to be shocked at the extraordinary ignorance on the topic of heart scanning among my colleagues. The number one killer of Americans and you still rely on stress tests?

Why this perception that heart scans are "wrong too often"? What this cardiologist means, I believe, is that when people are taken to the cath lab for catheterization, a substantial number of those with positive heart scan scores don't have "blockage". But I could have told him that even before the heart catheterization.

There is an expected and well-documented likelihood of finding significant "blockage" based on your heart scan score. At Tim's scary score of 3,447, what is the likelihood of "blockage" of 50% or more? It's around 40-50%. That means that half the people at this score will have a blockage sufficient to justify inserting stents or undergoing bypass surgery, half will not. There will indeed be many plaques, but none severe enough to block flow.

Does that make the heart scan wrong? I don't think it does. Just because you don't need a major procedure to "fix" blockages does not mean that no heart disease is present. Without preventive efforts, Tim's heart attack risk remains an alarming 25% per year--whether or not he gets stents or bypass. The only treatments that substantially reduce this risk (in an asymptomatic person) are preventive efforts, not procedures.

Yet cardiologists like the one Tim consulted at the Cleveland Clinic regard heart scans as something "he doesn't believe in". I would suggest a return to the textbooks and published literature and re-thinking how heart disease should be managed.

Heart scans should provide an opportunity for prevention, not an opportunity for profit.

More on the “Rule of 60”

Despite its apparent simplicity, there’s a lot of thought and wisdom in the Rule of 60.

What if you achieve only a single value in the Track Your Plaque “Rule of 60”? What if, for instance, you got LDL down to 60 mg/dl, but ignored the fact that your HDL was 41 mg/dl and triglycerides were up to 145 mg/dl? Can you still do pretty well?

Probably not. In fact, this specific combination of low HDL and high triglycerides tells me several things:

1) LDL is really much higher than suggested by the 60 mg/dl, which is a calculated value, often much higher. Recall that calculated LDL is prone to immense inaccuracy. When measured, the LDL is commonly somewhere between 120 and 160 mg/dl. However, when you raise HDL to 60 and reduce triglycerides to 60, much of the inaccuracy is removed, i.e., calculated LDL becomes more accurate. LDL can be measured as LDL particle number (NMR), apoprotein B, or direct LDL.

2) LDL particles are small. This is yet another reason why the weight-based LDL measures can be inaccurate. Imagine you have two identical glass jars full of marbles. One jar has small marbles, the other has large marbles, but both jars have the same weight in marbles. Which jar has more marbles? The one with small marbles, of course. The same phenomenon occurs with LDL particles: at the same weight, you can have different numbers of LDL particles. It’s the number of particles that better determine risk for heart disease, not the weight.

3) Triglycerides of 145 mg/dl is actually below the target advised by the National Cholesterol Education Panel Adult Treatment Panel-III guidelines, i.e., you’re okay by conventional standard. But look beneath the surface, and you’ll find that triglycerides at 145 mg/dl are associated with flagrant excesses of VLDL lipoprotein particles and a greater likelihood of a postprandial (after-eating) disorder (increased IDL or postprandial triglycerides), both of which add to coronary plaque.

4) This pattern is also commonly associated with higher blood sugar, higher blood pressure, increased inflammation (e.g., C-reactive protein), increased fibrinogen—all the facets of the metabolic syndrome, or pre-diabetes.

In fact, some of the most aggressive plaque growth—increasing heart scan scores—will occur with this specific pattern. So just achieving one facet of the Track Your Plaque Rule of 60 does not suffice. It’s the whole package that really stacks the odds in your favor of stopping or dropping your heart scan score.
All posts by william-davis

American Heart Association stamp of approval

The American Heart Association (AHA) has a program called the Heart-Check Mark, an "approval" process that permits a food manufacturer to affix the AHA logo and stamp of approval on various food products.

A company simply makes application to the AHA. The application and product details are reviewed and then approved or turned down.

To date, 106 companies have obtained the AHA stamp of approval on 768 products. What kinds of products are on the approved list? Here's a sample:

--Honey Bunches of Oats

--Kellogg's Frosted Mini-Wheats

--Cocoa Puffs cereal

--Cookie Crisp cereal ("The great taste of chocolate chips in every bite!")


There are 764 others. If you doubt this, just go to the store and take a look at the product containers.

