Homocysteine and coronary plaque

If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.

More Vitamin D and HDL

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

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

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

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

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

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

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

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

Thin ice

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

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

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

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

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

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

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

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

Vitamin D and cancer

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

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

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

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

http://tinyurl.com/f93vl

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

Lipoprotein(a), menopause, and andropause

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

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

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

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

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

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

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

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

The Paleo approach to meal frequency

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:


We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.



In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.


The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Even mummies do it


Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Life Extension article on iodine

Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

The healthiest people are the most iodine deficient

Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

It's the score, stupid

Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Heart Scan Blog Redux: Cheers to flavonoids

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.

Fatal underdose

Since vitamin D has been the topic of a fair amount of media coverage, I've received many questions about this fascinating "nutrient." A day doesn't go by without several nurses, friends, even fellow physicians stopping me to ask about vitamin D.

When I inform them that the average dose for females in this region (upper Midwest) is 4000-5000 units per day, 5000-6000 units per day for males, they are all surprised. "Then why did they say just take your multivitamin every day, or just drink your milk on the news?"

Many people are even more surprised, sometimes completely turned off, when they hear that, to be truly confident of adequate vitamin D dosing, a blood level of 25(OH) vitamin D3 needs to be checked. Now we're talking real hassle!

But there is no other way to do it. In order to obtain the full potential benefits of vitamin D, such as reduction in blood sugar and sensitization to insulin, reduction in cancer risk (especially prostate, colon, and breast), reductions in blood pressure, increased bone density, not to mention markedly increasing the likelihood of stopping or reducing your heart scan score, then achieving a desirable blood level of 25(OH) vitamin D is necessary.

Checking a blood level of vitamin D is no more difficult than having a cholesterol test, unless, of course, your doctor balks at the idea. (Time for a new doctor if that occurs.)

All too often, someone will be convinced they are taking a sufficient dose of vitamin D of, say 2000 units per day, only to discover that their blood level of 25(OH) vitamin D is something like 17 ng/ml--severe deficiency, sufficient to leave them exposed to all the undesirable consequences of vitamin D deficiency. Even though 2000 units per day represents 500% of the Institute of Medicine's recommended Adequate Intake for adults, to those familiar with the Track Your Plaque program it likely sounds like a child's dose.

Many variables enter into the equation in your body that determines your need for vitamin D: body size (heavier or larger people need more, with obese people often requiring enormous doses); sex (men need more than women); age (aging results in dramatic loss of ability to activate vitamin D in the skin); race; skin color (darker skinned people require more). Trying to guess your need is a fool's game. It's also a game that can seriously compromise your health and your hopes of ever stopping or reducing your heart scan score.



The message is clear: You cannot guess what your vitamin D need is. You cannot properly judge your vitamin D requirement by your age, body size, sex, or any other characteristic. Having a tan or a lack of a tan is a lousy indicator, as well. A simple blood level of 25(OH) vitamin D is an absolute necessity to gauge your vitamin D status, both before starting and while on your supplement.

Members of Track Your Plaque: Watch for the 30-some page booklet, The Track Your Plaque Complete Handbook on Vitamin D and Heart Health, which will be released in the next day or two.


Copyright 2008 William Davis, MD

Is direct-to-consumer drug marketing a failure?

According to the poll just completed by 80 participants on The Heart Scan Blog, 50% of respondents said they were less likely to take a drug after viewing an advertisement for it. A whopping 3 (4%) said that they would be more likely to take the drug after viewing an advertisement.

I find that interesting. If half the people responding are less likely to become customers of a drug company, then how does the drug industry justify running around-the-clock, every-few-minute ads? Spending by the drug industry for direct-to-consumer (DTC) advertising has ballooned over the past few years, and is now well over $30 billion dollars per year.

