All posts by william-davis

China fiction?

10. July 2010 William Davis (39)

Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger.

Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition.

Her comments on the relationship of wheat to heart disease:

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?

Carbohydrate-LDL double whammy

9. July 2010 William Davis (14)

Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:

--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall.
--Small LDL particles are more adherent to glycosaminoglycans in the artery wall.
--Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls.
--Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL.
--Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall.

Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.)

Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.)

Here's a great demonstration of this phenomenon by Younis et al:

"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference.

Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation.

So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.

To lose weight, prick your finger

8. July 2010 William Davis (45)

We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket.

Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated.

Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow.

To do this, you will need:

1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.)
2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece.
3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars.

No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.

Iodine update

2. July 2010 William Davis (30)

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.

Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.

Why haven't you heard about lipoprotein(a)?

1. July 2010 William Davis (26)

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

How to have a heart attack in 10 easy steps

29. June 2010 William Davis (48)

If you would like to plan a heart attack in your future, here are some easy-to-follow steps to get you there in just a few short months or years:

1) Follow a low-fat diet.

2) Replace fat calories with "healthy whole grains" like whole wheat bread.

3) Eat "heart healthy" foods like heart healthy yogurt and breakfast cereals from the grocery store.

4) Use cholesterol-reducing plant sterols.

5) Take a multivitamin to obtain all the "necessary" nutrients.

6) Take the advice of your doctor who declares your heart "in great shape" based on your cholesterol values.

7) Take the advice of your cardiologist who declares your heart "like that of a 30-year old" based on a stress test.

8) Take a statin drug to reduce LDL and c-reactive protein while maintaining your low-fat diet.

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.

There you have it: An easy, 10-step process to do your part to help your local hospital add on its next $40 million heart care center.

If you would instead like to prevent a heart attack in your future, then you should consider not doing any of the above.

Kick inflammation in the butt

25. June 2010 William Davis (0)

C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?

Life without Lipitor

25. June 2010 William Davis (17)

One of the most common reasons people come to my office is to correct high cholesterol values without Lipitor. (Substitute "Lipitor" with Crestor, simvastatin, Vytorin, or any of the other cholesterol drugs; it's much the same.)

In the world of conventional healthcare, in which you are instructed to follow a diet that increases risk for heart disease and not advised to correct nutrient deficiencies like vitamin D and omega-3 fatty acids, then a drug like Lipitor may indeed provide benefit.

But when you are provided genuinely effective information on diet, along with correction of nutrient deficiencies, then the "need" and apparent benefits of Lipitor largely dissolve. While there are occasional genetic anomalies that can improve with use of Lipitor and other statins, many, perhaps most, people taking these drugs really would not have to if they were just provided the right information.

Anyone following the discussions on these pages knows that wheat elimination is probably one of the most powerful overall health strategies available. Wheat elimination reduces real measured LDL quite dramatically. Provided you limit other carbohydrates, such as those from fruits, as well, LDL can drop like a stone. That's not what your doctor tells you. This approach works because elimination of wheat and limiting other carbohydrates reduces small LDL. Small LDL particles are triggered by carbohydrates, especially wheat; reducing carbohydrates reduces small LDL. Conventional LDL of the sort obtained in your doctor's office will not show this, since it is a calculated value that appears to increase with reduced carbohydrates, a misleading result.

Throw vitamin D normalization and iodine + thyroid normalization into the mix (both are exceptionally common), and you have two additional potent means to reduce (measured) LDL. Not restricting fat but increasing healthy fat intake, such as the fats in lots of raw nuts, olive oil, and flaxseed oil reduce LDL.

While I still prescribe statins now and then, a growing number of people are succeeding without them.

(Note that by "measured" LDL I am referring to the "gold standard," LDL particle number by NMR provided by Liposcience. A second best is measured Apoprotein B available through most conventional labs.)

In search of wheat: Emmer

23. June 2010 William Davis (13)

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

In search of wheat: Another einkorn experience

23. June 2010 William Davis (6)

Lisa is a trained dietitian. Unlike many of her colleagues, she has "seen the light" and realized that the conventional advice that most dietitians are forced to dispense through hospitals, clinics, and other facilities is just plain wrong.

