All posts by william-davis

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.

While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?

Fred Hahn's latest book, adapting slow burn techniques for kids.

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:

I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna

No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

I don't like to stray too far off course from discussions of heart disease and related issues in this blog. But the question of bone health comes up so often that I thought I'd discuss the strategies available to everybody to stop, even reverse, osteoporosis.

Coronary atherosclerotic plaque and bone health are intimately interwoven. People who have coronary plaque usually have osteoporosis; people who have osteoporosis usually have coronary plaque. (The association is strongest in females.) The worse the osteoporosis, the greater the quantity of coronary plaque, and vice versa. The two seemingly unconnected conditions share common causes and thereby respond to similar treatments.

Incredibly, rarely will your doctor tell you about these strategies. Your doctor orders a bone density test, the value shows osteopenia or osteoporosis, and a drug like Fosamax or Boniva is prescribed. As many people are learning, drugs like this can be associated with severe side-effects, such as jaw necrosis (death of the jaw bone), a dangerous and disfiguring condition that leads to loss of teeth and disfigurement, followed by reconstructive surgery of the jaw and face. These are not trivial effects.

Note that drugs are approved by the FDA based on assessment of efficacy and safety, NOT proven equivalence or superiority to natural treatments.

In order of importance (greatest to least), here are strategies that I believe are important to regain or maintain bone health. Indeed, I have seen many women increase bone density using these strategies . . . without drugs of any sort.

1) Vitamin D restoration--Vitamin D is the most important control factor over bone calcium metabolism, as well as parathyroid function. As readers of this blog already know, gelcap forms of vitamin D work best, aiming for a 25-hydroxy vitamin level of 60-70 ng/ml. This usually requires 6000 units per day, though there is great individual variation in need.

2) Vitamin K2--If you lived in Japan, you would be prescribed vitamin K2. While it's odd that K2 is a "drug" in Japan, it means that it enjoys the validation required for approval through their FDA-equivalent. Prescription K2 (as MK-4 or menatetranone) at doses of 15,000-45,000 mcg per day (15-45 mg), improves bone architecture, even when administered by itself. However, K2 works best when part of a broader program of bone health. I advise 1000 mcg per day, preferably a mixture of the short-acting MK-4 and long-acting MK-7. (Emerging data measuring bone resorption markers suggest that lower doses may work nearly as well as the high-dose prescription.)

3) Magnesium--I generally advise supplementation with the well-absorbed forms, magnesium glycinate (400 mg twice per day) or magnesium malate (1200 mg twice per day). Because they are well-absorbed, they are least likely to lead to diarrhea (as magnesium oxide commonly does).

4) Alkaline potassium salts--Potassium as the bicarbonate or the citrate, i.e., alkalinizing forms, are wonderfully effective for preservation or reversal of bone density. Because potassium in large doses is potentially fatal, over-the-counter supplements contain only 99 mg potassium per capsule. I have patients take two capsules twice per day, provided kidney function is normal and there is no history of high potassium.

5) An alkalinizing diet--Animal products are acidic, vegetables and fruits are alkaline. Put them together and you should obtain a slightly net alkaline body pH that preserves bone health. Throw grains like wheat, carbonated soft drinks, or other acids into the mix and you shift the pH balance towards net acid. This powerfully erodes bone. Therefore, avoid grains and never consume carbonated soft drinks. (Readers of this blog know that "healthy, whole grains" should be included in the list of Scams of the Century, along with Bernie Madoff and mortgage-backed securities.)

6) Strength training--Bone density follows muscle mass. Restoring youthful muscle mass with strength training can increase bone density over time. The time and energy needs are modest, e.g., 20 minutes twice per week.

Note that calcium may or may not be on the list. If on the list at all, it is dead last. When vitamin D has been restored, intestinal absorption of calcium is as much as quadrupled. The era of force-feeding high-doses of calcium are long-gone. In fact, calcium supplementation in the age of vitamin D can lead to abnormal high calcium blood levels and increased heart attack risk.

These are benign and easily incorporated strategies. They are also inexpensive. I challenge any drug to match or exceed the benefits of this combination of strategies. Keep in mind that strategies like vitamin D restoration provide an extensive panel of health benefits that range far beyond bone health, an effect definitely NOT shared by prescription drugs.

The thoracic aorta lives happily within the chest.

The aorta is the main artery of the body that emerges from the heart, located just under the sternum. It is the "tree trunk" from which all the major arteries branch off to the rest of the body: the arms, brain, abdominal organs, pelvis, and legs. The aorta receives the high-pressure blood ejected directly out of the heart muscle.

However, there are evil forces in the body that work to weaken the aorta. When the aorta is weakened, it enlarges. Enlarged aortas also tend to grow atherosclerotic plaque. Plaque in the aorta poses long-term risk for stroke and and mini-strokes ("transient ischemic attacks," or TIAs), due to fragmentation.

There are many enlarged aortas in this world. I see at least several every week. It is fairly common, particularly in people with high blood pressure and cholesterol abnormalities, as well as those who are overweight. Smokers get it really bad.

