Lessons from the 20-year statin experience

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

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

Small LDL particles and increased HbA1c--An evil duo

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

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

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

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

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

Unforgiving small LDL particles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Do the math: 41.7 pounds per year

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

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

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

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

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

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

We got the drug industry we deserve

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

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

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

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

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

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?
Is an increase in heart scan score GOOD?

Is an increase in heart scan score GOOD?

In response to an earlier Heart Scan Blog post, I don't care about hard plaque!, reader Dave responded:

Hello Dr Davis,

Interesting post about hard and soft plaque. I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).

After the first scan we started aggressively going after my LDL, HDL and Trig...196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 [The Track Your Plaque target values]-

So the increase is a surprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.



Dave's doctor then responded to him with this comment:

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago. Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT [i.e., calcium score]. It is only the safe, calcified plaque that can be measured with the EBT. [Emphasis mine.] For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque. There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque. We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above."


Huh?

This bit of conventional "wisdom" is something I've heard repeated many times. Is it true?

It is absolutely NOT true. In fact, the opposite is true: Dave's substantial increase in heart scan score from 235 to 419 over 22 months, representing a 78% increase, or an annualized rate of increase of 37%. This suggests a large increase in his risk for heart attack, not a decrease. Big difference!

Dr. Paulo Raggi's 2004 study, Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy in 495 participants addresses this question especially well. Two heart scans were performed three years apart, with a statin drug initiated after the first scan, regardless of score.

During the period of study, heart attacks occurred in 41 participants. When these participants were analyzed, it was found that the average annual increase in score over the three year period was 42%. The average annual rate of increase in those free of heart attack was 17%. The group with the 42% annual rate of increase--all on statin drugs--the risk of heart attack was 17.2-fold greater, or 1720%.

The report made several other important observations:

--20% of the heart attack-free participants showed reduction of heart scan scores, i.e., reversal. None of the participants experiencing heart attack had a score reduction.
--Only 2 of the 41 heart attacks occurred in participants with <15% per year annual growth, while the rest (39) showed larger increases.
--The intensity of LDL reduction made no difference in whether heart attacks occurred or not. Those with LDL<100 mg/dl fared no better than those with LDL>100 mg/dl.

Dr. Raggi et al concluded:

"The risk of hard events [heart attack] was significantly higher in the presence of CVS [calcium volume score] progression despite low LDL serum levels, although the interaction of CVS change and LDL level on treatment was highly significant. The latter observation strongly suggests that a combination of serum markers and vascular markers [emphasis mine] may constitute a better way to gauge therapeutic effectiveness than isolated measurement of lipid levels."

This study demonstrates an important principle: Rising heart scan scores signal potential danger, regardless of LDL cholesterol treatment. Yes, LDL reduction does achieve a modest reduction in heart attack, but it does not eliminate them--not even close.

These are among the reasons that, in the Track Your Plaque program, we aim to correct more than LDL cholesterol. We aim to correct ALL causes of coronary plaque, factors that can be responsible for continuing increase in heart scan score despite favorable LDL cholesterol values.

So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

Just don't let your doctor's ignorance permit the heart attack that is clearly in the stars. Take preventive action now.

Comments (30) -

  • Anonymous

    11/20/2007 5:41:00 PM |

    Dr Davis,

    What should Dave do?  He appears to have improved his LDL:HDL ratio as well as his total C to HDL ratio substantially, but his CAC score jumped significantly.  Maybe look at other risk factors?

    The info here gives no indication of median blood pressure for Dave.  LP(a)?  No indication of particle sizes. But, which of these or others would be most likely to be Dave's downfall in attempting to mitigate a future hard endpoint?

    I don't ask this lightly, I myself am trying to follow the TYP program and keep my high-for-my-age 29 CAC score from growning.  But, I'm frankly not looking forward to my rescan in about a year.  I'm a bit worried about the, "What if my scan shows a dramatic increase?  What then?"

    Thank you for the valuable information you provide.