Unfortunately, despite the views of the highly-educated, curious, think-for-yourself, health information-seeking sorts of people who read this blog, drug companies still come out on top by DTC advertising. Estimates vary, with a 2006 U.S. Government Accountability Office study reporting that, for every $1 DTC advertising, sales are increased by $2.20. A 2000 Harvard study showed a higher return of $4.40 for every advertising dollar spent.

I'm sure the drug companies themselves have a very tight accounting handle on their own set of figures. We may not be terribly fond of these people and their often suspect tactics, but they're not stupid. They are certainly not stupid when it comes to making money.

Interestingly, 80% of the funds spent on DTC advertising focus on the 20 or so most popular drugs, all of which are used for treatment of chronic conditions like high cholesterol and high blood pressure, markets that are large and long-term. It pays very little to advertise drugs that may serve small markets for a short period. The implicit message is that this is not at all about informing the public. It is about advertising to grow revenues and profits--pure and simple.

It makes me wonder what the results of our poll would have been had we conducted it in 2000 before many people hadn't yet been brought to the brink of vomiting from the endless onslaught of commercial after commercial, complete with smarmy spokespeople (a la Lipitor's Dr. Robert Jarvik). What will it show in two years? Will the broader public join the more informed people who read this blog and become increasingly inured to the hard sell tactics?

For further discussion of this topic, click here for a reprint of an August, 2007 New England Journal of Medicine study, A Decade of Direct-to-Consumer Advertising of Prescription Drugs provides background, along with commentary on the impact of DTC drug marketing since the FDA allowed it 10 years ago. (Because it is a study and not an editorial, the editors fall short of making any recommendations for improvement or calling for a moratorium.)


Copyright 2008 William Davis, MD

Cheerios and heart health



Anna responded to the Heart Scan Blog post, Can you say "sugar"? with the following wonderfully telling comment:

A measured bowl of Cheerios and a bit of milk (whole, because it's what I had), equal to 75 grams of carbohydrate, gave me the highest ever blood glucose reading from a food (not counting glucose solution from a Glucose Tolerance Test). I was attempting a "homemade" version of a 3 hr GTT before going to my doctor with my concerns about my BG.

My BG started to rise very fast within 15 minutes after eating the cereal, peaked at about 250 mg/dL at 45 minutes, then slowly dropped. By about 60-75 minutes, I experienced strong hunger and carb cravings as the BG began to slowly drop, and by about 2.5 hours after eating, my BG had suddenly dropped quite low (in the low 70s) and I had developed a nasty hypoglycemic feeling (shaky, irritable, craving sugary foods, headache, etc.).

It's hard for me to see "heart healthy" Cheerios (or any other highly processed breakfast cereal) as anything other than a bowl of pre-digested sugar that contributes to roller coaster blood glucose and insulin levels, which a great way to start anyone's day. Certainly, I don't do well with Cheerios because I clearly have a damaged glucose regulatory system (probably a diminished or absent first phase insulin response, but I can't imagine that it is doing any good for people with healthy glucose regulation, either.

I banned prepared cold cereals from our house. If my 9 yr old son gets cereal at all at home, it's whole groats (not even rolled or steel cut because those aren't truly "whole grain" anymore), soaked overnight in some water and a tsp of plain yogurt (soaking neutralizes phytates and reduces cooking time), then cooked about 8-10 minutes (water added as necessary). Sometimes I add a bit of quinoa or almond meal prior to soaking to boost the protein content a bit. I garnish with a pat of butter, some heavy cream, and a dusting of cinnamon. If I'm feeling *really* indulgent, I drizzle about 1 tsp of Grade B maple syrup on top (Grade B is stronger in flavor and so less can be used). I don't eat this cereal myself, and truthfully, I'd rather my son not, either, but he sometimes wants cereal. It's the least damaging compromise I can come up with that we can both live with.



I have also seen diabetic effects from Cheerios: rises in blood sugar, exagerration of small LDL, drops in HDL, rises in triglycerides. Yes, it may reduce LDL a small quantity, but so what?