What the heck is going on here? Most of us with any judgment know that these products are pure sugar. They may contain "no more" than 15-40 grams sugar per sugar, but the principal products--corn, wheat, fructose--mean that these products are, in effect, nearly pure sugar. Yet they carry the AHA stamp of approval.

What do products like this cause? It's a long list but the major effects include:

--Obesity

--Diabetes

--Drop in HDL

--Rise in triglycerides

--Small LDL particles

--Heightened inflammation (i.e., C-reactive protein)

--Mental cloudiness


Need I go on? Why are products like these and many others deserving of the AHA heart-check approval? Because they lack high fat and saturated fat (3.0 grams, 1.0 grams respectively, by AHA criteria). In other words, just lacking these ingredients means that, to the AHA, they qualify as "heart healthy."

By that same line of reasoning, many candy bars are "heart healthy", as are many cookies and cupcakes.

What's the reason behind this extraordinary absurdity? Is the AHA stupid?

There may be many reasons, but one very suspicious fact becomes immediately obvious when you realize these endorsements product a substantial revenue source for the AHA, since companies must pay for the right to use the heart-check approval mark. Also, just look at the major contributors (millions of dollars) to the AHA: ConAgra, General Mills, Kraft, etc.) You get the picture.

Does this make the AHA evil? Not necessarily. But it seriously erodes credibility. it also should make you very leery of any advice that comes from such an agency that is reluctant to bite the food manufacturer hands that feed it.

In my view, we simply cannot rely on the AHA for genuine, unbiased heart health advice.

"Your heart scan score means nothing"

Charles was visibly confused.

He'd gotten his CT heart scan after hearing one of the local scan center's ads on the radio. His score 2773, obviously in the 99th percentile for any age.

"Do you think the score means anything? My primary doctor said that it was meaningless because it was all in the deep wall of the artery. He said that it has nothing to do with risk for heart attack. As long as I feel good, he says don't do anything."

What exactly did his doctor mean, in the "deep wall of the artery"?

What the doctor is referring to is the fact that some people with a long history (many years) of diabetes or kidney failure (also for many years) tend to develop calcium deposits in the media, or muscular layer of arteries. The media is the tissue thin layer just below the intima, the most inner layer of arteries that we usually associate with atherosclerotic plaque and the layer that is most prone to calcium accumulation that we score on heart scans.

Aging, generally into your late 70s, 80s, and onwards, also increases the likelihood of medial calcification. Lastly, longstanding deficiency of vitamin D encourages medial calcification.

Is there any way to distinguish intimal vs medial calcification on a heart scan? No, there is not. Having read many thousands of CT heart scans, I can tell you that there is no practical way in 2007 to tell the difference.

Then how did this doctor "know" that Charles' calcium was "deep walled" or medial? Simple: He didn't. This was yet another example of ignorance based on old thinking. Unfortunately, he did Charles a serious disservice by dismissing his heart scan score that predicted a 25% per year risk for heart attack.

Interestingly, whether calcium is intimal as in atherosclerotic plaque, or medial, both are strongly associated with risk for heart attack. In other words, if calcium is confined to the intima, heart disease risk is present. If calcium is limited to the media, risk is still present.

In all practicality, the only difference we make of the intima vs. media argument (that is, when the distinction has been made by some other means like intracoronary ultrasound, the test that is truly necessary to distinguish the two patterns) is that medial calcification may be more powerfully related to vitamin D deficiency. Thus, someone with heavy medial calcification may require closer attention to maintaining a perfect year-round blood level of 25-OH-vitamin D3. But that's the only practical difference.

Vitamin D toxicity?

"My primary care doctor said to stop the vitamin D because it's toxic. So I stopped it and I just take a multivitamin. He said that a multivitamin and two glasses of milk a day was all I needed."

So proclaimed Eleanor to me. This happens around once every week by doctors frightened of the vitamin D.

So I reminded Eleanor that, before starting vitamin D supplementation, her blood level of 25-OH-vitamin D3 had been 17 ng/ml--severe deficiency.

On 4000 units per day (oil-based gelcap), her blood level had been 37 ng/ml--still deficient, below the desirable range of 50-60 ng/ml. That's the dose Eleanor's doctor had declared "toxic."

When exactly does deficiency develop? There's not full agreement on this, but Dr. Michael Holick of Boston University, among the most experienced and insightful authorities on vitamin D, states that toxicity is more likely when blood levels exceed 150 ng/ml (Nutr Clin Pract. 2007 Jun;22(3):297-304).

