How old are you?

George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.

No high blood pressure

Primitive cultures that were, until recently, unexposed to the modern world, reveal some important insights into blood pressure.

The Yanomamo of South American, the Xingu Indians of Brazil, rural Kenyans, and the natives of Papua, New Guinea have average blood pressures of 103/63 mmHg. Even more incredibly, while 90% of modern Americans will develop high blood pressure as they age, the members of these primitive cultures do not develop age-related hypertension.

What's the secret? Perhaps the full "secret" of their remarkably low blood pressure has not been fully unraveled, but several observations have emerged:

--They are not exposed to modern processed foods like pretzels, crackers, and breakfast cereals.
--Low-carbohydrate foods. Carbohydrates are largely the product of the food industry, convenience foods bought in stores. No such thing in the jungle.
--Living outdoors, having to forage and hunt, walk to your destination, not drive or wait in line for food.
--Outdoor lives, wearing little more than a few strands of clothing, exposes you to plentiful vitamin D activation from sunlight exposure.
--Consuming wild game, rich in omega-3 fatty acids, enhances endothelial health and reduces blood pressure.
--Wild plants, roots, and berries, as well as wild game, along the coast, are richer in iodine.

The studies examining the habits of the Yanomamo and other primitive cultures focused principally on sodium intake. Indeed, the very low sodium intake of primitive cultures was associated with lower blood pressure--up to 6 mmHg reduction. But there's clearly more to learn than "cut your salt."

Name that food

What common food can:

• Cause destructive intestinal damage that, if unrecognized, can lead to disability and death?
• Increase blood sugar higher and faster than table sugar?
• Trigger an autoimmune inflammatory condition in the thyroid (Hashimoto’s thyroiditis)?
• Create intestinal bloating, cramps, and alternating diarrhea and constipation, often labeled irritable bowel syndrome?
• Trigger schizophrenia in susceptible individuals?
• Cause behavioral outbursts in children with autism?
• Cause various inflammatory diseases such as rheumatoid arthritis, ulcerative colitis, dermatitis herpetiformis, systemic lupus, pancreatic destruction, and increase measures of inflammation like c-reactive protein?
• Cause unexplained anemia, mood swings, fatigue, fibromyalgia, eczema, and osteoporosis?


The food is wheat. Yes, the ubiquitous grain we are urged to eat more and more of by the USDA (8-11 servings per day, according to the USDA food pyramid), American Heart Association, American Dietetic Association, and the American Diabetes Association. Wheat is among the most destructive ingredients in the modern diet, worse than sugar, worse than high-fructose corn syrup, worse than any fat.

What other common food can result in such an extensive list of diseases, even death?

Celiac disease alone, a severe intestinal inflammatory condition from wheat gluten, affects an estimated 3 million Americans (Celiac Disease Foundation). The medical literature is filled with case reports of deaths from this disease, often after many years of struggle with incapacitating intestinal dysfunction and the sufferer's last days plagued by encephalopathy (brain inflammation).

What happens when you remove wheat from the diet?

The majority of people quickly shed 20-30 lbs in the first few weeks, selectively lost from the abdomen (what I call “wheat belly”); blood sugar plummets; triglycerides drop up to several hundred milligrams, HDL increases, LDL drops (yes, wheat elimination is a means of achieving marked reduction in LDL cholesterol, especially the small, heart disease-causing variety); c-reactive protein plummets. In addition to this, intestinal complaints improve or disappear, rashes improve, inflammatory conditions like rheumatoid arthritis improve, diabetes can improve or be cured, and behavioral disorders and mood improve.

Along with the ill-fated low-fat dietary advice of the last 40 years, the advice to eat plenty of "healthy whole grains" is responsible for untold disease and suffering. Yes, if you start with a fast food and junk diet and replace some of the calories with whole grains, you will be better off. (That was the logic--the Nutritional Syllogism--of the studies that established the benefits of whole grains over processed, "white" grains.)

But eliminate wheat grains and health takes a huge leap forward. And, no, there is no such thing as wheat deficiency--B vitamins, insoluble fiber, some protein--can easily be replaced by other foods.

Heart Defects Simplified



For as long as I've known him, echocardiography technologist, Ken Heiden, has had a deep fascination with congenital heart disease. Ken has just written a wonderful book on congenital heart disease called Heart Defects Simplified.

While this is a bit off-topic for the Heart Scan Blog, I know that there is a serious lack of helpful information for people with congenital heart disease and parents of children with congenital heart defects. So I asked Ken to tell us something about his book.



