"Get regressive"

This caught my eye:



Niaspan, prescription niacin, now sold by Abbott Laboratories, is now promoting its advantages in regressing coronary plaque:



In patients with a history of coronary artery disease (CAD) and hypercholesetgerolemia, Niaspan (niacin), in combination with a bile acid-binding resin, is indicated to slow progression or promote regression of atherosclerotic disease.



And the new slogan: "Get regressive."



Interestingly, the new marketing campaign is based on relatively old data. They base this new claim on 3 studies:



1) Cholesterol-Lowering Atherosclerosis Study (CLAS)--a 1987

CRP House of Cards

Lew has coronary plaque with a heart scan score of 393. At age 53, that's in the 90th percentile (higher score than 90% of men in his age group).

On our search for causes of his coronary plaque, we identify low HDL of 41 mg/dl, high triglycerides of 202 mg/dl, small LDL (83% of total), calculated LDL of 133 mg/dl, and severe vitamin D deficiency with a starting blood level of 25-hydroxy vitamin D of 19 ng/ml.

His c-reactive protein: 4.1 mg/dl--above the cut-off of 2.0 mg/dl that the pharmaceutical industry is targeting as a mandate for statin therapy, particularly given the JUPITER data.

Lew instead eliminates wheat an

Lessons from the 20-year statin experience

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

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

Small LDL particles and increased HbA1c--An evil duo

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

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

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

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

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

Unforgiving small LDL particles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Do the math: 41.7 pounds per year

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

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

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

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

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

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

We got the drug industry we deserve

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

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

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

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

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

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra bagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")

The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!"

If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:

--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation.

--Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL.

--Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.

--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.

--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL.


While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.

Vitamin D and inflammation

We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack.

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.

In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.


Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.

Zitterman A, Frisch S et al.

BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis.
OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects.
DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program.
RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group.


(Calcitriol = 1,25-dihydroxy vitamin D.)


Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.

Even monkeys do it


It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound.

A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku:

“Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.”

Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."
In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning.

Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves.

Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication.

If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?



Image courtesy Wikipedia

Cath lab energy costs

In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory.

A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).

All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging.

Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath.

Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing.

At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs.

If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold.

By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluids.

That's just one procedure. The amount of trash generated by these procedures is staggering, much of it plastic. I don't know how much of the U.S.'s annual plastic trash burden of 62 billion pounds (source: EPA) originates from the the cath lab, but I suspect it is a big number in total.

So if you are truly interested in reducing your carbon footprint and doing your part to be "green," avoid a trip (or many) to the cath lab.

Wag the Dog

What if the system to provide heart care has already gotten as big as it should be?

Worse (for hospitals), what if it’s already far larger than it needs to be? Can the system continue to increase revenues if they’ve already attained titanic proportions and outgrown demand? After all, darn it, there are only so many sick people around.

Hospital administrators might have to face an unpleasant choice: downsize to strip excess capacity and suffer the consequences in a competitive market, or . . . fabricate demand for their services.

Like the Dustin Hoffman and Robert DeNiro characters in the movie, Wag the Dog, about how two media-manipulators divert public attention away from a Presidential sex scandal by fabricating a war, spin is everything. It’s enough to sidetrack public attention from a scandal, obscure a truth, send us on a useless detour.

If healthcare for the heart isn’t driven by need, but many still desire to reap the benefits of the procedure-focused system, why not increase the perceived need?

That’s precisely the course that many hospital systems have chosen to follow. If the market you serve has been tapped to its full potential, then grow the market.

Imagine if a company like General Motors were to operate this way. In 2006, for instance, GM sold 9.1 million automobiles. If GM executives were to decide that they’d like to outstrip Toyota by boosting sales by 10% to 10 million, how would they do it? They would first have to determine whether it was feasible to grow demand for their product. If deemed possible, the company would need to ramp up manufacturing capacity to anticipate increased demand. If they miscalculate, GM could be stuck with a costly surplus and have to swallow the costs, maybe selling leftovers at a loss. (We don’t mean to pick specifically on GM; they’re a fine company as far as we’re concerned. This is just a hypothetical illustration.)

But what if a company could concoct some sort of scheme to persuade the car-buying public that they just had to have their cars or trucks? In other words, they could, in effect, create demand for their products.

