What role cholesterol medication?

10. April 2006 William Davis (0)
A frequent conversation point among my patients, as well as participants in the www.cureality.com program, is "Are cholesterol medications really necessary?"

No, they are not. What IS necessary is to correct all manifest and hidden causes of coronary plaque. Among these causes, in my view, is LDL cholesterol of 60 mg/dl or greater. There are many other causes of coronary plaque--e.g., small LDL particles, unrecognized hypertension, Lp(a), hidden diabetic patterns, etc.--but reducing LDL to 60 mg is still an important part of a plaque-reversing effort.

Insofar as we wish to get LDL to this goal, the statin cholesterol drugs like Lipitor, Zocor, Crestor, etc. may play a role. However, they should only be considered after a full effort dietary program is pursued. Don't follow the American Heart Association's diet unless you want to fail. It's nonsense.

For a more detailed discussion of how to use nutrition and nutritional supplements to reduce LDL cholesterol, go to www.lef.org, the website for the Life Extension Foundation. I wrote an article for their magazine called "Cholesterol and Statin Drugs: Separating Hype from Reality". You'll find the article at http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1295&query=davis%20cholesterol%20natural&hiword=CHOLESTEROLA%20CHOLESTEROLS%20DAVI%20DAVID%20DAVIE%20DAVIES%20DAVIN%20DAVIO%20DAVISON%20DAVISS%20DAVIT%20NATURALBASED%20NATURALES%20NATURALIZED%20NATURALLY%20NATURALS%20NATURE%20NATURES%20cholesterol%20davis%20natural%20.)

Can your plaque-reversal efforts succeed without statin drugs? It depends on your causes. For instance, someone with small LDL and Lp(a) only may do great on our basic program and then add niacin. Unfortunately, another person with a starting LDL cholesterol of 240 mg/dl--sky high--will have more success with these drugs.

Believe me, I am no blind supporter of drug companies and their flagrantly profit-seeking practices which, in my view, are cut-throat, shoving anyone and anything out of their way to increase profits and market share. I share many of Dr. Dave Warnarowski's views on how vicious their tactics can be; see his recent Blog post at http://www.drdavesbest.com/blog/ called "I smell a rat".

Nonetheless, the deep and well-funded research of the pharmaceutical industry does yield some useful tools. You don't have to love the insect exterminator, but if your house is being eaten by termites, his services can be useful. Same thing with these drugs. Useful--not the complete answer, not even close, but nonetheless useful in the right situations. Sometimes antibiotics are necessary, even life saving. That's how cholesterol drugs are, too.

Take it all in the proper perspective. Your goal is not cholesterol reduction, per se, but plaque control, preferably reversal.

Supplement Mania!

9. April 2006 William Davis (3)
Ever hear of "polypharmacy"? That's when someone takes too many medicines. People will have lists of 15-20 prescription medicines, for instance, with crazy interactions and oodles of side-effects.

Well, how about "poly-supplments"? That's when someone takes a large number of nutritional supplements.

Let me tell you about a 45 year old man I met.

In an effort to rid himself of risk for heart disease that he felt was likely shared with his family (brother and father diagnosed with heart attacks in their late 40s), Steve followed a program of nutritional supplementation. You name it, he took it: hawthorne, anti-oxidant mixtures, vitamins C, E, B-complex, saw palmetto, 7-keto DHEA, velvet deer antler, gingko biloba, policosanol, chronium picolinate, green tea, pine bark extract, St. John's Wort, CoEnzyme Q10, papain and other digestive enzymes...He became a distributor for a nutritional supplement company to allow him to afford his own extraordinary program.

To satisfy himself that he had indeed "cured" himself of heart disease, he got himself a CT heart scan. His score: 470, in th 99th percentile. Steve's heart attack risk based on this score was around 10% per year. High risk, no question.

For weeks after his scan, Steve admitted walking around in a daze, not knowing what to do. Years of telling himself that he had effectively dealt with his heart disease risk, now all down the drain.

When we met, I persuaded him that to think that this collection of supplements would reverse heart disease was magical thinking. We trimmed his list down to the essentials and got him on the right track.

Heart disease is controllable and reversible, but not this way. Don't fool yourself into thinking that some collection of supplements will be enough to stamp out your heart disease risk. Just like taking an antibiotic when you don't have an infection achieves nothing, so does taking the wrong supplements.