    :LaughingCT

  • Dr. Davis

    11/20/2007 11:17:00 PM |

    I would urge Dave to follow all the principles of the Track Your Plaque program, including:

    1) Fish oil to provide minimum 1200 mg EPA + DHA per day

    2) Correction of all concealed lipoprotein patterns such as IDL and Lp(a)

    3) Vitamin D raised to 50 ng/ml--crucial!

    4) Normalization of blood pressure, including during exericse.

    5) Normal blood sugar (<100 mg/dl).

    Further efforts might be required, depending on the long-term effects on rate of plaque growth.

  • Ross

    11/21/2007 3:41:00 AM |

    My question is: how repeatable do you think the scores are on the CT scan?  Are they bulletproof (+/- 5% no matter where measured), consistent by analyst (+/- 5% with the same doctor analyzing the scan), or...?  

    I am currently visiting my brother in law, who is an FP doctor with a private practice.  One of his professional friends, a cardiologist who seems a cut above (thinks stenting is a cop-out), recently told him that he only trusted two centers in the mid-Ohio region to score a 16-slice CT scan accurately, and that even then, the variability was still too high for his taste.  Two numbers within 20% were within his expected error bars and weren't different enough to indicate any change to him.  Two different scan centers?  He wouldn't even compare the two scan scores.

    In my own job (software), I've had to manage human-measured numbers over and over again.  One observation keeps coming up: a single value doesn't mean much without an understanding of the accuracy of that value.  I really am curious about how you estimate confidence intervals on CT scan scores.

  • Dr. Davis

    11/21/2007 3:55:00 AM |

    Hi, Ross--

    Excellent questions.

    Several thoughts:

    1) 16-slice scanners are, unfortunately, prone to wider error in heart scan scoring, perhaps as much as 20%. The variation in scoring on an EBT or 64-slice device is far less.

    2) Variation from scan to scan, when expressed as percent, depends to a great degree on the score itself. Lumping all scores together, variation should be no more than 8-9%. However,a low score of, say 2, then repeated at 4 means 100% variation. However, the same absolute difference of 2 but with a score of 1002 and repeated at 1004 is <1% variation. Therefore, higher scores assume much less percent variation, usually <5%.

    3) Variation among different reading physicians tends to be a minor issue, since much of the scoring is done by standard criteria determined by software, not the human eye. The only real source of human variation comes from disputable areas, such as the mitral valve (which can sometimes encroach into the coronary area and appear like plaque) and the mouth of arteries, which can be debated as being in the aorta or in the coronary arteries themselves. However, these disputable areas are issues in <5% of scans.

  • Tom

    11/21/2007 4:30:00 AM |

    It's interesting that a 29 year old is able to track his plaque. I'm in my 60's now and recently found your site AFTER bypass surgery and a calcium score >700 via a 64 slice scan.
    In reading past comments, those of us having had the heart procedure are now unable to follow our progress via the cac score. Until this post I had hoped to use your recommended blood tests for indication of progress, but if LDL reduction achieves a modest risk reduction, we are left without a specific guide.
    Question: Was the progress in blood tests in dave's case a result of statins ?

  • Dr. Davis

    11/21/2007 12:46:00 PM |

    That's why lipoproteins are so important--they provide other indicators. In my experience, people who have LDL cholesterol as the sole cause of heart disease are a very small minority. The vast majority of people have multiple causes beyond LDL.

    Also, about 50% of people can still get a heart scan score after bypass surgery if you find a center willing to do a detailed analysis. You will need to ask.

    Also, I don't know what Dave did, since he is a reader and everything he posted is above. Are you there, Dave?

  • Dr. Davis

    11/21/2007 5:41:00 PM |

    Hi, Paul--

    I think your doctor might be confusing heart scans with CT coronary angiograms. She is right in saying that CT angiograms (using X-ray dye) require a lot of radiation; 100 chest x-rays worth with present technology.