As perverse as it sounds, that is exactly what occurs in healthcare for heart disease. The system long ago exceeded the necessary level of infrastructure to maintain a high-quality level of care accessible to most Americans. Instead, it continues to grow through a distortion of perception, delivering more services of increasing complexity to larger and larger numbers of people.

The size of the market is therefore a manipulable thing, something that can be massaged and cultivated. There are a variety of clever ways to exaggerate the need for heart procedures.

Why not raise the alarm for heart disease every chance you get? When a local sports figure survived a heart attack here in Milwaukee, St. _____ marketing department was right there, broadcasting the process in TV ads after his recovery. What could be more American than baseball, apple pie . . . and St. _____ Hospital? After his hospital discharge, the 57-year old local icon was shown on the sidelines with his team, back on the job, and at home with family, all beaming, just three months after a bypass operation. “I received only the very best care at St. _____ Hospital. They treated me like family. St. _____ doctors and nurses are the best!” Predictably, a two-month long spike in hospital testing followed filled with people worried whether they, too, might be in imminent danger. Several local cardiologists boasted of the many sports figures who came through the stress testing and heart catheterization labs, though virtually all checked out to be fine.

Though it can serve a legitimate purpose in some situations, stress tests are the ultimate example of a heart scam built on the perception of danger. Pull people in with promises of reassuring them whether or not they have heart disease, only to provide murky results that usually do no such thing. The pitfalls of the test are turned to advantage. The all too common equivocal or mildly abnormal result can be converted into a hospital procedure. (Imagine you could perform such alchemy on the uncertain calculations on your income taxes.)

With millions of stress tests performed every year and the push to perform more and more screening tests, the market has, in effect, been expanded—even though no increase in the disease itself has actually occurred.

Beware: As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine.

Copyright © 2026 Cureality.com

All posts by william-davis

Calcium reflects total plaque





People frequently ask, "Why measure coronary artery calcium? My doctor said that calcium only tells you if there's hard plaque, and that hard plaque is stable. He/she says that calcium doesn't tell you anything about soft plaque."

Is that true? Is calcium only a reflection of "hard" plaque? Is hard plaque also more stable, less prone to rupture and causes heart attack?

Actually, calcium is a means of measuring total plaque, both soft and hard. That's because calcium comprises 20% of total plaque volume. Within plaque, there may be areas that are soft (labeled "lipid pool" in the diagram). There are also areas made of calcium (shown in white arcs within the plaque). Even though this is just a graphic, it's representative of what is seen when we perform intracoronary ultrasound of a live human being's coronary artery. In other words, this cross section contains both "soft" (lipid pool) as well as "hard" (calcium) elements.

Is this artery "soft" or "hard"? It's both, of course. The artery compostion can vary millimeter by millimeter, having more soft or hard elements. The artery can also change over time in either direction. Thus, "soft" plaque may indeed be soft today, only to be "hard" in 6 months, and vice versa.

The essential point is that measuring just "soft" plaque provides limited information. What the CT heart scan does is provide a gauge of total plaque, soft and hard, and it does so easily, safely, precisely. If your score increases, the lengthwise volume of total plaque has also grown. If your score decreases, the total amount of plaque has also decreased.

Don't mistake marketing for truth

We're all so inundated with marketing messages for food. Unfortunately, many people confuse the messages delivered through marketing with the truth.

For instance:

Pork: "The other white meat." Pork is a high-saturated fat food.

"Bananas: A great source of potassium." Bananas are a high glycemic index (rapid sugar release), low fiber food.

"Pretzels: A low-fat snack." A high glycemic index food made from white wheat flour. It makes you fat and skyrockets blood sugar.

Jif peanut butter: "Choosy moms choose Jif." Do they also choose hydrogenated fats?

Hi-C: Upbeat jingles like "Who put the straw in my Hi-C fruit drink, a new cool straw that wriggles and bends? Who put the straw in my Hi-C fruit drink, with Vitamin C for me and my friends? Who was that man, I'd like to shake his hand, he made my Hi-C cooler than before!" What about the 25 grams of sugar per 4 oz serving? And the high fructose corn syrup that creates an insatiable sweet tooth, raises triglycrides 30%, and exagerates pre-diabetes?


Marketing is not reliable, unbiased information. If Ford boasts that their cars are superior to GM, do you say "Well then, I need to buy a Ford?" Of course not. Take marketing for what it is: A method of persuading people to buy. It may or may not contain the truth. It's a big part of the reason Americans are the fattest people on earth and are experiencing an explosion of chronic diseases of excess.

