More Vitamin D and HDL

I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.

"I have never seen regression"

At a presentation at the American College of Cardiology meetings in New Orleans yesterday (March 27, 2007), Dr. Arthur Agatston declared "I have been doing CT for many years, and I have never seen regression."

Whooooaaaa. Wait a minute here. I have great respect for the work Dr. Agatston has done over the years. He is, after the originator of the scoring algorithm that allows us to score CT heart scans (though a more accurate measure, the volumetric score, is the one we often use behind closed doors because of modestly increased accuracy and reproducibility). His diet program, the South Beach Diet, has achieved enormous success and is indeed an effective approach for both weight loss and correction of many weight-related causes of heart disease.

But he has never seen regression? Why would this be when we see it all the time? When we see heart scan scores drop 30%, it's hard to believe that with some savvy he has never seen regression (drop in score).

I can only attribute the difference to the more intensive endpoints we advocate (e.g., 60-60-60 for lipid values); the incorporation of adjuncts like fish oil, vitamin D, l-arginine; attention to non-cholesterol issues and intensified treatments for each. I doubt that the populations we see differ substantially.

As much as I admire Dr. Agatston's accomplishments, I believe that he is behind the times on this issue. No regression is so starkly different from the Track Your Plaque experience. I believe that relying only on statin drugs and diet will slow but will not stop plaque growth. It will also rarely, if ever, drop your score.

Attention to detail and a little insight into better preventive strategies really pays off. While not everyone in the Track Your Plaque experience will drop their score, a substantial number do. Many more slow plaque growth dramatically. And, as time goes on, our track record gets stronger and stronger.

COURAGE to do better

The results of the long-awaited COURAGE Trial were announced today at the American College of Cardiology meetings in New Orleans.

In this trial, 2200 participants with stable coronary disease (i.e., not unstable, in which heart attack or death is imminent) were randomly assigned ("randomized") to either angioplassty/stent or "maximal medical therapy." Medical therapy means such things as aspirin, beta blocker drugs, and statin cholesterol drugs. There was virtually no difference between the groups in rate of heart attack and death from heart disease over a period of up to 7 years.

These results have caused a stir in the media and my colleagues, trying to sort out of the implications. However, I think there's one observation in particular worth making for those of us who tend to scoff at the conventional approach to coronary disease. That is, 1 of 5 people had a heart attack or died from heart disease in both groups. That's a lot. Even more ended up with a procedure (angioplasty, stent, or bypass). In other words, the "maximal medical therapy" instituted in participants was hardly a success. Though angioplasty and stenting failed to prove superiority, both really stunk. Both permitted a lot of catastrophes to occur.

"Maximal medical therapy," in other words, is a laughable concept. It doesn't include raising HDL, suppressing small LDL, reducing Lipoprotein(a), addressing inflammatory issues. It does not include omega-3 fatty acids from fish oil, nor does it address the severe degrees of vitamin D deficiency that are proving, in the Track Your Plaque experience, to be among the most potent causes of atherosclerotic plaque known. It includes a sad attempt at diet, as advocated by the American Heart Association, a diet that, in my view, causes heart disease and is distorted by the powerful political and financial influence of food manufacturers.

If the trial were to be done again, I'd like to see the "maximal medical therapy" arm be represented by a more effective program like the Track Your Plaque approach.

Value of a zero heart scan score

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

You're at the cutting edge

If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health.

Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare."

Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies.

Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money.

Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust.

In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases.

If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans.

In our program, 18-30% reductions in heart scan scores are common.

A stent--just in case

Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart.

"The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."

Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)

Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?

That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower.

In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.

Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.

How will you know your score dropped?

This issue came up twice this week.

Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)

Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case.

So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan.

Bill was surprised. "Why another scan? I already had one!"

I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly.

Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth.

Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:

398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.)

250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.

525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following.

The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.
All posts by william-davis

The costs of doing drug business?

Here's a telling situation.