I know Lisa personally and we've had some great conversations on diet and nutritional supplements. I told Lisa about my einkorn experience and how I witnessed a dramatic difference between bread made from einkorn wheat and that made from conventional whole wheat. So she decided to give it a try herself.

Here's Lisa's experience:

This past Friday, June 18th, I conducted my "Einkorn Wheat Experiment".

7 am
FBG [fasting blood glucose] 97 mg/dl

8 am-9 am
1 hour high-intensity aerobic workout

10:05 am
BG 99

10:05 am
I embarked upon the journey of choking down, I mean enjoying, the hefty piece of Einkorn bread. Wow, was that bread dense! It was a lot of work chewing.

10:50 am
(45 minutes after consumption, wanted to see what BG did a bit before the 1 hr mark) BG 153

11:05 am
1hr PP 120

11:35 am
90 mins PP [postprandial] 113

12:05 pm
2 hours PP 114 ... at this time I ate an egg & veggie omelet for lunch.

12:50 pm
BG 100

Before dinner 5:10 pm
BG 88

I was surprised with the BG of 153. However, it was good to see my insulin response is reactive and decreased BG 33 points in 15 minutes to end up with a BG of 120 1 hr after the bread.

So, it appears my response is similar. A slight elevation of BG at the 1 hour mark, but not to the degree of conventional whole grain wheat bread.

Of note, also, was the fact that I cannot remember the last time I ate a piece of wheat bread of this magnitude that did not make me bloated... not at all: No cramps, no brain fog, no headache and, did I mention not bloated?

I believe you are on to something with tolerance of Einkorn wheat for those of us with wheat sensitivities, in addition to its apparent lower glycemic response.

Along with Lisa, I asked four other people with various acute intolerances (all gastrointestinal) to conventional wheat, i.e., people who experience undesirable effects from wheat within minutes to several hours, to eat the einkorn bread. None experienced their usual reactions.

Obviously, this does not constitute a clinical trial. Nonetheless, I find this a compelling observation: People like myself who generally experience distinct undesirable reactions to wheat did not experience these reactions with einkorn.

Note, however, that einkorn behaves like a carbohydrate. No different, say, from brown rice or quinoa. However, unlike modern whole wheat flour from Triticum aestivum, in this little experience there were no immune reactions, no neurologic phenomena, no gastrointestinal distress--just the blood sugar consequences.

While this may not be true for all people consuming einkorn, it suggests that primordial einkorn wheat is quite different from modern conventional wheat for most people.

All posts by william-davis

Wheat "debate" on CBC

11. October 2011 William Davis (29)

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

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

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

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

Carrot Cake

5. October 2011 William Davis (14)

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

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

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

Makes 8-10 servings

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

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

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

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

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

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

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

Why wheat makes you fat

1. October 2011 William Davis (32)

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

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

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

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

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

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

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

Just who is "Real Facts 2000"?

29. September 2011 William Davis (38)

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

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

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

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

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

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

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

Anybody from the media listening?

Almonds are the new wheat

29. September 2011 William Davis (31)

Once you eliminate this genetically-altered Frankengrain called modern wheat, the diet should center around vegetables, nuts, healthy oils like olive and coconut, fish, meats, cheese, olives, avocados and other real whole foods. This is, in fact, the diet that I have advocated in my heart disease prevention practice, as well as my online program for prevention and reversal of heart disease.

But what if you'd like a piece of cheesecake or a nice slice of dessert bread---but you don't want to gain two pounds, spend 48 hours in the bathroom suffering with diarrhea and cramps, 3 weeks of joint pains and leg swelling, wade through mental "fog," anxiety, and rage just because you had that momentary indulgence---as you would with wheat?

That's why I've been focusing on recipes that allow you to have something familiar, e.g., chocolate coconut bread or biscotti, but using ingredients that will not generate the metabolic contortions triggered by wheat.

On perusing these recipes, you will notice that there are recurring ingredient themes. Many of the same ingredients pop up time and again. Among the most frequent, versatile, user-friendly, and tasty: Almonds.

You can use almonds as ground whole almonds, ground blanched almonds for a finer texture, ground roasted almonds, almond butter (though, for maximum health benefits, I prefer the ground whole almonds). Ground almonds allow you to recreate muffins, breads, scones, pizza crust, pie crust, biscotti, and cookies with health benefits that exceed that of whole wheat---but with none of the downside: no weight gain, no high blood sugar, no triggering of small LDL particles (#1 cause of heart disease in the U.S.), no accumulation of visceral fat, no appetite stimulation.