Tattered Red Dress

"Are you taking your health to heart? Perhaps you understand the importance of eating a diet low in cholesterol or getting 30 minutes of exercise a day. But do you know your own risk of developing cardiovascular disease?


It’s time to take your heart health personally. Heart disease is the No. 1 killer of American women — and that means it is not “someone else’s problem.” As a woman, it’s your problem.

That’s where the Go Red Heart Checkup comes in. This comprehensive evaluation of your overall heart health can help you now and in the future. By knowing your numbers and assessing your risks now, you can work with your doctor to significantly reduce your chances of getting heart disease tomorrow, next year, or 30 years from now!"



So reads some of the materials promoted by the American Heart Association Red Dress campaign to increase awareness of heart disease in women. The effort is well-intended. There is no doubt that most women are unaware of just how common coronary disease is in females.

But I've got a problem with the solutions offered. "Know your numbers"? Eat healthy, don't be overweight, be active, don't smoke. That's the gist of the program's message--nothing new. In 2006, why would some sort of screening effort for detectin of heart disease not be part of the message? Why isn't there any message about the real, truly effective means to detect hidden heart disease in women--namely, heart scanning?

Does a 58-year old woman with normal blood pressure, LDL 144, HDL 51, 20 lbs overweight have hidden heart disease? I've said it before and I'll say it again: You can't tell from the numbers. She could die of a heart attack tomorrow without warning, or maybe she'll be dancing on our graves when she's 95 and never have experienced any manifestation of heart disease. The numbers will not tell you this.

I'm glad the American Heart Association has seen fit to invest its sponsors' money in a campaign to promote prevention. I wish they hadn't fallen so far short of a truly helpful message. Perhaps the sponsors (like Pfizer, maker of Lipitor) will benefit, anyway.

Panic in the streets

Several days ago, I wrote about a local prominent judge in my neighborhood who was unexpectedly found dead in bed of a heart attack at age 49.

As expected, I've received multiple calls from patients and physicians who want heart catheterizations. For instance, an internist I know called me in a panic. He asked that I perform a heart catheterization in a patient with a heart scan score of 768. I've been seeing this patient for about a year. He's without symptoms, even with strenuous exercise; stress tests (i.e., tests of coronary bloow flow) have been normal.

I remind patients and colleagues every day, day in day out: Having a heart scan score revealing some measure of coronary plaque is not a sufficient reason by itself to proceed with procedures. Fear of suffering a fate like the unfortunate judge is also not a reason to proceed with procedures.

Increased awareness of the gravity of heart disease is a good thing. Some good can come out of a needless tragedy like this. The lesson from the judge's unfortunate experience: he needed a CT heart scan. I'm told that the judge's doctor advised him that a heart scan was a waste of time. I hope that appropriate legal action for negligence is taken by the judge's family against this physician.

Not doing a heart scan is wrong. That's the lesson to learn. The lesson is not that everybody with coronary plaque needs a procedure. Had the judge undergone a simple heart scan, intensified prevention could have been instituted and he'd still be alive with his wife and children today.

The indications for procedures are unchanged by your heart scan. If a stress test is abnormal and indicates poor flow to a part of the heart, that would be a reason. If symptoms like chest discomfort or breathlessness appear, that's an indication. If there's evidence of poor heart muscle contraction, that's a reason to proceed with a procedure. But just having coronary plaque is not a sufficient reason.

Heart scan curiosities 1

Heart scans often reveal more than coronary plaque. From time to time, I'll show some curious findings that people have displayed during routine heart scans.

This 65-year old man had a relatively low heart scan score of 73, but showed an impressive quantity of calcification of his pericardium, the usually soft-tissue sack that encases the heart. The calcified pericardium is the white arcs that surround the heart in the center of the image.



Thankfully, because he's without any symptoms of breathlessness, excessive fatigue, or leg swelling, he won't need to have it surgically corrected. When the pericardium becomes rigid and encircles the heart, it can literally squeeze the heart, a condition called "constrictive pericarditis". The surgery is pretty awful.

This man's calcified pericardium likely resulted from one or more viral infections over his lifetime.

Annual physical

A judge who lives in my neighborhood was found dead in his bed this week from a heart attack. He was 49 years old. His teenage kids found him and performed CPR, but he was cold and long-gone by then.