WD: I've reviewed your book and have been thoroughly impressed with the clarity and detail with which you handle a complicated topic. You somehow manage to make it easy to grasp, far more than any other resource I've used in past. Do you feel that your book serves a previously unmet need?

KH: This book serves an unmet need in that it presents the complex subject of congenital heart defects in a simplified manner. Most books on this subject are anywhere from 300-1700 pages in length and tend to be written for doctors. Further, most of these books have very few diagrams, and they rely upon their explanations to describe these defects.

Heart Defects Simplified is 104 pages in length, describes the most common defects, including surgical repairs, in a two-page format with full-color diagrams on the left and complete descriptions on the right of each chapter. The book is particularly written for sonographers, nurses and parents, but it is valuable for anyone interested in this subject. It is particularly useful in clinical situations because it is convenient to lay out at your side with a coil-bound format and durable pages. Further, there are appendixes which include "Surgical Procedures in Alphabetical Order," "Prevalence of Congenital Heart Disease," "Scanning Protocols for Echocardiographers," "Imaging Tips," a glossary and a worksheet for echocardiographers.


WD: I know that many people with loved ones who have congenital heart defects, particularly parents of children with such conditions, are often kept in the dark about the details of the condition. Is your book suitable for the non-technical reader, such as parents?

KH: This book is an excellent resource for parents. It is written in language that is understandable by parents as well as technologists and nurses. The full-color diagrams provide invaluable insight into this very complex world. Most importantly, this book attempts to make the subject of congenital heart defects accessible to anyone who wishes to comprehend this subject.


WD: I understand that people with congenital heart defects and parents are active participants in online discussion groups. Will your book serve as a resource for people who participate in these groups?

KH: This book is not only a resource for sonographers and parents, but the book is accompanied by a blog (HeartDefectsforEveryone.blogspot.com) that attempts to address many of the concerns commonly encountered with congenital heart defects. This blog is a work in progress, but I hope to provide a forum for parents, healthcare personnel, and others to share their questions and concerns about congenital heart disease.

My experience with the omega-3 index

I just got back my own results from the Gene Smart laboratory reporting my omega-3 index and omega-6:omega-3 ratio.

My results:

Omega-3 index: 8.2%

Omega-6:omega-3 index: 3.2 to 1

Not too bad, but not as good as I'd expected. Hmmm.

Although the omega-3 index of 8.2% puts me in the lower risk category for sudden cardiac death, I was hoping for a level of 10% or slightly greater, the level that I believe is more likely to be related to plaque inactivation or reversal. I obtained this level of omega-3 averaging an intake of EPA and DHA of about 2500 mg per day.

I was somewhat disappointed by the omega-6:omega-3 index. Although it's clearly better than the American average range of 20:1, it is short of the ideal of 2:1 or even 1:1. Since I purposely avoid omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils, I wonder if I've overdone the nuts. The two ways to improve the omega-6:omega-3 ratio are to 1) decrease omega-6, or 2) increase omega-3. I'm going to do both.

So I thought I was doing pretty well. But there's clearly room for improvement.

Remember: If just reduction of cardiovascular risk is your interest, then a lackadaisical attitude towards these issues might work. But if your interest is elimination of risk and reversal of atherosclerotic plaque, then it pays to go the extra mile. In this case, knowing your omega-3 index and omega-6:omega-3 ratio might tighten up your program.

The Omega-3 Index: The higher, the better?

So you take a few fish oil capsules every day and eat fish once or twice a week. What is the blood and tissue level of omega-3 fatty acids generated by your habits?

A number of variables enter into the equation. For instance, if you take fish oil capsules, what is the concentration of omega-3 fatty acids? How well are they absorbed? After absorption, how effectively are omega-3 fatty acids incorporated into cell membranes?

Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.


The Omega-3 index and sudden cardiac death

Two large studies have demonstrated that higher omega-3 blood (the level in red blood cells, or RBCs) levels were associated with reduced likelihood of sudden cardiac death. The risk for sudden cardiac death was 10-fold higher for the lowest omega-3 RBC levels compared to the highest.



Harris WS 2008; adapted from Siscovick DS et al 1995 and Albert CM et al 2002
(The omega-3 Index was derived from whole blood omega-3 levels, which correlate with RBC omega-3 levels, and are thus “estimated.”)



What’s the average omega-3 RBC level for Americans? Most Americans have omega-3 RBC levels in the 2.5-4.0% range, consistent with the tallest bars at the left and associated with greatest risk for sudden cardiac death. People with heart disease can have levels less than 1%. Some authorities propose that this new measure be called the omega-3 index.

