All posts by william-davis

Followers of the Track Your Plaque program know that we advocate periodic fasts to reduce heart disease risk.

I came across an interesting report form an abstract presented at last week's American Heart Association meetings in Orlando:

(Read the report at HeartWire. You will need to register or sign-in.)

In this study, the investigators tried to determine why members of the Church of Jesus Christ of Latter-Day Saints (LDS) tended to have reduced risk of heart disease compared to others in the area but not in the LDS faith. While the reduced risk of heart disease in LDS members had been traditionally attributed to the no smoking policy advocated by the Mormon church, the investigators suspected that there was more to the reduced risk.

Of 515 people interviewed, periodic fasting, whether for religious or other reasons, was found to distinguish people who were less likely to have coronary disease by conventional catheterization (59% vs. 67%). (Since the study was published in only abstract form, it's not clear why all these people underwent heart catheterization in the first place.)

Nonetheless, it's an interesting observation and one consistent with the benefits we see when someone fasts: reduced blood pressure, reduced inflammatory responses, improved lipids and lipoproteins, weight loss.

Fasting can be an especially effective method to gain control over heart disease and coronary plaque if rapid control is desired. In fact, I wonder if the normally year-long process of plaque control that I advocate can be much abbreviated. Fasting, I believe, is a crucial component of rapid control, what I've talked about in Instant Heart Disease Reversal

There's also additional thoughts on fasting in my Heart Scan Blog post, For rapid success, try the "fast" track.

Fasting is not something to fear. It can be an enlightening process that can serve to abruptly sever bad habits, perhaps even turn the clock back on prior dietary and lifestyle excesses. My favorite variation on fasting is to use soy milk (yes, yes, I know! I can already hear the the soy bashers screaming!) as a meal substitute. It is an

Put lipstick on a dwarf

2. December 2010 William Davis (24)

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

1. December 2010 William Davis (47)

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?

28. November 2010 William Davis (25)

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 thedevelopment 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, 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

26. November 2010 William Davis (22)

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

24. November 2010 William Davis (14)

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?

19. November 2010 William Davis (20)

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?

13. November 2010 William Davis (48)

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?

10. November 2010 William Davis (24)

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

9. November 2010 William Davis (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

4. November 2010 William Davis (12)

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.

Don't be satisfied with "deceleration"

Whole grains and half truths

Fasting and heart disease