A close friend of the judge told me that he'd passed an annual physical just weeks before.

This sort of tragedy shouldn't happen. It is easily--easily--preventable. Had this man undergone a heart scan, a score of at least 400 if not >1000 would have been uncovered, and appropriate preventive action could have been taken. The conversation could have centered around the strategies to correct the patterns that triggered his plaque and how he could reduce his score.

Of course, hospitals make use of stories like this to fuel fear that brings hordes to their wards for procedures. Would the judge have required a procedure to save his life, had his heart disease been diagnosed at his annual physical? Not necessarily. Hospitals and cardiologists would try to persuade you that procedures have an impact on mortality. This is simply not true. In fact, the mortality benefits of procedures are questionable except in the midst of acute illness (e.g., unstable chest pain symptoms or heart attack).

Don't be falsely reassured by passing a physical. A physical does nothing to screen you for heart disease. An EKG and stress test, if included, is a lame excuse for heart disease screening. Remember that a stress test is a test of coronary blood flow, not for the presence of coronary plaque. The unfortunate judge most likely had a 30% "blockage" that did not block flow, but ruptured and closed an artery off sometime in the night when he died. A stress test even on the day of his death would not have predicted this.

A CT heart scan would have uncovered it easily, unequivocally, safely.

A curious case of regression

Randi came to me at age 43. Before I'd met her, she'd undergone two heart scans about one year apart. The initial score was 57--not terribly high, but very high for a 41-year old, pre-menopausal female. Recall that rarely do women have any heart scan score above zero before age 50. Randi's 2nd scan had yielded a score of 72, a 27% increase.

Randi even had her lipoproteins assessed and she had the dreaded Lp(a). So when I met her, we discussed the possible choices in Lp(a) treatment: niacin and estrogens as primary treatment, along with LDL reduction to rock-bottom numbers, along with adjunctive DHEA, almonds, ground flaxseed, and fish oil. Sandi was okay with the adjunctive treatments and was already slender and active (BMI <25), and did not show Lp(a)'s evil partner, small LDL. But Randi had no interest in estrogens, even bio-identical preparations, because of the usual uncertainties associated with estrogen replacement. She also proved to be one of the people truly intolerant to anything but the most minute dose of niacin, experiencing prolonged flushing and abdominal cramps with any dose >250 mg.

Randi even attempted a trial of the Mathias Rath concoction of high-dose vitamin C, lysine, and proline as treatment for Lp(a), but we saw no effect on Lp(a).

Unfortunately, this left Randi's Lp(a) essentially uncorrected. Another scan one year later: 90, another 25% increase. 18 months after that, another scan: 120, a 30% increase.

Now 47-years old, Randi had resigned herself to not being able to control her plaque. We'd run out of options. At that point, I'd started to have everyone's vitamin D blood level assessed and then replaced with vitamin D. I did this with Randi, too.

A year after her last scan, she underwent another. The score: 92, a 23% reduction--substantial reversal following a course of unrelenting progression.

Randi and I, of course, both rejoiced with this unexpected success. But it raised some interesting questions: How important is Lp(a) when vitamin D is normalized and small LDL is not a part of the picture? How consistent with regression be with this strategy over time? Would normalization of vitamin D have stopped plaque from becoming established in the first place?

I hope these issues will clarify over time. For now, I'm thrilled with Randi's success. She remains on her present, "incomplete", though successful program.

Note: I would not ordinarily advise a young woman to undergo serial heart scanning with this frequency. Randi had unusual access to a scan center through a relationship with the staff. I am nonetheless grateful for the lessons her experience have taught us.

Fortune teller

Whenever your doctor uses your cholesterol values--total, LDL, HDL, triglycerides--to judge your heart disease risk, he/she is trying to act as your fortune teller.

In some states, fortune telling is illegal, a misdemeanor. The New York State lawbooks say:

A person is guilty of fortune telling when, for a fee or compensation which he directly or indirectly solicits or receives, he claims or pretends to tell fortunes, or holds himself out as being able, by claimed or pretended use of occult powers, to answer questions or give advice on personal matters or to exorcise, influence or affect evil spirits or curses; except that this section does not apply to a person who engages in the aforedescribed conduct as part of a show or exhibition solely for the purpose of entertainment or amusement.
(Source : Wikipedia)

Rather than occult powers, your physician claims to use "medical judgement" to tell your fortune. Except for that distinction, it might be construed as a misdemeanor.