Subsequent studies have shown that the omega-3 index has greater power to discriminate who will have a heart attack or die from sudden cardiac death better than any other common laboratory measure of coronary risk, including LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol to HDL ratio, homocysteine, and c-reactive protein.

Just as hemoglobin A1c offers a 3-month look into blood glucose levels, the omega-3 index reflects your long-term omega-3 intake. The quantity of RBC omega-3s also closely parallels the quantity of omega-3s in heart tissues.


What is an ideal omega-3 index?


The above studies relating RBC omega-3 levels and sudden cardiac death suggest that a level of 6.3-7.3% is associated with far fewer fatal events?but events are not eliminated at this level. Is there even greater benefit with levels higher than 6.3-7.3%?

A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks. This suggests that even higher levels are necessary to prevent non-fatal events.

Should we target 10%? 12%? Maybe higher? Any higher and we are toeing the level achieved by the Inuits, the “Eskimoes” of Greenland, northern Canada and Alaska who have been observed to have a low rate of heart disease.


What’s your omega-3 index?

The appreciation of the importance of omega-3 fatty acids marks one of the greatest health revelations of the last 50 years. We can now measure it.

The ability to measure the proportion of omega-3 fatty acids in red blood cells may provide yet another means for all of us to further reduce risk for cardiovascular events.

If you are interested in knowing your omega-3 index, we are now making the fingerstick test kits available by going here.

Vitamin D increased my cholesterol

A friend told me this story.

Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day.

However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl.

"It must have been the vitamin D! So I stopped it right away."

Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain.

Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:

Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5

This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol.

One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer.

Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL.

So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl.

So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program.

This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misinformation.

Nutrtional ignorance is not unique to the U.S.

Heart Scan Blog reader from Australia, Michaela, also a mother of a son with a complex congenital heart defect, wrote this series of e-mails to me. (Published with Michaela's permission.)


I've been reading the article, Valve disease and Vitamin D from April '07, by Dr William Davis. I'm hoping you may have some information on the topic. I'm hoping someone will have time to help me.

I have been supplementing my 15 year old son with Vit D for 4 months but only 1000 (U) per day. I would like to increase the dosage but am not sure if I would do him more harm than good.

I have been researching vitamins and supplements on the net for a few months and have been amazed at what I have found. I only wish I had done it years ago. My son has been let down by the Australian Medical Profession and it's a race against time now to keep him well and avoid a heart transplant.

My son was born with aortic stenosis and had a valvotomy at 4 weeks of age. This damaged the aortic valve and he had a Ross Repair procedure at aged 3. This left him with a damaged heart muscle and leaking aortic & pulmonary valves. In May '08, his heart grew more enlarged, causing the mitral & tricuspid valves to also leak.

I took him to Bangkok in Feb this year where he had 70 million of his own Adult Stem Cells directly injected into his heart muscle with the hope of strengthening the muscle and eventually valve replacement.

My son has recovered from the surgery and is once again symptom-free, thanks to the wonderful advice followed by the Author & Cardiologist, Stephen T. Sinatra. I have followed his supplement regime and what a difference! Of course, this won't last while my son's valves continue to leak.

My son has also developed secondary hyperparathyroidism, bone thinning and hypothyrodism. Vit D & Calcium have something to do with this I believe.

My Australian Doctors have never made mention of any vitamins or supplements .... EVER! Transplant is all they will consider and we are not having it.

If you have any info or links to any sites which may be useful to me, could you email them to me? I would be grateful for any help I could get.

Sincerely
Michaela



I responded to Michaela's e-mail:

Hi, Michaela--

Vitamin D is extremely important. Sometimes, hyperparathyroidism and calcium derangements are caused by vitamin D deficiency. You might be able to get help with this from an endocrinologist, since they are the ones who deal with hyperparathyroidism. An endocrinologist might even be familiar with several recent studies that document this phenomenon:

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Vitamin D deficiency and primary hyperparathyroidism

Also, see the discussions at www.vitamindcouncil.org from Dr. John Cannell.

Because of the complexity of your son's health, it might be hazardous to stray too far away from conventional care though you and I know that there are limitations to that perspective. For that reason, I would urge you to press for answers from a knowledgeable endocrinologist.

I hope you find the answers you need.

William Davis, MD



Several months later, Michaela provided this update:

Hi Dr Davis,

I wrote to you back in July regarding my 15 year old son's need for a Heart Transplant through a failed Ross Repair and the possible Vitamin D connection. You sent me some valuable links and I thank you again for that.