What does heart scanning mean to you?

8. April 2006 William Davis (0)
CT heart scans can mean different things to different people.


What does a heart scan mean to you? There are several possibilities:

1) A way of reducing uncertainty in your future.

2) A tool to crystallize your commitment to health.

3) A device to help you track how successful your heart disease prevention program is.

4) A trick to get you in the hospital.

5) A moneymaking tool for unscrupulous physicians hoping to profit from "downstream" testing, particularly heart catheterizations.


Like anything, heart scans can be used for both good and evil. How can you be sure that your heart scan is put to proper use--for your benefit and not someone else's profit?

Simple: Get educated. Understand the issues, be armed with informed questions.

If, for instance, you're a 55-year old female with a heart scan score of 90, active without symptoms, and you're told to have a heart catheterization right off the bat---run the other way. This is bad advice. A heart procedure like catheterization at this score in an asymptomatic woman is very rarely necessary. That decision can only be made after a step-by-step series of decisions are made by a truly interested, unbiased party. (A stress test is almost always required in this situation before the decision can be made to proceed with a catheterization.)

Unfortunately, in 2006, getting unbiased advice from your doctor is still a struggle. That's why we started Track Your Plaque---unbiased information, uncolored by drug or device company support, with an interest in the truth.

Coronary disease is drying up!

7. April 2006 William Davis (1)
I had an interesting conversation with a device representative this morning. He was a sales representative for a major medical manufacturer of stents, defibrillators, and other such devices for heart disease.

Since I'm still involved with hospital heart care and cardiac catheterization laboratories, this representative asked me if I was interested in getting involved with some of the new cardiac devices making it to market over the next year or two. "The coronary market is drying up, what with coated stents and such. We've got to find new profit sources."

Well, doesn't that sum it up? If you haven't already had this epiphany, here it is:

HEART DISEASE IS A PROFITABLE BUSINESS!

Why else can hospitals afford billboards, $10 million dollar annual ad campaigns, etc.? They do it for PROFIT. Likewise, device and drug manufacturers see the tremendous profit in heart disease.

The representative's comments about the market "drying up" simply means that the use of coated stents has cut back on the need for repeat procedures. It does NOT mean that coronary disease is on the way out. On the contrary, for the people and institutions who stand to profit from heart care, there's lots of opportunity.

Track Your Plaque is trying to battle this trend. Heart disease should NOT be profitable. For the vast majority of us, it is a preventable process, much like house fires and dental cavities.

Mammogram for your heart

6. April 2006 William Davis (0)
With the booming popularity of "64-slice CT scans", there's a lot of mis-information about what these tests provide.

These tests are essentially heart scans with added x-ray dye injected to see the insides of the arteries. However, to accomplish this, a large quantity of radiation is required. In addition, the test is not quantitative, that is, it is not a precise measure that can be repeated year after year.

It is okay to have a 64-slice CT coronary angiogram. It is NOT okay to have one every year. That's too much radiation. However, a heart scan can be repeated every year, if necessary, to track progression or regression. Once stabilization (zero change) or reduction is achieved, then you're done (unless your life takes a major change, like a 20 lb weight gain).

The tried-and-true CT heart scan is the gold standard--easy, inexpensive, precise, and repeatable. Not true for 64-slice angiograms.

Is your doctor using "leeches"?

4. April 2006 William Davis (0)
What if you went to your doctor for a problem and he/she promptly placed leeches on your body?

Yeccchhhh! Would you go back? I'd bet that you'd run the other way as fast as your bleeding legs could take you. Outdated health practices like "bleeding" are outdated for good reason.

Then why would you allow your doctor to approach your heart disease prevention program by checking cholesterol and then waiting for symptoms to appear? That miserable approach leads to tragedy and death all too often--ask Bill Clinton! He might as well have had leeches!

Don't allow your doctor's ignorance or disinterest impede your prevention program. Get your coronary plaque measured, then attack it from all sides by knowing all causes, hidden and obvious. That's why Track Your Plaque is such an effective program.

