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.
All posts by william-davis

Track Your Plaque and non-commercialism

If you're a Track Your Plaque Member or viewer, you may know that we have resisted outside commercial involvement. We do not run advertising on the site, we do not allow drug companies to post ads, we do not covertly sponsor supplements. We do this to main the unbiased content of the site.

We've seen too many sites be tempted by the money offered by a drug company only to see content gradually drift towards providing nothing more than cleverly concealed drug advertising. I personally find this deceptive and disgusting. Ads are ads and everyone knows it. But when you subvert content, secretly driven by a commercial agenda, that I find abhorrent.

That said, however, I do wonder if we need the participation of some outside commercial interests to help our members. In other words, many (over half) of the questions and conversations we have with people is about what supplement to take, or what medication to take. While we cannot offer direct medical advice online (nor should we) because of legal and ethical restrictions, I wonder if could facilitate access to products.

Many people struggle, for instance, with trusted sources for l-arginine, vitamin D, fish oil. Other people struggle with finding a heart scan center because of the changing landscape of the CT scanning industry. Could we somehow provide a clear-cut segment of the website that clearly demarcates what is commercial and non-Track Your Plaque-originated, yet at least provides a starting place for more info?

Ideally, we would have personally tried and investigated everything there is out there applicable to the program. But that's simply impossible at this stage.

I feel strongly that we will never run conventional ads on the site. Nor will we ever permit any outside commercial interest to dictate what and how we say something. The internet world is full of places like that. Look at WebMD. I find the site embarassing in the degree of commercial bias there. We will NEVER sell out like that, regardless of the temptation. People with heart disease are all conducting a war with the commercial forces working to profit from them--hospitals, cardiologists, drug companies, medical device companies (yes, even they advertise to the public, e.g., implantable defibrillators--no kidding). Genuine, honest, unbiased information is sorely needed and not from some kook who either knows nothing about real people with real disease, or has a hidden agenda like selling you chelation.

I'd welcome any feedback either through this Blog or through the contact@cureality.com.

The nattokinase scam

A conversation about vitamin K2 commonly leads to confusion. Several people have asked about something called nattokinase.

The scientific data on the potential role of vitamin K2 deficiency in causing both osteoporosis and vascular calcification is fascinating. Along with vitamin D3, vitamin K2 may be an important factor in regulation of calcium metabolism. Supplementation may prove to be a major strategy for inhibition of vascular calcification.

Obtaining K2 in the diet is tricky, since it's present in just a handful of foods: egg yolks, liver, traditional cheeses, and natto. This is where the confusion starts.

Natto is a Japanese fermented soy product. I've had it and it's quite disgusting. Nonetheless, Japanese who eat natto experience less fracture. (A parallel study in heart disease has not been performed.) Natto is also a source of another substance called nattokinase.

Advocates (otherwise often known as supplement distributors) claim that nattokinase is a "fibrinolytic", or blood clot-dissolving, preparation that "improves blood flow, protects from blood clots, and prevents heart attacks and strokes."

Don't you believe it. This is patent nonsense. There are several problems with this rationale:

--Any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. That's why all medically used fibrinolytics are given intravenously. Drug companies have struggled for years to encapsulate, modify, or somehow protect protein (or polypeptide) products taken orally from degrading this way. They've never succeeded. That's why, for instance, growth hormone (a polypeptide) remains an injection, not an oral agent. An oral growth hormone, by the way, would sell like mad, so the drug companies would very much like to figure out how to bypass the degradative effects of stomach acid. One of the "researchers" behind the nattokinase claims boasts that he has single-handedly figured out how to protect the nattokinase molecule in the gastrointestinal tract. However, he won't tell anybody how he does it. Right.

--Fibrinolytic agents are extremely dangerous. In years past, we used to treat heart attacks with intravenous fibrinolytic agents like tissue plasminogen activator, urokinase, streptokinase, and others. They have fallen by the wayside, for the most part, because of limited effectiveness and the unavoidable dangers of their use. Fibrinolytics are "dumb": they dissolve blood clots in both good places and bad. While they might dissolve the blood clot causing your heart attack, they also degrade the tiny clot in your cerebral (brain) circulation that was protective. That's why fatal brain hemorrhages, bleeding stomach ulcers, and blood oozing from strange places can also occur with fibrinolytic administration. Believe me, I've seen it happen, and I've watched people die from them.