I just wanted to let you know, I think you have given me the answers. I increased Lee's Vitamin D supplement to 6000U a day and, along with the recommended nutritional supplements of US Cardiologist Dr Stephen T Sinatra, there have been remarkable improvements! Lee also had 70 million of his own Adult Stem Cells injected into his heart in February. As we know, Stem Cell Therapy takes time and Lee was looking like time was quickly running out.

I have removed him from the transplant list. He is now reading normal Kidney function, the BNP (Brain Natriuretic Peptide, a measure of heart failure] has dropped by 7000 and his liver size has reduced to where it no longer causes him discomfort. The liver tests show it's still affected but it's function is improving each month. His last Echo was in early July and there had been a reduction in the size of his heart, which is so important.

To the Doc's, Lee can't get better, there is only transplant or death so you can imagine the surprise on their faces to see him looking and feeling so well with their tests to back it up. Still, even though it's staring them in the face, they don't want to know about it. They have no interest in what supplements he is on or Stem Cell therapy. God help their other patients. I view them in the waiting room and think of them as lambs to the slaughter.

We are not spoiled for choice with Doc's here in Western Australia. I have to take what I can get and there is not many who would take on Lee's case. He was number 1 on the transplant list and a most urgent case. Not many were willing to even look at him with his cardiac history and all I had to help was the arrogant Doc's at the Advanced Heart Failure Unit. They were not at all interested in his secondary hyperparathyroidism. I suppose it didn't matter what else he had compared to his heart problems.

Anyway, I'm writing to thank you. Lee would be transplanted or dead now if it wasn't for Dr's like you sharing their knowledge online. I wish I had researched things years ago, Lee might not have sunk so low if I had. I don't know if the transplant can be held off indefinitely, but like I tell Lee, "Stay well. There are amazing people out there doing amazing things, if you can just hang on. The miracle is around the corner." He's so well, you'd have to see him to believe it. But I have 7 kids and Lee is as physically active and as well as the other 6! For how long he can stay like this, I don't know but if his ejection fraction [a measure of left ventricular strength] can keep climbing and his body gets stronger, I have hope for another attempt at valve replacement.

I'm still shocked and angry that nutritional supplements have never been mentioned in the 15 years I've been dealing with cardiologists. Surely they know about them. I have read through dozens of reports online of the benefits of them--Why haven't they?! Thank God for the online Doc's such as yourself, the valuable info would never make it out of a Doctor's office in Western Australia! I've had to leave my country for Stem Cell therapy and then implore overseas Doc's for advice and information. What does that say for the Australian Medical Profession? Not a lot! They put him in the position he is in yet don't want to help get him out.

I'm so very grateful to you, thank you and God bless.

Michaela



Note: The above is not meant to be an implicit endorsement of stem cell therapy. This was just part of Michaela's story about her son.

Eat cranberries

Most people already know that cranberries are useful for preventing urinary tract infections. Cranberries can also be useful for preventing other sorts of infections, such as dental cavities and stomach ulcers because of cranberry's ability to block bacterial adhesion.

Cranberries can also be a useful component of a heart healthy program.

Several unique properties of cranberries contribute to various aspects of heart health:

• Cranberries are a rich source of pectin--Pectin is a soluble fiber, the sort that binds bile acids in the intestinal tract and naturally reduces LDL cholesterol.
• Cranberries are a rich source of polyphenols and flavonoids--Including the wonderfully fascinating anthocyanins, the flavonoids that confer the beautiful red color. Surprisingly, cranberries are richer in polyphenols and flavonoids than blueberries, strawberries, and grapes. Cranberry juice is also rich in these compounds. However, beware of cranberry juice "cocktail," which is diluted with other liquids such as high-fructose corn syrup. Like grapes, cranberries are a source of resveratrol, the polyphenol also found in red wines that some believe is responsible for reduced risk for heart disease and extending life.
• Cranberries have high antioxidant activity--Cranberries are among the highest in antioxidant capacity against superoxide radicals, hydrogen peroxide, and hydroxyl radicals, oxidizing factors believed to underlie heart disease, cancer, and aging. Cranberries also reduce the oxidation of LDL cholesterol particles.
• Cranberries block uric acid production--Cranberries have the unique ability to block the activity of an enzyme, xanthine oxidase, that converts xanthine to uric acid. Uric acid is believed to add to heart disease risk and is the factor responsible for gout.
• Cranberries increase HDL cholesterol--Cranberry juice increases HDL by 3-4 mg/dl.