I often wonder why more doctors aren't using this unbelievably powerful approach to deal with heart disease. But when I see colleagues implanting stents, defibrillators, and the like for many thousands of dollars per patient, the answers are obvious. Given a choice of a rational, effective program of prevention that pays the doctor a few hundred dollars for his time, versus $2000 to $10,000 for a procedure, you can see that the temptation is irresistible for many physicians.

All in the family--What to do if there's heart disease in your family

3. April 2006 William Davis (0)
What should you do if a close relative of yours is diagnosed with coronary disease?
This question came up recently with a patient of mine. The patient--a strapping, 47 year old businessman who looked the absolute picture of health--was undergoing bypass surgery. Although I'd met him for the purposes of plaque reversal, he was already having symptoms and his stress test was flagrantly abnormal, all discovered after a heart scan score of 765. On the day after the patient's bypass, the patient's brother came to me. Understandably concerned about his own health, he asked what he should do. The answer: get a heart scan.
Measure the disease with the easiest test available. If his heart scan score is zero, great--he's at exceptionally low (near zero) risk for heart attack. A modest program of long-term prevention is all that's necessary. What if his score is like his brother, should he get in line for his bypass? No, absolutely not! But he will need two things: 1) a stress test to ascertain whether or not he's safe (60% likelihood a stress test would be normal), and 2) an effort to determine how the heck he got so much plaque. (We favor lipoprotein testing, of course, for greatest diagnostic certainty.)
Message: Learn from the lessons your own family provides. Don't let this valuable information go to waste.
All posts by william-davis

Are you hungry?

6. December 2011 William Davis (43)
Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

30. November 2011 William Davis (22)
If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

19. November 2011 William Davis (29)
At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

14. November 2011 William Davis (73)
More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

2. November 2011 William Davis (0)
Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

30. October 2011 William Davis (53)
Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

21. October 2011 William Davis (39)
Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

19. October 2011 William Davis (33)
Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

14. October 2011 William Davis (21)
Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

14. October 2011 William Davis (6)
A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI."

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.
All posts by william-davis

Medicine ain't what it used to be

15. June 2011 William Davis (0)
The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

15. June 2011 William Davis (19)
I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

11. June 2011 William Davis (10)
The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

8. June 2011 William Davis (31)
Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

3. June 2011 William Davis (16)
In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

1. June 2011 William Davis (34)
I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

28. May 2011 William Davis (11)
An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

26. May 2011 William Davis (28)
People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

24. May 2011 William Davis (17)
Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

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

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

14. May 2011 William Davis (3)
So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 
All posts by william-davis

Heart Scan Blog Redux: Cheers to flavonoids

13. November 2009 William Davis (32)
Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


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

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

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

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




Regarding the variable flavonoid content of wines, he states:

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

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

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

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

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

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

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

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

Spain--Moderate in general.

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

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

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

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

Can wheat elimination cure ulcerative colitis?

13. November 2009 William Davis (0)
Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



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



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



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



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



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



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



Postprandial pile-up with fructose

12. November 2009 William Davis (20)
Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

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

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



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

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

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

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

Track Your Plaque: Safer at any score

11. November 2009 William Davis (0)
Imagine two people.

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

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

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

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

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

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

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

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

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

Triglyceride and chylomicron "stacking"

10. November 2009 William Davis (24)
Continuing the comments started in Grazing is for cattle, here's an interesting study from the Oxford Center for Diabetes, Endocrinology and Metabolism.

Volunteers were fed a test meal breakfast of Rice Krispies, a banana, and a chocolate milkshake (76.4 grams carbohydrates, 51.9 grams fat, 12.2 grams protein). Lunch was served 5 hours later and consisted of a cheese sandwich and a second chocolate milkshake 43.4 grams carbohydrates, 49.6 grams fat, 24.0 grams protein). Frequent blood samples were then assessed over the day. (Don't try this at home: These are obviously very dangerous foods!)

Here's the pattern of triglycerides that was observed (1st dotted vertical line = breakfast, 2nd dotted vertical line = lunch):



Note that triglycerides only begin to decline 3-4 hours after breakfast, only to peak higher after lunch.


Here's the pattern observed for chylomicrons, the "granddaddy" of lipoproteins that derives from intestinal absorption of fatty acids:



Both graphs from Heath RB et al Am J Phyiol Endocrinol Metab 2006.


With chylomicrons, note a similar pattern to triglycerides: Chylomicrons begin to decline at 3-4 hours, only to peak higher after lunch.