The Cheerios "heart healthy" claim is based on a piece of research apparently performed by Dr. Donald Hunninghake at the University of Minnesota and reported in 1998:

A study conducted at the University of Minnesota Heart Disease Prevention Clinic and published as "Cholesterol-Lowering Benefits of a Whole Grain Oat Ready-to-Eat Cereal" in the May issue of the Nutrition in Clinical Care journal in 1998, showed that people can lower their blood cholesterol by an average of 3.8% over six weeks by enjoying 3 cups of cold cereal made with 100% whole grain oats everyday as part of the meals and snacks in a healthy lower-fat diet.

(Unfortunately, I could not locate the actual publication. It doesn't mean it doesn't exist; I just couldn't locate it. Perhaps it's in a small journal not entered into the online publication database.)

The purported effects of Cheerios should not be confused with that of actual, intact oat bran, as suggested by studies such as those of Brenda Davy et al, High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men, in which significant reductions in LDL particle number and small LDL (NMR) were obtained. (This study was also supported by Quaker Oats.) Several studies have shown that oat bran does indeed reduce LDL cholesterol, sometimes as much as 30-50 mg/dl. Cheerios can not even come close to this.

If Cheerios were nothing more than finely pulverized oats, then perhaps it wouldn't be so bad. But add corn starch and sugar, and you have ingredients that have potential to distort LDL particle size and yield blood sugar-escalating effects like those described by Anna.

The gravity of perpetuating these myths is brought home by a testimonial posted on the website for Cheerios:

“I had unexpected open heart surgery a year ago. As I adopted heart health habits during my recovery, I realized that I should have been eating the Cheerios cereal I carried around in a plastic baggie so many years for my kids!”

Beverly
Scotch Plains, NJ



It makes me shudder.


Copyright 2008 William Davis, MD

The IF Life: Intermittent fasting

There's a wonderful blog called The IF Life: Intermittent Fasting and Instant Freedom. It is written by personal trainer (and apparently former corporate bigshot), Mike O'Donnell.

Mike has a great take on brief, intermittent fasting that I found helpful and I believe you will also.






Intermitent Fasting 101: How to Start, Part I

The biggest question people have is how to effectively use IF (intermittent fasting) to achieve their goals and maximum results. These results and goals can vary by each person with fat loss, muscle gain, better health, improved performance in your sport of choice and more. With that comes the individuality of what is a person’s insulin resistance, current body composition (bodyfat%), daily lifestyle, eating habits, macronutrient ratios (carbs/protein/fat), type of exercise program, frequency and volume of training, recovery demands, and so forth. You are unlikely to find 2 people with the same set of parameters and same exact responses to an IF protocol. What does this mean? Well just that we need to start with a basic IF program, and then learn how to monitor results and adjust as we go. Even down the road things will change as you will improve health, lower insulin resistance and maybe change performance and recovery needs. So nothing is ever just one set way. Life is dynamic (always changing and evolving) and so should be the way we see our own journey for health and fitness.

What is IF?

For those that may not be familiar to the term, intermittent fasting is just taking times of fast (no food) and working them into your lifestyle. This can be either daily or a couple times a week (will get into that more below). Benefits include improving insulin resistance (which you will hear alot about as being the #1 key marker in so many health factors including weight loss, muscle gain, performance, recovery, anti-ageing and disease prevention) and giving the body a chance to do some internal cleaning (or housework), which can lead to improved immune function and overall health. If you want to see studies of all the benefits of IF/CR, please the resources page.


How do I begin to IF?

Is there only one set way in which to do IF? No. I could easily come up with 10 different IF protocols based on 10 people’s individual’s needs, lifestyle, exercise, goal, macronutrient ratios, and so forth. We will keep it simple and give the 2 most frequent and basic options.