In short, you just have your chocolate almond biscotti or mocha cupcake and enjoy it, no health price to pay. So I call almonds the new wheat, except better.

Being regular is dangerous to your health

25. September 2011 William Davis (21)

No, I'm not referring to your daily morning ritual in the bathroom. I'm talking about heart rate.

Counterintuitively, a perfectly regular heart rate is a marker of poor health. People with perfect regularity of heart rate have more heart attacks, for instance.

Regularity of heart rate occurs more commonly in people with hypertension and other metabolic derangements, and it signals increased risk for both heart attack and death. A perfectly regular heart rate, i.e., no variation in the time interval from beat to beat, suggests that the parasympathetic nervous system, the component of automatic ("autonomic") nervous system control that is associated with the relaxation response, feelings of well-being, quiet, and relaxation, is weak. It also means that the opposing sympathetic nervous sytem that regulates the "fight or flight," adrenaline-like response is allowed to be dominant. Dominance of the sympathetic over the parasympathetic system generates regularity of heart rate. Heart rate also tends to be faster, e.g., 85 beats per minutes rather than 55 or 60 beats per minute. So perfect regularity, as well as increased rate, is undesirable.

What we want is irregularity of heart rate. But not irregularity that occurs chaotically with no rhyme or reason. More precisely, we want variability in heart rate. And we want variability to occur in synchrony with breathing, i.e., the respiratory cycle.

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

Heart rate in healthy people typically varies 15-20 beats per minute within the respiratory cycle, e.g., 60 bpm at end-exhalation, 80 bpm at end-inspiration.

Restoration of increased heart rate variability is associated with reduced blood pressure, reduced blood sugars (HbA1c), reduced inflammatory markers and cortisol (associated with stress), even an increase in DHEA levels. Feelings of well-being and calm also develop.

Among the strategies to consider to restore heightened heart rate variability and slowed heart rate include:

--Omega-3 fatty acid supplementation
--Exercise
--Weight loss
--Deep breathing exercises
--Meditation, prayer, and biofeedback

For our Track Your Plaque purposes, we are folding in the HeartMath strategies, i.e., use of a heart rate monitor that calculates heart rate variability in the context of respiratory cycle. If you've not already done so, take a look at the two Special Reports devoted to this topic on the Track Your Plaque website.

You mean weight loss is hazardous to your health?

23. September 2011 William Davis (11)

In my last Heart Scan Blog post, What is this wacky thing called weight loss?, I discussed how weight loss is associated with distortions in cholesterol and blood sugar values that can be very confusing, often leading your doctor to wrongly and unnecessarily prescribe drugs--since he/she likely rarely sees weight loss.

Blog reader, Donald K., posted his enlightening story:

I experienced this very thing.

After losing serious weight from the eliminating wheat, processed, and sugary foods (1 year in total) I lost 130 pounds. When I was nearly finished I went to see my doctor. He wanted to put me on statins. I explained to him how the data does not support application to me (no evidence of heart disease) and I got the mantra about standards of practice, etc, etc. I held my ground and decided I am much happier eating dairy, eggs, grass fed beef, wild caught fish, and as much raw foods (nuts, veggies, fruits) as my body desires to treat my health parameters.

Maintaining weight, it is easy. My BMI (23 down from 40) has remained constant for a few months now. You are right: metabolic processes definitely change. I no longer have sensations of glucose fluctuations or an uncontrolled appetite. I can only imagine the improved hormone regulation and metabolic communication going on inside my body.

The symptoms from obesity, all gone. Goodbye sleep apnea, hypertension, hemorrhoids, arrhythmias, gastroinestinal disruptions, smelly body, chaffing thighs, and others not mentioned. The positive effects are just as dramatic, but I don’t want to ramble on.

Weight loss? What is it? Getting your life back!

Brace yourself: If you are following the nutrition advice posted here and in the Track Your Plaque program, or the discussion I've initiated in Wheat Belly, then you may find yourself in the very same health predicament as Donald. Arm yourself to protect yourself against the drug-wielding ways of doctors. No, weight loss to achieve ideal weight is definitely not bad for health. But your doctor's misinterpretation of its effects can be!