This is the first study to examine the effect of sequential meals on such postprandial (after-eating) patterns. But it makes the graphic point that, if insufficient time is permitted between meals, both triglycerides and chylomicrons will "stack" themselves higher and higher. (Chylomicrons are subjected to processing by the enzyme, lipoprotein lipase, to form highly atherogenic, or plaque-causing, chylomicron remnants.)

While not examined in this study, my bet is that "grazing," i.e., eating small meals or snacks frequently, is an extreme instance of triglyceride, chylomicron, and chylomicron remnant stacking. That can only lead to one thing: accelerated heart and vascular plaque.

What is a healthy vitamin D blood level?

9. November 2009 William Davis (32)
When measuring blood levels of vitamin D (as 25-hydroxy vitamin D), what constitutes a desirable level?

There's no study that directly examines this question, no study that enrolled thousands of people and assigned a placebo group and groups receiving escalating doses of vitamin D and/or achieved higher levels of vitamin D, then observed for development of cancer, diabetes, depression, heart disease, multiple sclerosis, osteoporosis, osteoarthritis, etc. Such a study would requires many thousands of participants (particularly to observe cancer and multiple sclerosis incidence), many years of observation, and many tens of millions of dollars. Nope, only a drug company could afford such costs.

So we have to piece together various observations and extrapolate what we believe to be the ideal level of vitamin D. Epidemiologic observations in several cancers (breast, colon, prostate, and bladder) suggest that a 25-hydroxy vitamin D level of 30 ng/ml or higher is desirable (with less cancer incidence above this level). Other data suggest a level of 52 ng/ml or greater is desirable. Unfortunately, much cancer research looked at intake of vitamin D from food and supplement sources, rather than actual blood levels. We also have to factor in the great individual variation in vitamin D metabolism, with a single dose yielding variable blood levels (as much as a 10-fold difference). There's also the variation introduced by vitamin D-receptor variation (genetic polymorphisms).

A new study using vitamin D administration helps chart the desirable levels of vitamin D.

Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

In this New Zealand study, 42 women (23 to 68 years old) were given 4000 units vitamin D, 39 women given placebo. Median 25-hydroxy vitamin D levels increased from 21 nmol/L (8.4 ng/ml) to 75 nmol/L (30 ng/ml). Both HOMA (a measure of insulin sensitivity) and fasting insulin levels improved, with greatest improvement seen at 25-hydroxy vitamin D levels of 80-119 nmol/L (32-47.6 ng/ml) or greater.

We also know that a vacation on a Caribbean beach in a bathing suit will increase vitamin D blood levels to the 80-110 ng/ml range without ill-effect (at least in young people who maintain the capacity to activate vitamin D in the skin, a phenomenon that declines as we age).

So do we really know the truly ideal level of vitamin D to achieve? I believe that, given the above observations, it is reasonable to extrapolate that the ideal vitamin D blood level likely lies somewhere above 50 ng/ml. We also know that vitamin D toxicity (i.e., hypercalcemia) is virtually unheard of until vitamin D blood levels approach 150 ng/ml, and even then is inconsistent. The health benefits of vitamin D supplementation are so tremendous, that I am not willing to wait for the prospective data to explore this question fully. For now, I aim for a blood level of vitamin D of 60-70 ng/ml (150-175 nmol/L).

Grazing is for cattle

5. November 2009 William Davis (17)
Many dietitians and nutritionists advise many people today to "graze," i.e., to eat small snacks every couple of hours. They argue that it blocks the drop in insulin and blood sugar that can trigger greater appetite and claim it can facilitate weight loss.



This is an absurd notion. Humans are not meant to graze. Humans are meant to find a wild boar or other animal, kill it, gorge on the meat, organs, and fat, then revert to berries, roots, leaves, and other foraged foods until the next kill. A human living in the wild does not have a cupboard or refrigerator full of ready-to-eat snacks to graze on.

The several hours after a meal is the most dangerous for creating coronary atherosclerotic plaque, i.e., the post-prandial period. In other words, eat dinner and, for the next 6-12 hours, your intestinal tract degrades the food; food byproducts are absorbed into the blood or lymph system. The blood is literally flooded with the byproducts of your meal.