In other words, Eleanor and her doctor should not be concerned with toxicity, but with the persistent levels of deficiency she is suffering.

Some authorities call the behavior of vitamin D "bi-phasic": Deficiency is toxic, excessive levels are toxic. We're really just trying to achieve a middle ground in vitamin D levels that are above deficiency but below toxicity.

In reality, deficiency is exceptionally common. In fact, it's the rule around here (northern U.S.), with >95% of everybody we check severely deficient in winter, mildly-moderately deficient in summer. Very few people approach normal levels year round without supplementation.

Toxicity, on the other hand, is exceedingly rare. I have seen it once in a woman who was taking a toxic dose of 50,000 units a day on the instructions of her (mis-guided) doctor. Thankfully, no ill-effects developed from this little "experiment."

So, it's not toxicity that is the overwhelmingly common worry, but deficiency, severe and sustained.

Non-profit hospitals

Take a look at your local hospital and you're likely to notice several curious things:

1) It is likely non-profit, meaning it enjoys a non-profit status with the Internal Revenue Service and enjoys the tax benefits of not paying taxes on profits. This provides an advantage to tax-protected hospitals. 70% or more of hospitals in the U.S. are "non-profit."

2) Non-profit or no, many hospitals operate under the guise of a religious affiliation, e.g., St. Mary's Hospital, Trinity Hospital, All Saints', Jewish Hospital, etc.

3) Executives in non-profit hospitals can make capitalistic salaries. One CEO of a Milwaukee hospital took home $3.7 million dollars in salary last year. That's not including the very substantial perks and business interests in the spin-off businesses the hospital owns, including pharmacies, drug and medical device disitributors, even a venture capital division. "Non-profit" does not have to mean that executives within the operation can't benefit handsomely.

That same hospital system spends over $10 million dollars in a year in local marketing for TV ads, print advertising, etc. Ads are slick and professionally produced.

Make no bones about it: These are "non-profit" for tax purposes only . They are for-profit in every other sense of the phrase, including rich rewards for the insiders.

Guess how those fat executive salaries and large marketing budgets are paid for? That's right: the 12-inch incision in your chest; the four stents, defibrillator, and repeated nuclear stress tests; the revolving door of hospitalization after hospitalization that typifies the "heart patient" experience.

See the hospital for what it is: In the 21st century, it is no longer a charitable operation worthy of your volunteer time and donations. It is a business no different than Home Depot, IBM, or--Enron. Yes, they do perform needed services, as well. But the perverse equation that often determines who needs hospitalization and who doesn't, who needs a heart procedure and who doesn't, is not always based on necessity but on financial return. Just ask the CEO.

What's the best lipoprotein test?

This is a frequent question from Track Your Plaque Members and others interested in improving their heart disease prevention program beyond that of simple-minded cholesterol testing.

I obtain lipoprotein testing every day on patients. I can tell you with the confidence of having done thousands of these tests that plain, old-fashioned cholesterol testing is like relying on riding a scooter to work compared to an 8-cylinder modern automobile. The scooter might get you there, but any rain, snow, or long distance to travel and you can just forget it.

All too often, lipoprotein testing uncovers abnormalities that standard cholesterol testing simply fails to uncover.

So, among the various lipoprotein tests available, which is best?


There are three commercial tests available today:

1) Gel electropheresis (GGE)--often known by its "brand" name as the Berkeley lipoprotein profile, after Berkeley HeartLabs. GGE uses a gel with an electric field applied to cause lipoproteins to migrate, based on particle size and charge.

2) Vertical auto-profile (VAP)--a form of centrifugation, or high-speed spinning of blood plasma to separate lipoprotein particles.

3) Nuclear magnetic resonance (NMR)--the idea of putting plasma in an NMR (also known as MRI) device to characterize blood proteins.

All three tests do an excellent job. All are competitively priced. All have validating data--lots of it--to justify their broad use (though health insurers, in their vast wisdom, would still have you believe that the tests are "experimental").

But is one better?

Having done many of all three (though least of VAP), I am partial to Liposcience's NMR. (By the way, I receive no fees from Liposcience to use their test, nor to promote it in any way.)

I believe NMR is superior in a few ways:

1) I believe that the LDL particle number is the best way to truly quantify LDL, better than apoprotein B and "direct" LDL.

2) It provides what I believe to be more accurate small LDL measures.

3) It provides intermediate-density lipoprotein (IDL), a post-prandial, or after-eating, measure not available on the other two.