Conventional thinking is that, once an aorta enlarges, it will inevitably continue to enlarge at the average rate of 2.0 mm per year (resulting in 1.0 cm enlargement over 5 years). For this reason, conventional discussions on the topic of thoracic aortic aneurysms all say something like "Enlarged aortas should be monitored yearly. Surgical replacement should proceed when the aorta reaches a diameter of 5.5 cm."

This is because an aortic diameter of 5.5 cm is associated with much greater likelihood that the aorta will rupture (fatal within minutes) or the internal lining will tear, a "dissection." The surgery is a major undertaking that involves opening the chest and usually replacing the aortic valve and inserting a synthetic aorta. The procedure is high-risk, especially if any branch arteries are involved.

So putting a stop to any further aortic enlargement is a worthwhile goal. Unfortunately, conventional thought is that there is nothing you can do to stop the inevitable growth of the thoracic aorta.

Nonsense. There are a number of efforts you can make to halt further increase in aortic diameter. (My experience in this is anecdotal and unpublished, but now numbers several hundred patients.)

There are two categories of factors that cause the aorta to increase in diameter:

1) Internal pressure--Think of blood pressure as the internal inflating pressure on this "balloon." Keeping the "inflating pressure," i.e., blood pressure, low exerts substantial effect on slowing growth of aortic diameter. I aim for normal BP or lowish BP (less than 130/80, preferably 100/70).

2) Factors that weaken the aortic wall--Processes like inflammation, glycation, lipoprotein deposition, and nutritional deficiencies will serve to weaken the supportive tissue of the aorta. For that reason, correction of lipoprotein abnormalities (e.g., small LDL and lipoprotein(a)), reductions in carbohydrate intake and thereby blood glucose/glycation, and "normalization" of vitamin D, vitamin C supplementation (for collagen crosslinking), and omega-3 fatty acids all play a role.

To push even farther, there may be additional advantage to following strategies that impair the production and activity of a crucial enzyme that lives within the aortic wall: matrix metalloproteinase, or MMP. MMP degrades the collagen and other supportive tissues within the aorta, weakening it and permitting expansion. Blocking MMP may prove to be among the most powerful new strategies to halt aortic expansion.

Compounds that have potential MMP-inhibiting effects include:
--Vitamin D--A substantial effect
--Resveratrol--One of the polyphenols from red wine
--Doxycycline--This old antibiotic often used for acne treatment has, in preliminary studies, shown important MMP-blocking effects and slowed aortic expansion.

Anyway, there you have it. A bit complicated, but a "recipe" that has failed me only rarely.

Here's an interesting example of what you might call "extreme carbohydrate intolerance."

May is a 44-year woman who has now had her 7th stent placed in her coronary arteries. She lives on a diet dominated by breads, breakfast cereals, muffins, rice, corn products, along with some real foods.

Her conventional lipid panel and other lab values:

Total cholesterol 346 mg/dl
Triglycerides: 877 mg/dl
HDL cholesterol: 22 mg/dl
LDL cholesterol: incalculable
(Recall that LDL cholesterol is usually a calculated, not a measured value. The excessively high triglycerides make the standard calculation invalid--more invalid than usual.)

Fasting blood glucose: 210 mg/dl
HbA1c (a reflection of previous 60-90 days average glucose): 7.2% (desirable 4.5% or less)
ALT (a "liver enzyme"): 438 (about five-fold normal)

At 5 ft even and 138 lbs (BMI 27.0), May appears small. But the modest excess weight is all concentrated in her abdomen, i.e., in visceral fat.

By lipoprotein analysis via NMR (Liposcience), May's LDL particle number was 2912 nmol/L, or what I would call a "true" LDL of 291 mg/dl. (Drop the last digit.) Of the 2912 nmol/L LDL particles, 2678 nmol/L, or 92%, were small.

The bad news: This pattern of extremely high triglycerides, extremely high LDL particle number, low HDL, predominant small LDL, and diabetes poses high-risk for heart disease--no surprise. It earned her 7 stents so far. (Unfortunately, she has made no effort whatsoever to correct these patterns, despite repeated advice to do so.)

The good news: This collection is wonderfully responsive to diet. LDL particle number, small LDL, triglycerides, blood glucose, and HbA1c drop dramatically, while HDL increases. Heart disease will at least slow, if not stop.

It's amazing how far off human metabolism can go while indulging in carbohydrates, particularly a genetically carbohydrate-intolerance person. (Actually, I wouldn't be surprised if May's diet, as bad as it seems to you and me, still fits within the dictates of the USDA food pyramid.) The crucial step in diet to correct this smorgasbord of disaster is elimination of carbohydrates, especially that from wheat, cornstarch, and sugars.

Heart Scan Blog reader and dietitian, Lisa Grudzielanek, provided this recipe in response to the post, What's for breakfast?

Lisa, by the way, is one of the rare dietitians who understands that organizations like the American Dietetic Association have made themselves irrelevant. She therefore advocates diet principles that work, not just echoing the idiocy that emanates from such organizations, often driven by economics more than science. Lisa works in the Milwaukee area and has proven a useful resource person for my patients who have required extra coaching in the Track Your Plaque diet principles.