Cranberries are only modest sources of sugars, with 7.19 grams “net” carbohydrates (total carbohydrates minus fiber content) per cup of whole raw cranberries.

The best way to eat cranberries is to consume the real thing: eat the whole berry, as in sugar-free cranberry sauce or added to baked dishes like chicken. Second best are dried cranberries. However, be careful of the overly-sweetened dried cranberries that contain added sugar (for a total of 78 grams sugar per cup--far too much). Unsweetened dried cranberries can be purchased, or you can dry them yourself.

Cranberry juice is another way to obtain the health benefits of cranberries; the unsweetened juice, while quite tart, is the best with 30.5 grams sugar per 8 oz--so don't drink more than 4 oz at a time. The more common cranberry juice “cocktails” are generally too sugary and/or too dilute for full health benefit.

The cranberry harvest season in Wisconsin, Michigan, Oregon, Massachusetts, and New Jersey is just getting underway, so we should be seeing fresh cranberries on store shelves or farmers' markets any day now.

Procedures 'R Us

Kay came to the office for an opinion.

Over the past 8 months, she'd received a stent to the left anterior descending coronary artery and, during a separate procedure, a stent to the left subclavian artery.

"My cardiologist was very capable doing procedures. But when I asked, 'What do I do now?' he barely said a word and handed me a presciption for Crestor."

This kind of incredible neglect is the norm: Write a prescription for statin drug, delegate dietary advice to the hospital dietitian who advocates a heart disease-causing low-fat diet, followed by hospital discharge. You are expected to report any recurrent symptoms (which are inevitable), at which point you might "qualify" for another procedure.

It would be malpractice if it were not the prevailing standard in the community. Yes, the prevailing standard is neglect--neglect to identify, quantify, and correct all the identifiable causes of heart disease; neglect to discuss the nutritional methods that actually correct the abnormal patterns that cause heart disease; neglect to discuss nutritional supplements or medications beyond statins that further reduce heart disease risk and "need" for more procedures. In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures.

I see consultation after consultation involving stories just like Kay's. People are frightened and they sense intuitively that nobody raised the question of why they have a potentially fatal disease.

Don't allow yourself to fall victim to this incredibly neglectful mode of practice, the one that has enriched hospitals, the drug industry, many cardiologists, but does little to address the actual disease.
MESA Study: Track Your Plaque-Lite?

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD

Comments (11) -

  • Mike

    1/4/2008 3:52:00 PM |

    The part of the study that caught my attention was "Current and former smokers had higher incident CAC rates than never smokers, but this difference was not statistically significant once other risk factors were considered. "

  • Barry

    1/4/2008 5:14:00 PM |

    Dr Davis,

    I recently came across your blog and it peaked my interest. I have been tracking my lipids for several years now.

    Let me give you a little background. My dad had by-pass surgery when he was in his forties. He spent the rest of his life watching his diet and lipids and blood pressure. In 2005 he died from coronary failure a month after turing 71.

    Because of my family history, and lipid levels (LDL 130, HDL <40), my physician wanted to start me on advicor. I resisted and tried to moderate my lipids through diet and exercise. I used the low fat diet approach and got nowhere. So I started on Advicor late in 2003. By March of 2004 my profile was right where my doctor wanted it: LDL 76, HDL 41, TriG 98. I continued on Advicor and had my lipid profile and liver enzymes checked every 6 months. I started keeping my scores in a spreadsheet and have been tracking them ever since.

    After taking Advicor for a while I started reading about the side effects, about the additional predictors for heart disease, and the limitations of the physician "approved" diets.

    After doing all this reading, I wanted to try once again to moderate my lipids through diet. In January 2006 I stopped taking advicor and changed my diet so as to reduce carbohydrate. I started eating cheese omlets cooked in butter for breakfast. I did not avoid red meat. I stopped eating rice, potatoes, and white flours, etc. As a result of these changed my HDL went up from 40 to 50. My TriG went down to a low of 73. Unfortunately, my LDL went up to 130-140. So after about a year I went back on Advicor but kept my diet similar (except I went back to whole grain cereal for breakfast). The other change I made last year is I started on an aggressive exercise program. I exercise 4-5 times a week for 50-60 minutes, keeping my heart rate at the 80% level. I also got a bicycle and started biking on the weekends (that has been quite fun and rewarding - I did an MS-150 ride this past October). I've only lost a few pounds 210 to 195. At 6'3" my BMI is barely in the "normal" range. I have recently switched Doctors due to other factors, but my new doctor wants to keep me on Advicor.