Liz had been on prescription niacin, Niaspan, 1500 mg per day (3 x 500 mg tablets) for several years to treat her severe small LDL pattern and familial hypertriglyceridemia (triglycerides 500-1000 mg/dl). Because her health insurance had been paying for the "drug," she insisted on taking the prescription form.

A change in insurance, however, meant that the Niaspan was no longer covered. Her pharmacy wanted to charge $227 per month.

Liz came to the office in tears, worried that she was going to have to choke up $227 per month. I reminded her that, as I had told her several years ago, she could easily replace the Niaspan with over-the-counter Sloniacin or Enduracin. Both release niacin over approximately 6 hours, just like Niaspan.

Here are the prices I've seen with Sloniacin, 100 tablets of 500 mg:

Walgreens: $15.99
Walmart: $12.99
Costco: $8.99

So the most expensive source, Walgreens, would cost Liz just under $15.99 per month to take 1500 mg per day.

$15.99 versus $227.00 per month for preparations that are highly similar. Hmmmmmm.

I wonder what the $211.01 extra per month goes towards? Admittedly, Abbott Labs, the current company selling Niaspan (after Abbott acquired Kos), has invested in a few clinical trials, such as ARBITER-HALTS6. But does supporting research justify this much difference, a difference that amounts to $2532 over a year? If just 100,000 patients are prescribed Niaspan at this dose (a typical dose), this generates $253 million.

Is the cost of developing and marketing a supplement-turned-drug that great? Is this justifiable? Is it any wonder that our health insurance premiums continue to balloon?

I use Sloniacin and Enduracin almost exclusively.

Measurement

A crucial component of self-empowerment in healthcare is to be able to measure various health parameters. More and more measurement tools are entering the direct-to-consumer arena.

Quantification of various phenomena is important in managing many aspects of health. Imagine a carpenter trying to build a house without the use of a tape measure, level, or other measuring tools. In health, as in building a house, measurement, adjustment, and correction are critical.

Among the most helpful health measurement tools:

Blood glucose meters--Blood glucose meters aren't just for diabetics. They are among the most powerful weight loss tools available.

Blood pressure cuffs--There's no better way to assess blood pressure than to assess it under all the varied conditions of life: When you're tired, when you're excited, when you're upset, when you're happy, hungry, stomach full, morning, night. This is a lot better than the one isolated measure in the doctor's office.

Digital thermometers--Your first a.m. oral temperature is a great way to assess thyroid status. We aim to maintain first a.m. oral temperature around 97.3 degrees F, the normal human temperature upon arising that reflects normal thyroid function. (No, Dr. Broda Barnes fans, axillary temperatures should NOT be used due to flagrant variation from right armpit to left armpit, modifying effects of clothing and ambient temperature, etc. Oral temperature tracks internal, "core," temperature fluctuations reliably, including circadian variation, far better than axillary temperatures.)

Fingerstick blood tests--An incredible number of blood tests are now available just by performing a simple fingerstick in your kitchen or bathroom. You can get 25-hydroxy vitamin D, lipids, thyroid measures (TSH, free T3, free T4), hormones (DHEA, testosterone, estrogens). And the list is growing rapidly. Salivary tests are also growing in number for many of the same measures.

A variation on fingerstick blood tests are devices like CardioChek that allow you to do a fingerstick, but also run the test on your own device at home. (The CardioChek device tests total cholesterol, triglycerides, and HDL.)

Urine pH--You can dipstick your own urine to assess the relative acidity or alkalinity of your lifestyle. Acid pH (7 or below) suggests that diet is weighed too heavily in favor of animal products and grains. An alkaline pH (above 7) suggests plentiful vegetables and fruits, not counteracted by animal products and grains.

There are many more, including the ZEO device to monitor sleep quality, RESPeRATE for reduction of blood pressure, HeartMath to manage stress and augment the parasympathatic (relaxation) response. We've come a long way compared to the health monitoring devices of just 25-30 years ago.

Anyway, that's a partial list. Given the rapid advances in technology that allow such home tests, I anticipate a much longer list in the coming few years.