    However, a plain heart scan to generate a heart scan score requires 4 chest x-rays worth on an EBT device, 8-10 on an 64-slice multi-detector device.

    See the Track Your Plaque Special Report, Radiation and Heart Scans: The Real Story at http://trackyourplaque.com/library/fl_06-021radiation.asp.

  • Anonymous

    11/21/2007 6:01:00 PM |

    Regarding repeatability, there is a 2005 study by Serukov, Bland, and Kondos that shows that the repeatability is a function of the square root of the calcium score, and that volume score is more repeatable than Agatston score. The reference is

    “Serial Electron Beam CT Measurements of Coronary Artery Calcium: Has Your Patient's Calcium Score Actually Changed?” Alexander B. Sevrukov, J. Martin Bland and George T. Kondos, American Journal of Roentgenology 2005; 185:1546-1553
    http://www.ajronline.org/cgi/content/full/185/6/1546

    In this report, the standard deviation of the difference between two sequential calcium scored is

    SDAG130 = 2.515 *sqrt(avg score)
    SDVol130 = 1.758 *sqrt(avg score)

    This results in the following values, where SDA is the standard deviation for the Agatston score and SDV is the standard deviation for the volume score.

    Score-SDA--%SDA--SDV--%SDV
    5-----5.62---112%---3.93--79%
    10----7.95---79%----5.55--56%
    20----11.2---56%----7.86--39%
    50----17.7---35%----12.4--25%
    100---25.1---25%----17.5--18%
    200---35.5---17%----24.8--12%
    300---43.5---14%----30.4--10%
    400---50.3---12%----35.1---9%
    500---56.2---11%----39.3---8%
    600---61.6---10%----43.0---7%
    700---66.5----9%----46.5---7%
    1000--79.5----7%----55.5---6%

    These values show why many people use 15% as a breakpoint - only if the score has changed by more than 15% can it be said that the change is real. And this is only true for scores above 200 or so.

    Harry

  • Anonymous

    11/21/2007 7:17:00 PM |

    My cardiologist told me that EBT scanning is not recommended for anyone under the age of 30. Is this true? If so, how do I (29 years) reliably know that I am at risk?

    I discovered your blog recently. Since I have a very bad family history of diabetes, high blood pressure, and cholesterol, I decided to visit a cardiologist last month so that I can request for an EBT scan. He said that I'm too young for that, and has instead asked me to take a Carotid IMT and Stress test - are these tests reliable enough to provide insight on my risk? Could these tests return "false positive" values?

    I had found during a blood test I did this July only to find that my triglycerides were at 600!! The other cholesterol values were bad too - totalC-HDL-LDL-Tri (255-31-Not measurable-600)

    Since then I have found your blog, lost around 25 lbs and did a VAP recently (I asked for NMR and all I got from doctors - what? What the heck is that?) So I settled for a VAP, since they knew about it.

    I did a VAP along with a comprehensive blood test and the measures that came up high were.

    LIPID related:
    Total LDL-C Direct:130 (Normal<130)
    Real LDL-C:110 (N<100)
    Sum Total LDL-C: 130 (<130)
    Remnant LIPO (IDL+VLDL3): 30 (<30)
    HDL-2:9 (>10)
    VLDL3: 14 (<10)

    Non-LIPID related high values:
    Uric Acid: 8.3  (4.0-8.0)
    Fasting Glucose: 104 (65-99)
    Creatine Kinase Total: 631 (<=200)


    LP PLA2 is normal: 164 (115-245)
    HBA1C suggests prediabetic: 5.7 (Normal <6%)


    Due to my very high value of CK Total, I researched online and found that this can increase due to high exercise, and I had it repeated after taking rest, and it returned normal results. My doctor was really surprised about this and initially hesitant to fractionise my CK. I feel empowered that I am able to take charge of my health and preventative care with the
    information that is available online (of course, one needs to tread that carefully and make an informed decision due to various conflicting opinions out there).