Perhaps I'm biased because I use the NMR most frequently. But I've used it because I felt it yielded superior, more clinically believable, data.

In truth, all three laboratories do an excellent job and you'd be served fine by obtaining any of the three. But my heart goes to NMR.

Vitamin K2, aspirin, fish oil and blood thinning

An interesting question came up from one of our Track Your Plaque Members on the Forum.

"I am now taking 9 mg of vitamin K1 and 1000 mcg of K2.

Does taking this supplement with this much K1 have a counteracting effect on the thinning/anticlotting properties of aspirin and fish oil that I also take?"


Great question (along with lots of other greater discussions we have on the Forum.)

The answer: Vitamin K should have no effect on the platelet-blocking effects of aspirin or fish oil. The majority of blood clot inhibiting effects of aspirin and fish oil arise from their ability to keep blood platelets from "clumping" (just like the TV commercials for Plavix).

Vitamin K, on the other hand, participates in the liver production of blood clotting factors (like II, VII, IX, and X, among others for you curious ones).

Thus, vitamin K-dependent clotting factors and platelet-blocking are two separate pathways to forming blood clots. Some of us refer to the difference as "red clots" from the vitamin K pathway and "white clots" from the platelet pathway, since they really do have this different physical appearance.

The vitamin K2 conversation, like that about vitamin D, is fascinating for its potential to provide the missing link between the tightly-tied fortunes of bone health and atherosclerosis. Why is someone with a high CT heart scan score far more likely to have osteoporosis? Vitamin D and K2 deficiency may provide the missing link for many people.

"Drug no cure for gluttony"

That's the headline I'd like to see associated with rosiglitazone, brand name Avandia.

The recent negative press, whether deserved or not, surrounding the prescription drug rosiglitazone for pre-diabetes and diabetes highlights the fact that drugs never--never--substitute for what we can achieve with lifestyle changes.

Typically, rosiglitazone reduces blood sugar a few milligrams, reduces C-reactive protein, and very modestly reduces triglycerides and its associated evil lipoprotein friends. It also causes an average weight gain of 8 lb in the first year of use.

What will weight loss achieve, especially if accomplished through dramatic reduction or elimination of processed carbohydrates and wheat products, along with fish oil supplementation, vitamin D normalization, and exercise? Extraordinary benefits, far superior to what is achievable with this drug. In fact, while rosiglitazone is a Band-Aid for this process, the lifestyle changes can represent a cure in many or most instances.

It should come as no surprise that a drug that does nothing more than increase sensitivity to insulin cannot erase the devastating effects of an unhealthy life. Take rosiglitazone but neglect exercise, don't bother with vitamin D, indulge in pretzels and breakfast cereals, gain more weight . . . It serves the drug company's agenda better than it serves health.

Rosiglitazone not so rosy?

Dr. Steve Nissen of the Cleveland Clinic published a study that suggests that the pre-diabetes and diabetes drug, rosiglitazone, may increase likelihood of heart attack by 43%.

I say "suggests" because the analysis was something called a "meta-analysis", a re-examination of data obtained by pooling unrelated studies and reanalyzing the data. Strengths of this sort of analysis: Sometimes trends that are not evident in smaller studies finally become evident in the larger numbers of participants obtained through pooling of data. Downside: Any statistician will tell you that a meta-analysis can only suggest an association, it cannot prove it.

Nonetheless, we are talking about people's lives. As they say, if you are taking this drug, also known by the brand name, Avandia, then talk to your doctor. I think that this is sound advice, as there are a number of factors to weigh in decision making. For instance, how far along the diabetic path are you? Have you had negative experiences with other agents?

It will, unfortunately, be months to years before confirmatory evidence on this question become available. In the meantime, Nissen will accuse the drug industry of pushing drugs through the FDA approval process without full safety data. GlaxoSmithKline, the manufacturer of Avandia, will counter with claims of weak data, the existing trials not confirming Nissen's findings, etc. We've seen it before.

My take on this is to step back and look at the broad picture. Do we need yet another reason to say that it's far better to maintain normal body weight, dramatically reduce reliance on processed carbohydrates and wheat, exercise, and following other insulin-sensitizing strategies, rather than rely on insulin-sensitizing drugs? (That's what rosiglitazone is supposed to do.) Metabolic syndrome, also known as pre-diabetes, or diabetes is present to various degrees in two thirds of all adults I meet. Nearly all of it is self-inflicted. Nearly all of it is curable with the above lifestyle strategies if undertaken early enough in the process.