For some perspective on how far these devices have come, here's a great graphic of an early sphygmomanometer, or blood pressure gauge.


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

At 5 ft 7 inches, he weighed in at 273 lbs, putting his BMI at a sobering 42.8. (A BMI of 30 or above is classified as "obese.") In addition to lipoprotein(a), Jack had an extravagant quantity of small LDL (the evil "partner" of lipoprotein(a)), high triglycerides, and blood sugars in the diabetic range. With a heart scan score of 1670, Jack had little room for compromises.

Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.

So I taught Jack how to check his blood sugars using a fingerstick device, what I call the most important weight loss tool available. I asked Jack to check his pre-meal blood glucose and his one-hour after-meal blood glucose and not allow the after-meal blood glucose to rise any higher than the pre-meal. For example, if blood glucose pre-meal was 115 mg/dl, after-meal blood glucose should be no higher than 115 mg/dl.

If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.

Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.

What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.

Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger.

The two kinds of small LDL

You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.

Wheat-free pumpkin bread

Try this recipe for a wheat-free, gluten-free yet healthy "bread." Unlike many gluten-free foods that send blood sugar skyward, this will not.

Ingredients:
2 cups ground almond meal (Buy it from Trader Joe's--70% cheaper than other grocery stores.)
1/2 cup ground flaxseed
1/2 cup sour cream (full-fat, of course)
15 oz canned pumpkin (Trader Joe's is bisphenol A-free)
2 medium to large eggs
1/2 cup chopped walnuts or pecans
4 tablespoons butter, melted
2 teaspoons baking powder
2 teaspoons cinnamon
1 teaspoon nutmeg or allspice
Dash of salt
Choice of non-nutritive sweetener (I used 3 teaspoons Trader Joe's stevia extract powder, the one mixed with lactose. Two tablespoons of Truvia, 1/2 teaspoon of the more concentrated stevia extract, or 1/2 cup Splenda are other choices. You can taste the mixed batter to gauge sweetness if in doubt.)

Preheat oven to 350 degrees F. Grease baking pan (e.g., 10 x 6 inch). The pan should be big enough so that the mix will not be more than 2 inches deep, else it will require much longer to bake. (If you have only smaller pans, you will need to cook longer while the pan is covered with aluminum foil.)

Mix all ingredients thoroughly in large bowl. Pour mix into greased baking pan.

Cover with aluminum foil and bake for 30 minutes. Remove foil and bake for additional 30 minutes or until inserted toothpick or knife comes out dry.

Serve with cream cheese or as is.

(I'd have some pictures, but the kids and I ate it up before I thought to take any photographs.)

Vitamin D: Deficiency vs optimum level

Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.

Dr. Dowd hits a bullseye with this remark:

The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?

Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.

I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)

The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.

Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.

Large LDL counts, too

Chad is a 43-year old father of five kids.

Earlier this year, he developed chest pain that got worse and worse. He ended up with a total of five stents in all three coronary arteries. After a devastating experience with Lipitor that resulted from a ruptured tendon, he came to me for an option.

Chad's lipoproteins:

Slow Burn works

I have been impressed with the results I've been obtaining with Fred Hahn's Slow Burn strength training technique.

Because I have limited time to hang around the gym, any technique that provides outsized results in a limited amount of time, I have to admit, appeals to me. In past, I'd be lucky to squeeze in one or two strength training sessions per week, devoting the rest of the time to biking outdoors, biking on a sedentary bike (while playing XBox), jogging, or doing strenuous yard work like digging trenches and planting shrubs.

Over the years, I've gradually lost muscle, since the strength training effort suffered with my time limitations.

So Fred's time-efficient Slow Burn idea struck a chord. Having now done it with some regularity, usually 1-2 times per week since mid-September, I have gradually added back visible muscle. My Slow Burn workouts, involving 8-10 different movements, seem to have restored the muscle I've lost, with a very modest time effort.