Daily Fasting: Typically done every day and only giving the person a smaller eating window in which to get their calories. (for example, a 18hr daily fast would mean someone would only eat every day between the hours of Noon and 6pm). You will see varying times from 15-19 hours for daily fasting.
Fasting 1-3x a week: This could also be called alternate day fasting/calorie restriction (for those doing it every other day). This is just fasting of usually longer periods 18-24 hours but only 1-3x a week. Many variations to play with here.
“But which one is better and how to I do it now if I want…….”. Whoa, slow down. I know many have questions but let’s still try to keep this simple for now and expand into more specifics later. So far many people have experimented with both types of IF and have seen great results. But you also have to take into account all the other variables such as what is the person eating in that window? Is is junk food? Is it low carb? How many times a week are they doing it? Are they overweight and wanting just fat loss? Are they lower bodyfat but looking for improved performance and health? How many times a week are they exercising? What kind are they doing and what intensity? The list can go on and on, but let’s start to analyze the 2 types of IF and let you decide which one best suits your lifestyle.

Daily Fasting (15-19 hours):

The Advantages are:

--simple eating strategies for every day
--even people that may not eat 100% clean foods can see weight loss due to the smaller window and lower calorie total per day


The Disadvantages are:

--Can possibly lower metabolism if calories are too low for too long (not what you want if your #1 goal is weight loss)
--Not getting enough food in the smaller window may also lead to muscle loss for more active people (not good)
Fasting 1-3x a week:


The advantages are:

--Allows a person to make sure they are getting enough calories on the non-fasting days, and then just keeps to a simple small feed window (if any) on the IF days.
--Simple thinking for people who do not have experience in how to eat clean to eat one day, and then eat in a smaller window the following day (alternate day fasting/CR). This can achieve fat loss for people who are mostly overweight and may not be too active. (of course don’t get me wrong, that eating healthy is our main goal but this can be a good step for some people to start their weight loss jounrey and learn how to make better choices as they go)


Disadvantages:

--Doesn’t force a person to make better choices with their food (as one could probably eat junk one day, and then fast the next and still lose weight). Not something we want long term because this is not going to improve your other health markers (diseases prevention, insulin resistance) like a good IF program on healthy foods.


Again I can’t say it enough, as there are so many variables to play with in an IF program. Some people may say “well it didn’t work for me” or “I didn’t gain any muscle”. Well unless I know everything about what you do for exercise daily, your total calories, when you eat and your macronutrient ratios (protein/carbs/fats), I can’t even begin to help. IF is a simple tool to start with, but you have to take full responsibility for your own health and progress and learn when it is not working and when to change things up! Like I said, if it is NOT working then stop IF and rethink your attack plan (or get a professional to coach you on it).

So to sum up, here are some examples of what you can play with:

Daily Fasting of 15-19 hours. I would highly suggest that if you do this make sure you are recovering from your exercise and start only Mon-Fri and give yourself the weekends to eat all day (hopefully with healthy choices of course)


Fast 1-2x a week to start if you have never done any fasting or do not know how to eat healthy and control your macronutrients. Start with 1-2 days a week with fasts of 18-20 hours (I wouldn’t start with 24 hr fasts to begin as most people can not handle the hunger cravings and in turn will just end up eating all the wrong foods when they do eat) and say eat only from say 1pm-6pm for example. Drink lots of water (add lemon, your liver will appreciate it! and it will help with the hunger). For example, fast Wed and Sun (or whatever days fit into your schedule)

Or you can do a mixed approach and fast every other day for a small eating window. For example eat all day Mon, only 12-6pm on Tues, all day Wed, 12-6pm on Thurs, etc. Start with bigger eating windows and make them smaller as you get used to fasting. This approach may work for people who have alot of weight to lose and can not (I should really say “will not” as everything is a choice!) eat 100% healthy for the moment. This approach may not work for more advanced people who have a high activity level unless you are getting a ton of health calories in that fasting window.
“So What Do I Eat on the Fasting Days?”