Postprandial abnormalities are emerging to be a potent, and much underappreciated, means of causing heart disease and atherosclerosis in other vascular territories (especially carotid arteries and thoracic aorta).

Not eating--i.e., the fasting state--for extended periods is good for you. Encouraging people to graze amplifies atherosclerotic risk, since it creates an abnormal prolonged postprandial state.

The disastrous results of a low-fat diet

4. November 2009 William Davis (16)
Rob was never that committed to following the program in the first place.

I met Rob because of a modest heart scan score and consultation for a cholesterol abnormality. Rob had been cycled through all the statin agents by his primary care physician, all of which resulted in terrible muscle aches that he found intolerable.

I started out, as usual, characterizing his cholesterol abnormality with lipoprotein testing (NMR):

LDL particle number 1489 nmol/L
LDL cholesterol (Friedewald calculation) 143 mg/dl
Small LDL 52% of total LDL
HDL 50 mg/dl
Triglycerides 82 mg/dl

(LDL particle number is the emerging gold standard for LDL quantification, superior to calculated or Friedewald LDL cholesterol for prediction of cardiovascular events.)

Rob is a busy guy. After only a couple of brief visits, life and work got in the way and Rob let his attentions drift away from heart health. Since the information I provided made little impact on his thinking, he reverted to the low-fat diet his primary care doctor had originally prescribed and that he read about in magazines and food packages. He also ran out of the basic supplements I had advised, including fish oil and vitamin D, and just never restarted them.

A couple of years passed and Rob decided that just poking around on his own might not cut it. So he came back to the office. We repeated his NMR lipoprotein analysis:

LDL particle number 2699 nmol/L
LDL cholesterol (Friedewald calculation) 229 mg/dl
Small LDL 81% of total LDL
HDL 53 mg/dl
Triglycerides 78 mg/dl


Two years of a low-fat diet had caused Rob's LDL particle number to skyrocket by 81%, nearly all due to an explosion of small LDL. Recall that small LDL is more susceptible to oxidation, more inflammation-provoking, more adhesive--the form of LDL particles most likely to cause heart disease.

Also, note that, despite the enormous increase in small LDL, HDL and triglycerides remained favorable. This counters the popular rule-of-thumb offered by some that small LDL is not present when HDL is "normal."

Low-fat diets as commonly practiced are enormously destructive. In Rob's case, a low-fat diet caused both calculated Friedewald LDL as well as LDL particle number to increase dramatically. In many other people, low-fat diets increase calculated Friedewald LDL modestly or not at all, but cause the more accurate LDL particle number to increase significantly, all due to small LDL.

I'm happy to say that, once Rob witnessed how far wrong he could go on the wrong program, he's back on Track. (Sorry, pun intended.) He has resumed his supplements and eliminated the food triggers of small LDL--wheat, cornstarch, and sugars.

Dr. David Grimes reminds us of vitamin D

3. November 2009 William Davis (13)
In response to the Heart Scan Blog post, Fish oil makes you happy: Psychological distress and omega-3 index, Dr. David Grimes offered the following argument.

Dr. Grimes is a physician in northwest England at the Blackburn Royal Infirmary, Lancashire. He is author of the wonderfully cheeky 2006 Lancet editorial, Are statins analogues of vitamin D?, questioning whether the benefits of statin drugs simply work by way of increased vitamin D blood levels.


There is a fashionable interest in Omega-3 fatty acids, and these become equated with fish oil.

But fish oil is much more. Plankton synthesise the related squalene (shark oil) which, in turn, is converted into 7-dehydrocholesterol (7-DHC). The sun now comes into play and it converts 7-DHC into vitamin D (a physico-chemical process).

Small fish eat plankton, large fish eat small fish, and we eat large fish. So vitamin D passes through the food chain.

This has been a vital source of vitamin D for the the Inuits and also for the Scots and other dwellers of northwest Europe. (Edinburgh is on the same latitude as Hudson Bay and Alaska, further north than anywhere in China). In these locations there is not adequate sunlight energy to guarantee synthesis of adequate amounts of vitamin D, again by the action of sunlight on 7-DHC in the skin.

When the Scots moved from coastal fishing villages to industrial cities such as Glasgow, they became seriously deficient in vitamin D, and so the emergence of rickets. This was followed by a variety of other diseases resulting from vitamin D deficiency: tuberculosis, dental decay, coronary heart disease, and even multiple sclerosis and depression (the Glasgow syndrome).