What is this wacky thing called "weight loss"?

20. September 2011 William Davis (41)

I've discussed this before, but it has proven such an (encouragingly!) frequent issue that I thought it was worth discussing once again.

What happens when you lose weight?

The process of weight loss is characterized by multiple shifts in metabolic patterns that can be confusing. To the uninitiated eye, weight loss can look like a disastrous distortion in metabolism. The naive doctor on seeing your lab values, for instance, might insist you take a statin drug, a fibrate like Tricor (to reduce triglycerides or increase HDL), or simply berate you for your bad health habits--when it's actually a good thing you've accomplished.

So when you lose weight, say, 30 pounds in 3 months, what have you accomplished?

Energy stored as fat, especially from visceral fat stores, is mobilized into the bloodstream. It floods the bloodstream as fatty acids and triglycerides. These fatty acids and triglycerides don't occur in isolation, but interact with other particles and metabolic patterns. The resulting blood patterns include:

--Increased triglycerides--An increase in triglycerides, for instance, from 90 mg/dl to 200 mg/dl in the midst of weight loss is common.

--Reduced HDL--The flood of triglycerides leads to increased degradation of HDL, thus a drop. A drop in HDL from, say, 40 mg/dl to 27 mg/dl--very frightening to people--is exceptionally common.

--Increased blood sugar--The flood of fatty acids and triglycerides results in insulin resistance, leading to higher blood sugars. It is not uncommon for someone with pre-diabetes to develop diabetic-range blood sugars, or a non-diabetic to show pre-diabetic blood sugars.

--Increased small LDL particles--Though small LDL is highly variable during weight loss. When it does happen, it's probably from the interaction of VLDL (triglycerides) with LDL particles and the reaction that overloads LDL particles with triglycerides and conversion to small LDL particles.

So why don't doctors often recognize these patterns when a patient loses weight? Because they rarely see it. Most of my colleagues are accustomed to having patients come back with weight gain, getting heavier and heavier each time. Lose weight? Impossible! So they just don't recognize weight loss effects when they see it. As followers of The Heart Scan Blog know, a frequent conversation around here is "Am I too skinny?" or "How do I stop losing weight?"

The solution: Be patient. Be patient and wait about two months after a weight plateau has been achieved. That's when the numbers "settle down" and you see marked drops in triglycerides, increases in HDL, drops in blood sugar, reductions in small LDL.

As with many things, it's all about timing.

Why small LDL particles are the #1 cause of heart disease in the US

15. September 2011 William Davis (77)

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Even moore from Jimmy Moore

14. September 2011 William Davis (8)

The ubiquitous and irrepressible Jimmy Moore posted even more commentary about the Wheat Belly phenomenon here, what he calls "The Wheat Belly Bonanza."

Is low-carb really, at its core, little more than elimination of wheat? Sure, corn, rice, and sugar exert deleterious effects. But the dominant effect--by far--is the elimination of wheat. So is the low-carb movement really, at its core, a wheat-elimination movement?

Food (non-wheat-containing, of course) for thought.

All posts by william-davis

Diet by LDL

7. March 2012 William Davis (0)

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

5. March 2012 William Davis (5)

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

4. March 2012 William Davis (10)

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

8. February 2012 William Davis (7)

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health

60-year old man dies of high cholesterol

1. February 2012 William Davis (12)

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

30. January 2012 William Davis (42)

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

15. January 2012 William Davis (45)

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

7. January 2012 William Davis (27)

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.

(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

4. January 2012 William Davis (88)

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

1. January 2012 William Davis (11)

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . . . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.

Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)

Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

All posts by william-davis

More Vitamin D and HDL

2. April 2007 William Davis (8)

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

2. April 2007 William Davis (0)

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

30. March 2007 William Davis (0)

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

30. March 2007 William Davis (0)

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.

"I have never seen regression"

29. March 2007 William Davis (0)

At a presentation at the American College of Cardiology meetings in New Orleans yesterday (March 27, 2007), Dr. Arthur Agatston declared "I have been doing CT for many years, and I have never seen regression."

Whooooaaaa. Wait a minute here. I have great respect for the work Dr. Agatston has done over the years. He is, after the originator of the scoring algorithm that allows us to score CT heart scans (though a more accurate measure, the volumetric score, is the one we often use behind closed doors because of modestly increased accuracy and reproducibility). His diet program, the South Beach Diet, has achieved enormous success and is indeed an effective approach for both weight loss and correction of many weight-related causes of heart disease.