    Sorry for the long post, Doc. I have a newfound awareness of my health thanks to your blog, and am very much interested in knowing your inputs. I just hope that more physicians in our country follow your noble path and understand the true value and empowerment of preventive care.

    - Philip

  • Dr. Davis

    11/21/2007 8:09:00 PM |

    Hi, Philip--

    In general, 29 is very young, perhaps too young, unless there is an outstanding family history (e.g., father with heart attack at age 37). Although your lipid/lipoproteins are concerning, it would be highly unusual to have anything but a zero heart scan score at your age.

  • Dr. Davis

    11/21/2007 8:14:00 PM |

    Hi, Harry--
    Thanks for the help!

  • Neelesh

    11/22/2007 4:51:00 AM |

    Hi Dr. Davis,
      I've just bought the Track Your Plaque book, waiting for its arrival. I've had a heart attack a year back.I'm 30 years old with no family history, non-alcoholic, non-smoker and vegetarian.
    The event was attributed to ectatic arteries(Type-III) and a very high level of LP(a)- between 120-130. The standard lipid profile was also marginally higher. If I had not insisted for an LP(a) test after reading Dr Agatston's South Beach Heart Program, I would have never found the LP(a) factor.
       I was stented during the hospitalization and now I'm wondering how effective the heart scan will be, given that the accuracy reduces  with stented arteries (http://circ.ahajournals.org/cgi/content/meeting_abstract/114/18_MeetingAbstracts/II_692-a)

    Thanks!
    -Neelesh

  • Dr. Davis

    11/22/2007 2:35:00 PM |

    Hi, Neeleesh--

    I do advocate heart scanning in people with stents, but I generally suggest that only the unstented arteries be scored. It's imperfect, excluding the most diseased artery, but it's proven a useful compromise, leaving you with two "scorable" arteries.

    The study you cite, however, is not about heart scans, it's about CT coronary angiography, a study that yields "percent blockage" sort of information, not an index of plaque.

    Beyond Lp(a), you should strongly consider vitamin D normalization.  By your first name, I take it you are from India/Pakistan or similar background, an ethnic origin that is associated with severe vitamin D deficiency.

  • Neelesh

    11/22/2007 3:00:00 PM |

    Thanks Dr. Davis. And yes, I'm from India.

  • wccaguy

    11/22/2007 3:13:00 PM |

    Dr. Davis,

    I found your answer to Neeleesh to be interesting in the extreme.  I have a  follow up question to it.

    I don't have specific references for the two facts I have heard but couldn't reconcile:

    1   India has high coronary artery disease incidence.

    2   Your answer to Neeleesh states that vitamin d levels are low in India and Pakistan.  And that would help much to explain the high rate of coronary artery disease in these countries.

    3   And yet India is close to the equator and so vitamin d levels should be relatively high because of sun exposure right?

    The question then is this:  What is the cause of the low vitamin d level in those countries?

    Thanks!

  • Dr. Davis

    11/22/2007 4:00:00 PM |

    It is interesting, isn't it?

    I believe part of the explanation is that, the darker your skin complexion, the more you are "protected" from intense and prolonged sun exposure. But, activation of 7-hydrocholesterol to 25-OH-vitamin D3 may require many hours more exposure. Thus, a fair skinned person might activate D within minutes, while a dark skinned individual might require hours.

    Another factor that has not been thoroughly explored but has potential for yielding enormous insights: Vit D receptor genotypes. That is, vitamin D deficiency may express itself in different ways in different populations. Some might get colon cancer, others multiple sclerosis, others coronary disease.

    I believe that the dark-skinned phenomenon becomes especially an issue when migrating to sun-deprived climates such as the northern U.S.

  • wccaguy

    11/22/2007 6:12:00 PM |

    Hi Doc,

    Your explanation makes sense.

    I did a quick google search and found experts on the problem in India attributing it to the increasing extent to which Indians were staying indoors and not "being active."

    But the vitamin D issue throws the whole question of "activity" into question doesn't it?  It might not be the activity per se but instead the amount of sunlight reduction.