And so it was with the Inuits. When their diet changed from fish for breakfast, fish for lunch, fish for dinner, they became deficient of vitamin D and they developed diseases characteristic of industrial cities, where there is indoor work for long hours, indoor activities, and atmospheric pollution.

It is the vitamin D component of fish and fish oils that is important.

I recently saw an elderly lady from Bangladesh living in northwest England. I would have expected her to have a very low blood level of vitamin D, as her exposure to the sun was minimal. However the blood level was 47ng/ml, not 4 as expected. She eats oily fish from Bangladesh every day, showing its value as a source of vitamin D with subsequent good health. I expect her blood levels of omega-3 fatty acids would also be high.

But it is unfashionable vitamin D that is important, not fashionable omega-3.

David Grimes
www.vitamindandcholesterol.com


Excellent point. The health effects of omega-3 and vitamin D are intimately intertwined when examining populations that consume fish.

In this study of Inuits, it is indeed impossible to dissect out how much psychological distress was due to reduced vitamin D, how much due to reduced omega-3s. My bet is that it's both. Thankfully, we also have data examining the use of pure omega-3 fatty acids in capsule (not intact fish) form, including studies like GISSI Prevenzione.

Nonetheless, Dr. Grimes reminds us that both vitamin D and omega-3 fatty acids from fish oil play crucial roles in mental health and other aspects of health, and that it's the combination that may account for the extravagant health effects previously ascribed only to omega-3s.

Why does fish oil reduce triglycerides?

2. November 2009 William Davis (9)
Beyond its ability to slash risk for cardiovascular events, omega-3 fatty acids from fish oil also reduce triglycerides.

There's no remaining question that omega-3s do this quite effectively. After all, the FDA approved prescription fish oil, Lovaza, to treat a condition called familial hypertriglyceridemia, an inherited condition in which very high triglycerides in the 100s or 1000s of milligrams typically develop.

The omega-3 fraction of fatty acids are unique for their triglyceride-reducing property. No other fraction of fatty acids, such as omega-6 or saturated, can match the triglyceride-reducing effect of omega-3s.

But why does fish oil reduce triglycerides?

First of all, what are triglycerides? As their name suggests, triglycerides consist of three ("tri-") fatty acids lined up along a glycerol (sugar) "backbone." Triglycerides are the form in which most fatty acids occur in the bloodstream, liver, and other organs. (Fatty acids, like omega-3, omega-6, mono- or polyunsaturated, or saturated, rarely occur as free fatty acids unbound to glycerol.) In various lipoproteins in the blood, like LDL, VLDL, and HDL, fatty acids occur as triglycerides.

Of all lipoproteins, chylomicrons (the large particle formed through intestinal absorption of fatty acids and transported to the liver via the lymph system) and VLDL (very low-density lipoprotein, very low-density because they are mostly fat and little protein) particles are richest in triglycerides. Thus, we would expect that omega-3s exert their triglyceride-reducing effect via reductions in either chylomicrons or VLDL.

Indeed, that seems to be the case. The emerging evidence suggests that omega-3 fatty acids from fish oil reduce triglycerides through:

--Reduced VLDL production by the liver (Harris 1989)
--Accelerating chylomicron and VLDL elimination from the blood
--Activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma)--Omega-3s ramp up the cellular equipment used to convert fatty acids to energy (oxidation) (Gani 2008)

Combine omega-3 fatty acids from fish oil with wheat elimination and you have an extremely potent means of reducing triglycerides. Read a previous Heart Scan Blog post here to read how a patient reduced triglycerides 93.5% from 3100 mg/dl to 210 mg/dl in just a few weeks using fish oil and wheat elimination.
All posts by william-davis

Heart Scans: An Interview with Jimmy Moore

10. septam 2011 William Davis (2)
My friend, Jimmy Moore, of The Livin' La Vida Low Carb Show, posted this video of an interview I did with him.

I provide some background on how heart scanning came about and how it led to the creation of the Track Your Plaque program.

It reminds me how far we've come over the 8 years since the program got started. From its modest start as just an information resource to help people understand their heart scan score, to a comprehensive program that helps followers gain incredible control over coronary plaque and coronary risk that has now expanded to over 30 countries. High-tech heart procedures still dominate public consciousness, but the tremendous power of real heart disease prevention efforts are gaining more and more attention as each day passes.