Let's take three typical examples:

58-year old Laura has a high LDL of 195 mg/dl. Her HDL is 52 mg/dl, triglycerides 197 mg/dl. Does she have heart disease?

51-year old Jonathan has an LDL of 174 mg/dl, HDL 34 mg/dl, triglycerides 156 mg/dl. Does Jonathan have heart disease?

71-year old Marian has an LDL cholesterol of 135 mg/dl, HDL 84 mg/dl, triglycerides of 67 mg/dl.

None of the three have symptoms. They all feel well. Nobody is taking a statin cholesterol drug or other agent that would modify the numbers. Jonathan is around 30 lbs overweight. Nobody has an impressive family history of heart disease.

Can you tell who has heart disease and who doesn't? If you can, you're smarter than I am, because I certainly can't tell. But your doctor tries to divine your future by looking at these numbers.

Do they know something that we don't know? No. It's a crude odds game, a guessing game. A guessing game that frequently comes up on the losing end.

These are three real people. Laura, despite her high LDL, has no identifiable coronary heart disease. Jonathan has advanced coronary disease. These were his numbers just prior to his stent. Marian has a moderate quantity revealed by a CT heart scan score of 419.

Don't even try predicting your future from your cholesterol numbers--it simply can't be done. Every day, I see patients and physicians beating their heads over this dilemma. Telling your fortune using pretended occult powers is illegal. Telling your fortune using cholesterol numbers should be, too.

If you want to know if you have coronary plaque, that's the role of the CT heart scan. Plain and simple.

Heart scan score drops like a stone

Matt was dumbfounded when he found out about his heart scan score of 317 in the summer of 2005.

Earlier that year he'd unintentionally lost 20 lbs. in the space of two months and was feeling awful. He was diagnosed with diabetes and put on several medications. He told me that the heart scan score was just adding insult to injury.

As you'd expect in someone with diabetes, Matt had a low HDL, increased triglycerides, and small LDL. Blood pressure and inflammation (C-reactive protein) were issues as well.

Matt's primary care physician had put him on a statin cholesterol drug as soon as he heard about Matt's heart scan score, so we kept this going. What Matt's primary care physician didn't know was that his "true" LDL had been much higher than the conventional calculated LDL had suggested, so the statin agent was a reasonable solution. (Matt was also not terribly motivated to make dramatic changes in lifestyle or food choices. The statin drug was a compromise.)

We added fish oil and vitamin D to his regimen. Though recent data have cast doubt on the value of treating homocysteine levels of around 12.5, Matt's much higher value of 28 was treated with vitamins B6, B12, and folic acid, with a resultant homocysteine of 7.6.

17 months into the Track Your Plaque approach, and Matt's repeat heart scan score: 244, a 23% reduction.

How's that for an early Christmas gift?

"You don't have a uterus. You don't need progesterone"

I was talking with a hospital nurse recently who told me about her lack of energy, blue moods, and other assorted complaints. At age 49, she was exasperated. So I suggested that she ask her gynecologist about progesterone cream.

The gynecologist advised her, "You don't have a uterus. You don't need progesterone." He went on to explain that the only reason to take progesterone was to prevent uterine cancer caused by estrogen.

Then what about progesterone's weight loss benefits? It's effects on increased energy, improved mood, deeper sleep? These benefits, of course, have nothing to do with the uterus.

I've witnessed these benefits in women many times, both in the peri-menopausal period (which starts around your late 30's) and menopause.

Why talk about progesterone when our focus is heart disease and reduction of heart scan scores? Because if progesterone in a woman helps her feel better, more upbeat, and accelerates weight loss, she's more likely to succeed in her plaque-control program.

For additional comments on progesterone, read the Track Your Plaque interview with women's hormone expert, Dr. Nisha Jackson, Females, hormones, and weight control:
An interview with Dr. Nisha Jackson
found at http://www.cureality.com/library/fl_04-008njacksonhormones.asp. Dr. Jackson also has a book available called "The Hormone Survival Guide to Perimenopause".







Or, read Dr. John Lee's pioneering books, What Your Doctor May Not Tell You About Menopause: The Breakthrough Book on Natural Hormone Balance and What Your Doctor May Not Tell You About Premenopause: Balance Your Hormones and Your Life from Thirty to Fifty . (An edition that combines the two books is available, also.)

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