    And if, per your explanation, darker skinned people need more time in the sun than lighter skinned people for Vitamin D3 to be "activated" then than a decrease in sunlight would have more effect on darker skinned people than lighter skinned people.

    Very interesting...  And perhaps INCREDIBLY good news!!!

    Because it means that there might be a cheap effective treatment for the coronary disease epidemic in India.

    Does all that make sense?

  • wccaguy

    11/22/2007 6:19:00 PM |

    Just to follow up one more point on this D3 question...

    I guess what we need to do is find a study which shows a correlation between degree of skin pigmentation and Vitamin D3 activation?

    (I'm not sure if the word "degree" is the right word, but perhaps the question is understood anyway?)

    Answering that question would certainly set up the basis for a scientific study right?

  • Dr. Davis

    11/23/2007 12:56:00 AM |

    Yes, it does. It could serve as the basis for a tremendously interesting study.

  • Dr. Davis

    11/23/2007 1:09:00 AM |

    There are indeed a few studies that document this effect, e.g., Factors that influence the cutaneous synthesis and dietary sources of vitamin D (abstract viewable at Arch Biochem Biophys. 2007 Apr 15;460(2):213-7.)

    However, I am not aware of any study that examines the effect of vitamin D supplementation specifically in this population that tracks coronary atherosclerosis. One British study  in Bangladeshi adults did demonstrate dramatic reduction in inflammatory markers with vit D replacement (Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? at http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12454321&ordinalpos=22&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum  ).

  • Dave K

    11/24/2007 12:21:00 AM |

    Hi Dr Davis,

    Sorry - I have been offline for a couple of days.  Interesting discussion.  I will try and add some detail lipid info.

    July 2007 Blood work showed

    My Lp(a) is 7
    IDL = 10
    VLDL=11
    HDL-2 = 15
    HDL-3 = 50
    VLDL C = 18
    VLDL1+2 = 7

    Currently taking fishoil 1700 mg of DHA+EHA
    Vitamin D 800mg - just incresed to 2000
    Baby Aspirin
    Multivitamin
    Crestor
    Just started Zetia after getting this last scan result
    Eat basic South Beach phase 3
    BMI - 27
    Glucose is 105
    Exercise 4X week...
    Lp-PLA2=120

    Blood pressure high-normal but I don't know about during exercise.  Cardilogist scheduled me for a stress test after this volume increase.

    I have not has a blood test for Vit D.

    Also - I had an angiograham after the first scan because I was having chests pains .... it turned up that I had no blockages whatsoever.  So we judged the chest pains as non cardiac.

    So I am following your list pretty close.  I guess I just have to wait to see how these changes do.  How long would you wait for another scan?

    Not sure what else to add - your website says to consider L-arginie...


    I do have a specific question.  In the scan report it shows where the calcium was found.  Don't know the software, but there was one spot where it showed in the early report that it didn't show in this report (of course there was several new areas) - could that have actually been a reversal at that spot?

  • Dr. Davis

    11/24/2007 1:25:00 AM |

    Small LDL and a deficiency of large HDL, along with modest excess weight, high blood sugar, high blood pressure all suggest you are (or were) likely over-dependent on processed carbohydrates like wheat products. Your pattern would likely respond vigorously to reduction or elimination of these foods and weight loss. Niacin can help this pattern. In our experience, normalization of vitamin D is crucial.

  • Dave K

    11/26/2007 5:51:00 AM |

    Dr Davis,

    Few more data ....

    Some of the treatments have only been for the last 6 months or so.  The Statin was first (of course) and it took almost a year to get something I could tolerate.  The we talked about Vit D (700) and fish oil (800 Omega 3).  After a full Lipid scan around 9 months ago - we decided to add more fish oil.  So the full dosage I listed is only 6 months old or so.

    Also - I love my red wine and I know the number says two glasses and i rarely do two - so its three or four ... which might be my next step....