Egg Bake
My favorite breakfast is what I call an "egg bake." Others may refer to it as a "quiche."

Take a variety of fresh vegetables. This time of year is great for farmers' markets.

I typically use fresh chopped organic spinach, bell peppers, red & white onions, scallions, broccoli, mushrooms, cherry tomatoes halved and, if desired, meat (nitrite-free ham or leftover chicken breasts).

1) Chop veggies and place in casserole dish.
2) Add meat and handful of cheese of your choice.
3) Scramble 8 eggs & little bit of milk & pepper.
4) Add to casserole dish and mix/coat veggies with egg mixture.
5) Put in oven at 450 degress for 30 minutes.

Yummy, ready to eat breakfast that is so easy for the work week.

If you eliminate wheat from breakfast and otherwise adhere to a low-carbohydrate dietary approach, what is there to eat for breakfast?

If you take out English muffins, bagels, all breakfast cereals, pancakes, waffles, and toast, what's left to eat?

Actually, there's plenty left to eat. It just may not look like the traditional American notion of "breakfast." (The traditional idea of breakfast was is, in part, due to the legacy of Dr. John Harvey Kellogg, who, in the latter part of the 19th century, ran a sanitarium in Battle Creek Michigan. He and his brother, Will Keith Kellogg, discovered the idea of turning grains into flakes, the birth of the breakfast cereal. Subscribe to the idea of breakfast cereal for breakfast and you subscribe to the ideas of a man who would administer four enemas for you today to cure your cancer or rheumatism.)

Here are a few ideas. By no means is this meant to be a comprehensive list, just a starting point for a few new breakfast food ideas.

--Eggs--Of course, eat the yolk. Eat three yolks. Scrambled, "fried," (not really deep-fried, of course), hard-boiled, poached, as an omelette. Add pesto, olive oil, vegetables, mushrooms, salsa.

--Ground flaxseed--As a hot cereal with your choice of water, milk (not my favorite because of insulin effects; the fat is immaterial), full-fat soy milk (yeah, yeah, I know), unsweetened almond milk. Add walnuts, blueberries, etc. Ground flaxseed is the only grain I know of that contains no digestible carbohydrates.

--Lunch and dinner--Yes, if you cannot have breakfast foods for breakfast, then have lunch and dinner, meaning incorporating foods you ordinarily regard as lunch and dinner foods into your day's first meal. This means salads, leftover chicken from last night, soup, raw vegetables dipped in hummus or guacamole, stir fry, etc.

--Cheese--For something quick, grab a chunk of gouda or emmentaler along with a handful of raw almonds, walnuts, or pecans. Because of the excess acidity of cheese (along with meats, among the most acidifying of foods), I usually try to include something like a raw pepper or avocado, foods that are net alkaline.

--Avocados--Cut in half, scoop out contents. They're quick and delicious, when available.

I hesitate to mention it, but I sometimes will have tofu, cubed and flavored with whatever is available--soy sauce, miso, pickled vegetables. My mother was Japanese, so I'm comfortable with this, though many people are not.

Anyway, that's a partial list that nonetheless can get you started on a wheat-free, low-carb breakfast.

If you are just starting out, you will notice a number of fundamental changes. You may first experience the characteristic "withdrawal" effect: mental fog and fatigue that lasts about a week. Energy then picks up, often substantially. This is followed by gradually reduced appetite: You will be far less hungry. You will require less food, less often, since appetite will be driven by physiologic need, not the appetite-stimulating properties of wheat (and cornstarch, high-fructose cornsyrup and sucrose).

By the way, do not skip breakfast unless it's part of an occasional fasting effort. Skip breakfast, wind down metabolism, get fat. I am impressed at how consistent skipping breakfast backfires in those who think that it helps you control weight.

I also welcome any suggestions on what you eat as part of your wheat-free, low-carb breakfast. (Thanks for the great suggestions on the last blog post, Anna.)

This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.

Vitamin D Newsletter

August, 2007

Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.

Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.

Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada

Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.

Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.

Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.

Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.

Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.

Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.

Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your y^x function and "(score 2 / score 1)" as the "y".

Annual rate of plaque growth (APG) = ( score 2 / score 1 ) ^1/t - 1

Multiply the result by 100 to yield a percent.

“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) ^1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth

Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.

Human foie gras

Let go of my love handles

Surviving a widow maker

Fred Hahn's Slow Burn

Can I stop my Coumadin?

Homegrown osteoporosis prevention and reversal

Your enlarged aorta

Extreme carbohydrate intolerance

What's for breakfast? Egg bake

What's for breakfast?

Vitamin D and autism

Michael Pollan Podcast

Are you addicted to fructose?

Chicken Little

200 point drop in heart scan score

How tough is the Track Your Plaque 60-60-60 target?

Vitamin D2 belongs in the garbage

Angioplasty vs. Track Your Plaque

Plaque is like money

Triglycerides: What is normal?