The idea that a small dose taken orally is healthy is ridiculous. Even if nattokinase worked, why the heck would you take an agent that has known dangerous and very real consequences?

Don't let this idiocy reflect poorly on the K2 conversation, which, I believe, holds real merit and is backed by legitimate science. This is symptomatic of a larger difficulty with the supplement industry: Insane and unfounded claims about one supplement erodes credibility for the entire industry. It gives regulation-crazed people like the FDA ammunition to go after supplements, something none of us need. You and I have to sift through the nonsense to uncover the real gems in this rockpile, real gems like vitamin D3, omega-3 fatty acids from fish oil, and, perhaps, vitamin K2. But not nattokinase.

Blood pressure with exercise

Here's a frequently neglected cause for an increasing CT heart scan score: High blood pressure with exercise. Let me explain.

Paul's blood pressure at rest, sitting in the office or on arising in the morning, or at other relatively peaceful moments: 110/75 to 130/80--all in the conventional normal range.

We put Paul on the treadmill for a stress test. At 10 mets of effort (on the protocol used, this means 3.4 mph treadmill speed at 14 degree incline), Paul's blood pressure skyrockets to 220/105. That's really high.

Now, blood pressure is expected to increase with exercise. If it doesn't rise, that's abnormal and may, in fact, be a sign of danger. Normally, blood pressure should rise gradually in a stepwise fashion with increasing levels of exercise. But any blood pressure exceeding 170/90 is clearly too high with exercise. (Not to be confused with high blood pressures not involving exercise.) A handful of studies have suggested that a "breakpoint" of 170/90 also predicts heightened risk of heart attack over a long period.)

I see this phenomenon frequently--normal blood pressure at rest, high with exercise. This also suggests that when Paul is stressed, upset, in traffic congestion, under pressure at work, etc., his blood pressure is high during those periods, as well. I wouldn't be surprised to see other phenomena of underappreciated high blood pressure, like abnormally thick heart muscle (left ventricular hypertrophy), an enlarged thoracic aorta (visible on your heart scan), left atrium, perhaps even an abnormal EKG or abnormal kidney function (evidenced by an elevated creatinine on a standard blood panel).

Unfortunately, the treatments that reduce blood pressure are "stupid," i.e., they have no appreciation for what you are doing and they reduce blood pressure all the time, whether or not you're stressed, exercising, or sleeping.

Blood pressure reduction should begin with weight loss, exercise, reduction of saturated fats and processed carbohydrates (esp. wheat), magnesium replacement, vitamin D replacement. Think about CoQ10. After this, blood pressure medication might be necessary.

The message: Watch out for the blood pressures when you have a stress test. Or, if you have a friend who is adept at getting blood pressures, get a blood pressure immediately upon ceasing exercise. It should be no higher than 170/90.

Vitamin D2 vs. vitamin D3

An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.

World record heart disease reversal

A quick but important note.

Track Your Plaque Members:

Keep your eyes on the Track Your Plaque Member website for details and images of our most recent huge success story. Track Your Plaque participant, Neal, dropped his score more than anyone else before.

Although reduction of heart scan score is an everyday event around here, a 51% drop in score deserves to make news!

We will post the images of Neal's heart scans on the www.cureality.com Member website in the coming days.

Dose of fish oil

Dosing for fish oil is a perennial point of confusion. However, it's quite simple.

The active ingredients in fish oil are DHA and EPA, the so-called omega-3 fatty acids. Of course, if there's anything else in your capsules, such as omega-6, omega-9, or linolenic acid, these should not count towards the sum of EPA + DHA, since they do not exert the same benefits as the omega-3s.

The basic suggested starting dose for the Track Your Plaque program is 1200 mg of EPA+DHA. This is usually provided by taking 4 x 1000 mg capsules of fish oil, providing 180 mg EPA, 120 mg DHA per capsules, for a total of 1200 mg EPA+DHA.

About a third of people, however, will require greater doses of omega-3s to reduce triglycerides, VLDL, and/or intermediate-density lipoprotein (IDL). Most people will do fine with an increase to 1800 mg EPA+DHA, usually provided by 6 x 1000 mg standard capsules. A very occasional person (about 1 in 100) will require even higher doses.