    From your last response, I assume the VLDL and IDL levels are the ones you would target hardest at this point.

    Don't do a lot of sugar or wheat... Do eat Oatmeal everyday with rasins or blueberries.

    Oh and my other question was with this kind of increase how long would you wait for the next scan?

  • Dr. Davis

    11/26/2007 12:08:00 PM |

    Dave-

    I generally recommend waiting a year after all identifiable causes have been corrected. However, given your minimal doses of vit D, I usually have my patients wait at least six month after vitamin D blood levels are corrected.

  • Dave

    11/26/2007 8:01:00 PM |

    Dr Davis,

    Thank you ... keep up the great work and I'll keep reading... and tracking.

    Dave

  • G

    11/27/2007 12:39:00 AM |

    Neeleesh and DR. D,

    This Canadian physician appears to have a lot of indepth awareness of the diff phenotypes. He suggests (in the author's response) that D2 may not work as well in East Indians (may worsen glycemic control) versus D3 (the more biologically active vitamin D). Very fascinating!!

    http://www.cfp.ca/cgi/reprint/53/9/1435
    Repletion of vitamin D with vitamin D2 is common
    practice, and vitamin D2 can be used safely when monitored
    to achieve normal levels of 25(OH)D. This might
    take 2 to 3 months, as discussed in your letter and in my
    paper, because the half-life is about 2 weeks. Using vitamin
    D3 (1000 to 5000 IU) daily, depending on the level
    of deficiency, will also achieve this goal. I also agree
    that the goal is to achieve levels of 25(OH)D higher than
    100 nmol/L, preferably 100 to 125 nmol/L.
    My concern regarding vitamin D2 is that it is a synthetic
    analogue and might interact with the vitamin D
    receptor differently in various cell systems. It has been
    reported that vitamin D3 might improve glycemic control.
    7 Vitamin D2 has been reported to cause worsening
    of glycemic control in people of East Indian descent.8
    Is this because of vitamin D receptor polymorphism, or
    because of enhanced 24-hydroxylase enzyme activation,
    or is it due to how vitamin D2 interacts with the receptor?
    Until this has been sorted out, I feel safest using
    vitamin D3. There are about 2000 synthetic analogues
    of vitamin D. The search is on for one that can cross the
    blood-brain barrier to treat certain types of brain cancers
    without causing hypercalcemia.9 But then again,
    what other effects would this compound have? There
    are still so many unknowns.
    The first step is to recognize that most Canadians
    do not get enough vitamin D, especially in the winter
    months, because of where we live. This recognition
    might reduce the need for expensive drugs to treat
    various conditions and might improve the well-being of
    many Canadians.
    An ounce of prevention is worth a pound of cure.
    —Gerry Schwalfenberg MD CCFP
    Edmonton, Alta
    by e-mail

    here's the orig article which is one of the most excellent summaries I've seen so far -- great minds think alike -- they advise > 50ng/ml like DR. Davis as well!
    http://www.cfp.ca/cgi/reprint/53/5/841

  • Neelesh

    11/27/2007 4:05:00 AM |

    D,
    Interesting study indeed. Thanks for the information. I guess I have a lot of things to discuss with my cardiologist next week. Smile
    -Neelesh

  • chickadeenorth

    12/2/2007 11:16:00 PM |

    Hi to Gerry Schwalfenberg MD CCFP, do you know any Dr In Edtmn who practices Track your Plague, if so could you suggest names to help me. I live out by Jasper and need a skilled Dr in this treatment program, I would travel to Edtmn.Many thanks.
    chickadeenorth
    (hope its ok for me to ask this here)

  • cadoce66

    4/5/2008 8:37:00 PM |

    hi my aunts 63 yrs and she underwent an angioplasty with a medicated stent .. Shes on PLAVIX and her artery was 90% blocked and she had an evolving AWMI...
    Please advise what she should taketo prevent another blockage or heart attack!
    Thanks!

  • buy jeans

    11/3/2010 10:34:10 PM |

    So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

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