Wheat Belly #5 on New York Times Bestseller list!

9. septam 2011 William Davis (66)
The New York Times just released its bestseller list due for release September 18th, 2011 . . . .

Wheat Belly is #5!! (That darned Jane Fonda woman elbowed me out for the #4 spot!

[caption id="attachment_4452" align="alignright" width="574" caption="Wheat Belly hits #5 on New York Times Bestseller List--in 1st week!"][/caption]

Interview with Jimmy Moore of Livin' La Vida Low-Carb

7. septam 2011 William Davis (11)
Here's my podcast interview with Jimmy Moore, host of the Livin' La Vida Low-Carb Show. (If you want to fast forward to the interview, go to time marker 41:20 on the slidebar.)



In the podcast, I talk about how the Track Your Plaque program and its focus on lipoprotein testing, along with the need to reverse the incredible epidemic of diabetes and pre-diabetes, led to elimination of all wheat from the diet and the book, Wheat Belly.

An open letter to the Grain Foods Foundation

4. septam 2011 William Davis (94)
Readers: Please feel free to reproduce and disseminate this letter any way you see fit.


To:

Ms. Ashley Reynolds
490 Bear Cub Drive
Ridgway, CO 81432
Phone: 617.226.9927
ashley.reynolds@mullen.com


Ms. Reynolds:

I am writing in response to the press release from the Grain Foods Foundation that describes your effort to "discredit" the assertions made in my book, Wheat Belly: Lose the wheat, lose the weight and find your path back to health. I'd like to address several of the criticisms of the book made in the release:

" . . . the author relies on anecdotal observations rather than scientific studies."
While I do indeed have a large anecdotal experience removing wheat in thousands of people, witnessing incredible and unprecedented weight loss and health benefits, I also draw from the experiences already documented in clinical studies. Several hundred of these studies are cited in the book (of the thousands available) and listed in the Reference section over 16 pages. These are studies that document the neurologic impairment unique to wheat, including cerebellar ataxia and dementia; heart disease via provocation of the small LDL pattern; visceral fat accumulation and all its attendant health consequences; the process of glycation via amylopectin A of wheat that leads to cataracts, diabetes, and arthritis; among others. There are, in fact, a wealth of studies documenting the adverse, often crippling, effects of wheat consumption in humans and I draw from these published studies.


"Wheat elimination 'means missing out on a wealth of essential nutrients.'"
This is true--if the calories of wheat are replaced with candy, soft drinks, and fast food. But if lost wheat calories are replaced by healthy foods like vegetables, nuts, healthy oils, meats, eggs, cheese, avocados, and olives, then there is no nutrient deficiency that develops with elimination of wheat. There is no deficiency of any vitamin, including thiamine, folate, B12, iron, and B6; no mineral, including selenium, magnesium, and zinc; no polyphenol, flavonoid, or antioxidant; no lack of fiber. With regards to fiber, please note that the original studies documenting the health benefits of high fiber intake were fibers from vegetables, fruits, and nuts, not wheat or grains.

People with celiac disease do indeed experience deficiencies of multiple vitamins and minerals after they eliminate all wheat and gluten from the diet. But this is not due to a diet lacking valuable nutrients, but from the incomplete healing of the gastrointestinal tract (such as the lining of the duodenum and proximal jejunum). In these people, the destructive effects of wheat are so overpowering that, unfortunately, some people never heal completely. These people do indeed require vitamin and mineral supplementation, as well as probiotics and pancreatic enzyme supplementation.


I pose several questions to you and your organization:

Why is the high-glycemic index of wheat products ignored?
Due to the unique properties of amylopectin A, two slices of whole wheat bread increase blood sugar higher than many candy bars. High blood glucose leads to the process of glycation that, in turn, causes arthritis (cartilage glycation), cataracts (lens protein glycation), diabetes (glycotoxicity of pancreatic beta cells), hepatic de novo lipogenesis that increases triglycerides and, thereby, increases expression of atherogenic (heart disease-causing) small LDL particles, leading to heart attacks. Repetitive high blood sugars that develop from a grain-rich diet are, in my view, very destructive and lead to weight gain (specifically visceral fat), insulin resistance, leptin resistance (leading to obesity), and many of the health struggles Americans now experience.