A 190 lb, 5 foot 2 inch woman, or a 220 lb, 5 foot 10 inch man, both of whom are surprised that they have pre-diabetes really need to get a grip on reality and health. To me, it's no surprise that drugs do not reverse all the nasty manifestations of lifestyle gone berserk. It should also come as no surprise that the complex, chaotic physiologic mess created by metabolic syndrome and pre-diabetes is not perfectly managed by adding one drug.

The lipid distorting effects of weight loss

Roger experienced a near-fatal heart attack 6 years ago. He survived thanks to the quick action of bystanders who initiated CPR and called 911. An emergency catheterization was performed and a stent implanted into the closed right coronary artery. But that's not why I tell Roger's story.

Since then, Roger has become comfortable with the idea that he has heart disease. His initial commitment to good nutrition and exercise has waned, as it often does in us distractable humans. So Roger gained about 30 lbs through a long winter, inactivity, eating frozen dinners, and the cookies and baked goodies his daughters made him.

As a result of the weight gain and inactivity, Roger's HDL dropped to 32 mg/dl, triglycerides rose to 211 mg/dl, blood sugar crept up into the pre-diabetic range of 116 mg/dl. Undoubtedly, small LDL was out of control beneath the surface. His tummy reflected the weight gain, flaccid and overhanging his belt.

I read Roger the riot act. I reminded him of what he had experienced and nearly didn't survive. Weight loss and a re-invigoration of his nutrition and exercise efforts was going to be crucial.

Roger listened and took it to heart. Over three months, he lost 24 lbs, a phenomenal result. However, his repeat lipid panel showed an HDL of 28 mg/dl, triglycerides 234 mg/dl, blood sugar unchanged.

"I don't get it! I lose all this weight and the number get worse?!" Roger was understandably upset after his enormous effort.

I told Roger that after a profound weight loss, lipids can go berserk for up to two months after weight has stabilized. Typically, HDL drops and triglycerides rise--the opposite of what we want. But wait another two or so months after weight has stabilized and the numbers begin to look beautiful.

Why does this crazy effect happen? I really don't know and I've never heard a satisfactory explanation for it. But it is very real and quite predictable.

The lesson: after a substantial weight loss, be patient. Check your lipid numbers too soon and you might be confused or disappointed. If you do check them, bear in mind that additional time may need to pass before you see the weight loss fully reflected.

Cholesterol reduction and wheat

In my previous post, Identical twins and the explosive influence of weight , we witnessed an excellent example of the profound influence of food choices and weight control on lipoproteins. The heavier twin among these 35-year old male twins (Steve) had an LDL particle number over two-fold higher than his more slender counterpart (Alfred).

The heavier twin, Steve, got here through numerous and longstanding dietary excesses: fast foods, saturated fats, sweets, processed foods. The conventional answer to Steve's lipid dilemma would be to modestly reduce his reliance on saturated fat, exercise, and limit snacks.

How far would that get Steve? Not very far at all. With regards to his high LDL particle number of 2256 nmol/l (representing an "effective" LDL cholesterol of around 225 mg/dl), it would be reduced a little, perhaps 10%.

Notice, however, that 72% of all Steve's LDL particles are small (1639/2256). This is the pattern that responds dramatically to a sharp reduction in processed carbohydrates, especially wheat-containing products.

If Steve were to eliminate all wheat products--all breads, breakfast cereals, pretzels, cookies, cakes, pasta, crackers--LDL particle number will drop dramatically, perhaps 50%, often more depending on the magnitude of weight loss. Small LDL will respond most obviously and will be sharply reduced, perhaps disappear. Incidentally, these changes might not be well reflected by the conventional calculated LDL cholesterol, since small LDL particles are well-concealed by standard measures.

Reducing corn products, white and brown rice, and potatoes would also add to the effect. But, in 2007, wheat products represent 90% of the problem for the majority of people. Reducing or eliminating wheat therefore yields the biggest effect by a long shot.

Steve therefore represents an excellent example of how reducing processed carbohydrates, esp. wheat-containing products, can yield an unexpected and paradoxical reduction in LDL cholesterol as evidenced by the highly accurate LDL particle number (or apoprotein B). Reducing saturated fat sources also helps, but it certainly will not yield the kind of results most people need. You've got to be smarter than the simple-minded conventional advice.

Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.