    My questions are these. Am I just fooling myself into a false sense of security by taking Advicor and monitoring my lipids? Should I continue this plan or make some mods?

    I anticipate that you will recommend a CT scan. Are they costly? Covered by insurance? Require a Dr's referral? What levels of radiation exposure do they impose?

    I look forward to hearing your reply.

  • Anonymous

    1/4/2008 6:50:00 PM |

    thats very interesting. The "conventional" risks only explain about 12% of plague increase and yet its well documented that statins reduce heart attack by somewhere between 30 and 40%.

  • Dr. Davis

    1/5/2008 1:55:00 AM |

    Hi, Barry-


    Thanks for your interest. However, I cannot answer direct medical questions, as good as they are.

    I would invite you to look at the website that this blog accompanies, www.trackyourplaque.com.

    Using conventional cholesterol as your index of risk is a fool's game. I could introduce you to hundreds of people who've had heart attacks and bypass surgery who thought they were being well served by conventional cholesterol. In my view, it is a model-T of medical testing.

  • Harry35

    1/5/2008 8:38:00 PM |

    I didn't find much value in this report because it doesn't look at percent changes in CAC, which seems to me to be the most important parameter to judge if plaque is growing at an unacceptable rate. Another thing about it, they didn't consider lipoprotein subclasses, but haven't most or all of the MESA subjects had NMR testing? Combining Otvos' NMR data on the MESA population with the CAC percent change data from this study could give some real insight into how and why plaque progresses. It looks like no one is going to do such a study. Is there any way a member of the public can get the raw data from the MESA studies, so we can do our own analysis? After all, MESA was funded by public funds, wasn't it?

  • Dr. Davis

    1/5/2008 9:30:00 PM |

    To my knowledge, NMR lipoprotein analysis was not performed as part of this study, or at least used for this type of analysis to predict events or progression of calcium scoring.

  • Harry35

    1/7/2008 12:09:00 AM |

    Yes, NMR results were not used in the study, but the study was done on 5756 subjects who participated in the MESA test. Mora did a study of the NMR results 5538 MESA participants, but didn't look at CAC progression (Atherosclerosis, 2007 May;192(1):211-7) Isn't it a pretty good possibility that these studies were both done on the same basic group of MESA participants? If so, the data is out there to do a study of the effect of lipoprotein subclasses on CAC progression, it just hasn't been done yet.

    Is it possible that the MESA data could be made available to us, or is the data totally  controlled by the people who collected it?

  • Dr. Davis

    1/7/2008 3:09:00 AM |

    Hi, Harry--

    I do believe that access is obtainable, though I am unsure how restricted. Go to http://www.mesa-nhlbi.org/default.aspx# for application information. I would like to do the same when some research time has been freed up.

  • Harry35

    1/8/2008 1:46:00 AM |

    Dr. Davis, from reading the MESA website, it looks like the MESA people aren't going to release the data except to qualified researchers working for established institutions or companies, and who will publish their results in a peer-reviewed journal. They aren't interested in making the data available to the general public, where it could be misinterpreted, thereby casting doubt on the overall MESA project.

    That leaves people like me out, because I just want to play with the data and look for possible correlations that haven't yet been investigated, like the effect of lipoprotein subclasses on CAC progression. Unless some established research group becomes interested in doing such a study and publishing the results, it probably won't get done. It's a bit frustrating, because it looks like the data is all there to do such a study, but there is no way to get them to release the data.

    It will probably take a fairly significant expenditure of time and analysis to investigate this and publish the results, so it will probably take a full time research group to do it. With all the other things you are doing, it may be difficult for you to take the time to do this kind of study. Perhaps with your contacts with clinical research people who might be interested in investigating this, (e.g., Otvos, Raggi, Budoff, Rumberger?) you could get the ball rolling.

    Also, it looks like a person can't get the data unless they specify exactly what they are looking for, which sort of rules out looking for correlations that haven't been previously suspected. There is something to be said for shoveling all the data into a stepwise multiple regression program and seeing what pops up as the most significant parameters, but with the tight controls they have on releasing data, this isn't likely to happen, which is unfortunate for those of us who have a personal interested in prevention.

  • Dr. Davis

    1/8/2008 2:46:00 AM |

    Hi, Harry--

    All is not lost. It may take a while, but there may be some possibilities.

    I've been giving it some thought. I can't give it high priority right now, given the need to get some of our own data analyzed and published. But I believe it is something we should explore in future.

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