If you ever decide to change your fish oil preparation, or if you change to a more concentrated form or another form such as liquid fish oil (e.g., Carlson's), paste (e.g., Coromega), or syrup (e.g., Pharmax Frutol), then you will need to examine the label to determine the dose of EPA+DHA. If, for instance, a teaspoon of liquid fish oil provides 360 mg EPA and 240 mg DHA, that's a total of 600 mg omega-3s per teaspoon. If your EPA+DHA dose is 1200 mg per day, then two teaspoons a day should provide it. Always adding up the EPA+DHA content of whatever preparation you choose will therefore allow you to mix, match, or change your dose whenever you like.

Niacin scams

As most of you know, niacin (vitamin B3) is an important tool for many in the Track Your Plaque program.

Niacin:

--raises HDL cholesterol
--reduces small LDL
--reduces lipoprotein(a)

And it's the most potent agent we have for all three patterns, despite just being a vitamin. Niacin also reduces LDL cholesterol, VLDL, IDL, triglycerides; reduces heart attack risk dramatically either alone or in combination with other agents.

Unfortunately, some people who are either afraid of the "hot flush" side effect, or experience excessive degrees of it, have resorted to two preparations sold in stores that have none of these effects.

Most notorious is "No-flush" niacin, also known as inositol hexaniacinate. This compound is an inositol sugar molecule complexed with 6 ("hexa-") niacin molecules. Unfortunately, it exerts none of niacin's effects in the human body. No-flush niacin has no effect on HDL, small LDL, or Lp(a), nor on LDL or heart attack.

In short, no-flush niacin is a scam. It's also not cheap. I've met people who have spent hundreds of dollars on this agent before they realize that nothing is happening, including a flush.

Likewise, nicotinamide does not work. It sounds awfully close to the other name for niacin, nicotinic acid. But they are two different things. Like no-flush niacin, nicotinamide has no effect on HDL, small LDL, Lp(a), etc.

Though I've discussed this issue in past, somehow these two "supplements" seem to sneak back into people's consciousness. You walk down the health food store aisle and spy that bottle of X-brand No-flush niacin, promising all the benefits of niacin with none of the bother. Then you remember that rough night you spent a few months back when the hot flush lasted longer than usual. That's when some people end up buying this agent making extravagant--and false--promises.

For now, for all its imperfections, niacin is still a pretty darn good agent for these patterns. Remember that the best strategy to minimize the hot flush effect is to drink plenty of water. We generally recommend taking the dose at dinner along with water. If the hot flush occurs, drink two large glasses of water (total volume 16-24 oz). Nine times out of ten, the flush is gone. It also dissipates the longer you take niacin.

Media mis-information

This is an excerpt from a popular health website, EverydayHealth.com:


A Cholesterol-Busting Vitamin?
Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter? Find out how niacin can help reduce cholesterol…

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. It is also inexpensive. However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.

Many people begin treatment at low doses (250 mg twice a day, for example) and, over six weeks or so, gradually build up to an amount that lowers lipid levels, anywhere from 1,000 to 2,500 mg split between two doses during the day. This gradual approach may help build tolerance to side effects such as facial flushing. Although niacin is available over the counter, you should not use it in quantities sufficient to lower cholesterol without a physician’s supervision. It is important to test liver function and levels of blood sugar and uric acid before beginning niacin therapy and during the course of treatment.


(Bold emphasis mine.)

At http://www.everydayhealth.com/publicsite/index.aspx?puid=548e8630-32d6-41dd-91a7-48e1cbac65ad&p=4




After an enticing headline, the article goes on to scare the pants off you. It also sounds like accurate information, delivered in an unbiased way, cold and straight.

If we were to use niacin this way, it would indeed be intolerable for most. Do not follow the above nonsensical advice. But that may have been the intention from the start.


Very telling are the fact that, both above and below the article were colorful advertisements for Lipitor, complete with Dr. Robert Jarvik’s (inventor of an implantable mechanical heart) soothing, professorial image.

Did they want to bait us with promising information about cholesterol and niacin, only to throw water on our fire and steer us towards something else?

That would be typical drug company marketing.

All in all, I’m grateful for the attention the media provides for health issues. Perhaps many people wouldn’t even be aware of niacin and other healthy strategies if some website, newspaper, or magazine article hadn’t talked about it.