That’s the best part, you should be able to eat unlimited healthy foods (healthy proteins, fats, veggies, fruit, nuts…see Paleo Diet in the resources page). If you are eating more processed foods, breads and other high calorie intakes then you may have to monitor and control portions. Please know this is NOT about chronic calorie restriction or starving yourself. When I do weeks of eating 1-7pm, I am eating a ton of protein and veggies (complex carbs pwo also). I am hardly starving myself. I am not taking in 4000 cal a day however, so my daily average of say 2200-2500 cal is still low compared to the alternative. If you want to lose weight of course you will need a calorie deficit to pull the “stored energy” out of fat cells. That is the advantage to eating “Paleo”, you can’t over eat on protein, healthy fats, fruits (in moderation) and veggies. If you are making bad choices or starving yourself on IF, you may lose the effectiveness or slow progress. All goes back to the fact that if it is not working, then change something up! (there is always something that can be changed…and food choices is the #1 place to start!) I don’t count calories, and by eating natural foods that have been around for 100s of years….I don’t need to! (eating healthy natural foods will not only help you lose weight but also improve your health and lower your risks of diseases….so eating for health should always be the #1 goal in any program)

Hopefully this will give a good overview while trying to keep it simple. Remember it’s your journey to take, measure progress and adjust things that are not working. Start with one approach, and modify it. Who knows, your approach may change every couple months and that is ok. Life is always changing and so should your approach to health and fitness (as the body always responds better to change than sticking with the same eating/exercise approach for a long period of time).

Can you say "sugar"?

All of these products bear the American Heart Association Check Mark of approval emblem, signifying that they are "heart healthy":


Kellogg's Frosted Mini-Wheats cereal

Ingredients:WHOLE GRAIN WHEAT, SUGAR, STRAWBERRY FLAVORED CRUNCHLETS (SUGAR, CORN CEREAL, CORN SYRUP, MODIFIED CORN STARCH, PARTIALLY HYDROGENATED COTTONSEED AND/OR SOYBEAN OIL, CITRIC ACID, GLYCERIN, NATURAL AND ARTIFICIAL FLAVOR, RED #40, BLUE #2), NATURAL AND ARTIFICIAL STRAWBERRY AND CREME FLAVOR, SORBITOL, GELATIN, REDUCED IRON, NIACINAMIDE, ZINC OXIDE, RED #40, PYRIDOXINE HYDROCHLORIDE (VITAMIN B6), RIBOFLAVIN (VITAMIN B2), THIAMIN HYDROCHLORIDE (VITAMIN B1), FOLIC ACID, BLUE #1, AND VITAMIN B12. TO MAINTAIN QUALITY, BHT HAS BEEN ADDED TO THE PACKAGING.










Orville Redenbacher popcorns









Dora the Explorer Cereal
























Cheerios
























The following requirements must be met to gain approval of the Check Mark program:

1) total fat 3.0 grams or less per serving

2) saturated fat 1.0 gram or less per serving

3) 20 grams or less cholesterol per serving

4) 480 mg or less sodium per serving

5) "Jelly Bean Rule": 10% of the Daily Value of 6 nutrients (e.g., fiber, vitamins A and C, etc.) must also be contained in each serving.


Had the Check Mark program focused on genuine nutrition and rated products by:

1) Healthy oil content

2) Sugar content or sugar-equivalents, i.e., glycemic index or load

3) Impact on HDL, small LDL, triglycerides

none of these products would have made the list, not even close.

Warfarin is scary stuff

Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.




Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.




Copyright 2008 William Davis, MD

Lipoprotein(a) Research Foundation

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

More on ASTEROID

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:


Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.



Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

LDL cholesterol, statins, and plaque regression

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

When is a calorie not a calorie?

One ounce of raw almonds (about 23 nuts) contains:


6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.


(From the USDA Nutrient Database)


Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.


The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).



Copyright 2008 William Davis, MD