It took a little getting used to. After Fred showed me how to do the movements--slow motion movement in both the "positive" and "negative" directions, with smooth, non-jerking transitions, one set per muscle group, each taken to muscle exhaustion--it left me unusually tired and sore the next day. This surprised me, given the limited time involved. Breathing is also very important; the usual exhale-during-the-positive, inhale-during-the-negative pattern is replaced by breathing freely during the entire set. I didn't get this at first and ended up with headaches that got worse with each set. Breathing freely relieved me from the effect.

I have strength trained since I was around 15 years old. Back in the early 1970s, I had about 2000 lbs of barbells and dumbbells in my garage in New Jersey, while also driving back and forth to the Morristown, NJ, YMCA to train with friends. The Slow Burn movements forced me to break habits established over nearly 40 years of conventional strength training.

I've also played around with mixing conventional movements with Slow Burn movements to keep it fresh. This also seems to work.

If you're interested in giving it a try, here's an animation that demonstrates what Slow Burn movements look like. Fred has also produced an excellent 3-DVD set of videos that more fully describe the practice.

Do your part to save on healthcare costs

While many of the factors that drive the relentless increase in health care costs are beyond individual control, you are still able to exert personal influence over costs. Just as in political elections, your one vote alone may not count; it's the collective effort of many people who share similar opinions that results in real change.

I just got the new monthly premium for my high-deductible health insurance: Up $300 per month, putting my family's total premium over $2000 per month---for four healthy people. (My son fractured his wrist playing high school hockey earlier this year; that may explain at least some of the increase.)

I'm going to shop around for a better deal. However, shopping is likely to only stall the process. It will not address the systemic problems with healthcare that continue to drive premiums up and up and up.

So what can you do to help keep costs down? Here are a few thoughts:

Never accept a prescription for fish oil, i.e., Lovaza. Just buy far less costly over-the-counter fish oil. I treat complex hyperlipidemias, including familial hypertriglyceridemia, ever day. I NEVER use prescription fish oil. A typical 4 capsule per day Lovaza prescription adds around $280 to $520 per month to overall health costs (though your direct out-of-pocket costs may be less, since you shove the costs onto others in your plan).

Never accept a prescription for vitamin D. Prescription vitamin D is the mushroom or invertebrate form anyway. Just buy the human (cholecalciferol, D3) form from your health food store or "big box" store. They yield consistent increases in 25-hydroxy vitamin D levels, superior to the prescription form. And they're wonderfully inexpensive.

Eliminate wheat from your diet. If there is a dietary strategy that yields unexpected and outsized benefits across a wide spectrum of health, it's elimination of this thing we're sold called "wheat," you know, the genetically-transformed, high-yield dwarf mutant that now represents 99% of all wheat sold. Blood sugar drops, pre-diabetics become non-prediabetics, diabetics reduce need for medication or become non-diabetic, cholesterol values plummet, arthritis improves, acid reflux and irritable bowel symptoms improve or disappear, just to mention a few. Wheat elimination alone, I believe, would result in incalculable savings in both healthcare costs and lives saved.

Be sure to obtain iodine. In the fuss to cut salt use, everyone forgot about iodine. Lack of iodine leads to thyroid disease, usually hypothyroidism, that, in turn, causes cholesterol values to increase, weight to increase, and heart disease risk to double, triple, or quadruple. Iodine supplementation is easy and wonderfully inexpensive.

Over time, I hope that all of us can help develop the effort to self-direct more and more of our own health. Our Track Your Plaque program has shown me that, not only can people take the initiative to direct aspects of their own health, they can do it better than 99% of doctors.  

I'm sure there are many, many other ways to help reduce costs. Any suggestions?

Calling all super-duper weight losers!






Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year.  Some have required two years.  Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is.  But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:








 

 

 

 

 

 

 

 

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.



 

 

 

 

 

 

 

 

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease  is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.

Why does wheat cause arthritis?

Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Why do morphine-blocking drugs make you lose weight?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Heart scan tomfoolery 2

In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.


Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart scan tomfoolery

Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve


Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.