But I do worry about bias. Was this an unbiased report? Or was it more like much of the physician-directed mail I receive, cleverly concealed propaganda from the drug manufacturers? Who wrote it? No author is listed. Could it have been ghost written by someone in the drug company itself, or an arm of the drug company? That’s a very common practice for the literature physicians receive, glossy, high-class materials paid for by drug companies, written by drug company-owned companies, but no company logo or name listed.

My point: Be skeptical of what the media tells us. There’s usually a good deal of truth in the reporting, but there’s also often just enough mis-information or slanting of content to make you behave or believe a certain way. “If niacin is this dangerous, maybe I really should take the Lipitor.”

A dirty little secret

Here's a dirty little secret many people don't know about.

If I implant a stent, I might get paid somewhere around $2000 for the heart catheterization, stent implantation, femoral artery closure device, hospitalization charges. That's not too bad.

But what if I'd like more? What if I'd like to squeeze this unsuspecting patient for more, or actually his/her insurance company?

Easy: Add on complex procedures to the basic procedure that yield more professional charges. For instance, I could perform laser angioplasty, a procedure that adds another couple thousand dollars. I might pull out the old rotational atherectomy device, a high-speed diamond tipped drill that also adds substantial professional charges. I might also use the intracoronary ultrasound device, an otherwise helpful device, but I might pull it out to use on everybody.

With the exception of ultrasound, all the "add-on" procedures were more popular in the early and mid-1990s--before they were shown in clinical studies to provide no advantage, perhaps even add to procedural risks.

Thus, a patient might undergo a heart catheterization, balloon angioplasty with stent implantation into the proximal left anterior descending coronary artery (LAD), followed by laser angioplasty of the mid-LAD, followed by intracoronary ultrasound of the vessel. Next, rotational atherectomy of the circumflex, followed by stent and ultrasound. Total charges for this 2-3 hour procedure? Somewhere around $8000 to the cardiologist. Of course, hospital charges are far more.

Ironically, patients are invariably impressed. Hearing that they went through all sort of high-tech procedures makes them grateful for receiving the benefits of the skills of their cardiologist. Of course, they would like have done as well with a far simpler procedure. Perhaps they didn't need the procedure at all.

If the excessive use of procedures and devices fails to benefit patients, why don't hospitals discourage it? Two reasons: 1) It's difficult to legislate or regulate decisions made on judgement, which can be a tough issue with many fuzzy edges, and 2) hospitals made oodles more money from the practice.

If you have a salesman in your new car lot and he outsells all his colleagues by 30-50% and makes you a couple hundred thousand a month more in sales. You've watched him at work and he's clearly good at it. But you suspect that he pushes the envelope of propriety frequently--badgering customers, add rustproofing to a little grandmother's car that will be driven 3000 miles a year, selling cars for prices far above what they would have sold for had the customer bargained more vigorously.
do you put a stop to it at the risk of pushing your star salesman away? Few would.

Only a minority of my colleagues are guilty of this despicable practice. I only know of a few who openly do it. Hopefully, you're not among their patients.

The party’s over

A good number of cardiology colleagues are vigorously bashing the outcome of the COURAGE Trial. Recall that COURAGE is the large clinical trial recently released that showed that, in people with stable angina (chest pains), people did equally well with “optimal medical therapy” as with stents.

The problem is that many of my colleagues wouldn’t know what to do in a world deprived of implanting 10 stents a day. Giving people nitroglycerin/statin drug/aspirin/beta-blocker day after day, week after week, would be an awfully dull world. All the excitement of the cath lab would be a lot more rare. We’d actually have to wait for a heart attack from some dumb smoker! All the money would disappear, too. After all, seeing a patient in the office pays, at best, $200 (and has to be stretched to cover overhead expenses like staff, malpractice insurance, and rent). Putting a stent in can pay $2000, $3000, $4000, often more. Put in several a day and—Wow! Now we’re talking money.

You can understand how upsetting it is to my colleagues who feel like the rug may be pulled out from underneath their practices and lives. Feel as sorry for them as you do for people who lose their jobs on an assembly line because of robotic technology. Or travel agents because everyone makes travel arrangements over the internet. Technology, in this information technology, marches on.

Cardiologists, cath labs, stent manufacturers, and the huge industry built around heart disease had their party. Now it’s time to clean the room and sober up. The party’s over.

The broader acceptance of “optimal medical therapy,” as lame as it is, will eventually open the door for many to demand for something even better. Ever hear of Track Your Plaque?

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.