But he has never seen regression? Why would this be when we see it all the time? When we see heart scan scores drop 30%, it's hard to believe that with some savvy he has never seen regression (drop in score).

I can only attribute the difference to the more intensive endpoints we advocate (e.g., 60-60-60 for lipid values); the incorporation of adjuncts like fish oil, vitamin D, l-arginine; attention to non-cholesterol issues and intensified treatments for each. I doubt that the populations we see differ substantially.

As much as I admire Dr. Agatston's accomplishments, I believe that he is behind the times on this issue. No regression is so starkly different from the Track Your Plaque experience. I believe that relying only on statin drugs and diet will slow but will not stop plaque growth. It will also rarely, if ever, drop your score.

Attention to detail and a little insight into better preventive strategies really pays off. While not everyone in the Track Your Plaque experience will drop their score, a substantial number do. Many more slow plaque growth dramatically. And, as time goes on, our track record gets stronger and stronger.

COURAGE to do better

28. March 2007 William Davis (0)

The results of the long-awaited COURAGE Trial were announced today at the American College of Cardiology meetings in New Orleans.

In this trial, 2200 participants with stable coronary disease (i.e., not unstable, in which heart attack or death is imminent) were randomly assigned ("randomized") to either angioplassty/stent or "maximal medical therapy." Medical therapy means such things as aspirin, beta blocker drugs, and statin cholesterol drugs. There was virtually no difference between the groups in rate of heart attack and death from heart disease over a period of up to 7 years.

These results have caused a stir in the media and my colleagues, trying to sort out of the implications. However, I think there's one observation in particular worth making for those of us who tend to scoff at the conventional approach to coronary disease. That is, 1 of 5 people had a heart attack or died from heart disease in both groups. That's a lot. Even more ended up with a procedure (angioplasty, stent, or bypass). In other words, the "maximal medical therapy" instituted in participants was hardly a success. Though angioplasty and stenting failed to prove superiority, both really stunk. Both permitted a lot of catastrophes to occur.

"Maximal medical therapy," in other words, is a laughable concept. It doesn't include raising HDL, suppressing small LDL, reducing Lipoprotein(a), addressing inflammatory issues. It does not include omega-3 fatty acids from fish oil, nor does it address the severe degrees of vitamin D deficiency that are proving, in the Track Your Plaque experience, to be among the most potent causes of atherosclerotic plaque known. It includes a sad attempt at diet, as advocated by the American Heart Association, a diet that, in my view, causes heart disease and is distorted by the powerful political and financial influence of food manufacturers.

If the trial were to be done again, I'd like to see the "maximal medical therapy" arm be represented by a more effective program like the Track Your Plaque approach.

Value of a zero heart scan score

27. March 2007 William Davis (1)

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

You're at the cutting edge

26. March 2007 William Davis (3)

If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health.

Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare."

Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies.

Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money.

Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust.

In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases.

If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans.

In our program, 18-30% reductions in heart scan scores are common.

A stent--just in case

26. March 2007 William Davis (3)

Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart.

"The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."

Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)

Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?

That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower.

In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.

Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.

How will you know your score dropped?

25. March 2007 William Davis (0)

This issue came up twice this week.

Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)

Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case.

So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan.

Bill was surprised. "Why another scan? I already had one!"

I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly.

Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth.

Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:

398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.)

250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.

525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following.

The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.

All posts by william-davis

Human foie gras

18. September 2010 William Davis (10)

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.

Let go of my love handles

14. September 2010 William Davis (44)

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.

Surviving a widow maker

11. September 2010 William Davis (19)

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.

Fred Hahn's Slow Burn

8. September 2010 William Davis (166)

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.

Can I stop my Coumadin?

5. September 2010 William Davis (20)

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.

Homegrown osteoporosis prevention and reversal

1. September 2010 William Davis (58)

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.

Your enlarged aorta

27. August 2010 William Davis (19)

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.

Extreme carbohydrate intolerance

25. August 2010 William Davis (26)

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.

What's for breakfast? Egg bake

20. August 2010 William Davis (42)

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.

What's for breakfast?

14. August 2010 William Davis (0)

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.)