How do you account for the psychologic and neurologic effects of the wheat protein, gliadin?
Wheat gliadin has been associated with cerebellar ataxia, peripheral neuropathy, gluten encephalopathy (dementia), behavioral outbursts in children with ADHD and autism, and paranoid delusions and auditory hallucinations in people with schizophrenia, severe and incapacitating effects for people suffering from these conditions.

How do you explain the quadrupling of celiac disease over the last 50 years and its doubling over the last 20 years?
I submit to you that, while this is indeed my speculation, it is the changes in genetic code and, thereby, antigenic profile, of the high-yield semi-dwarf wheat cultivars now on the market that account for the marked increase in celiac potential nationwide. As you know, "hybridization" techniques, including chemical mutagenesis to induce selective mutations, leads to development of unique strains that are not subject to animal or human safety testing--they are just brought to market and sold.

Why does the wheat industry continue to call chemical mutagenesis, gamma irradiation, and x-ray irradiation "traditional breeding techniques" that you distinguish from genetic engineering? Chemical mutagenesis using the toxic mutagen, sodium azide, of course, is the method used to generate BASF's Clearfield herbicide-resistant wheat strain. These methods are being used on a wide scale to generate unique genetic strains that are, without question from the FDA or USDA, assumed to be safe for human consumption.

In short, my view on the situation is that the U.S. government, with its repeated advice to "eat more healthy whole grains," transmitted via vehicles like the USDA Food Pyramid and Food Plate, coupled with the extensive genetic transformations of the wheat plant introduced by agricultural geneticists, underlie an incredible deterioration in American health. I propose that you and your organization, as well as the wheat industry and its supporters, are at risk for legal liability on a scale not seen since the tobacco industry was brought to task to pay for the countless millions who died at their product's hands.

I would be happy and willing to talk to you personally. I would also welcome the opportunity to debate you or any of your experts in a public forum.

Wiliam Davis, MD
Author, Wheat Belly: Lose the wheat, lose the weight and find your path back to health (Rodale, 2011)

Do you eat wheat? I thought so.

2. septam 2011 William Davis (85)
I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “

Here's some of their starting salvos on their Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly explodes on the scene!

29. out 2011 William Davis (64)


Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.



Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

Good fat, bad fat

27. out 2011 William Davis (11)
No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D or . . .

26. out 2011 William Davis (53)
You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

More lipoproteins zero!

26. out 2011 William Davis (18)
A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!


Diet: One size does NOT fit all

24. out 2011 William Davis (33)
Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.

This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


How important is high blood pressure?

24. June 2006 William Davis (0)

Control of blood pressure is crucial for coronary plaque control and stopping your heart scan score from increasing.

Dr. Mehmet Oz (of Oprah fame and a cardiac transplant surgeon at Columbia University) made graphic point of this on the ABC TV news show, 20/20, last evening on an episode called "Our Bodies: Myths, Lies, and Straight Talk". (See a summary on the ABC News 20/20 website at http://abcnews.go.com/2020/story?id=2109291&page=1)

Although I believe he somewhat overstated the case for hypertension (proclaiming "If you're going to remember one number, if you're going to focus and fixate on one number in your entire health profile, it better be your blood pressure"), he made the point that a blood pressure of 115/75 is what you should have for optimal health.

I couldn't agree more. Unfortunately, the old advice that desirable blood is 140/90 or less is absolutely wrong. At this level, we see flagrant increases in heart scan scores. We also progressive enlargement of the thoracic aorta, the large vessel that leaves the heart and branches to provide the major arteries of the body. Growth of the aorta to an aneurysm is also common at these formerly acceptable blood pressure. (The diameter of your aorta in the chest is an easily obtainable measure on your CT heart scan.)

The blood pressure you need for halting and reversing plaque growth on your heart scan is indeed 115/75 or less. (Not so low, however, that you're lightheaded.) This is the blood pressure that you were meant to have evolutionarily. It's also the blood pressure that helps tremendously in keeping your aorta from enlarging.

Watch for an upcoming exhaustive report on blood pressure and its plaque-raising effects and how to reduce it using nutritional strategies on the www.cureality.com membership website.

Is your doctor in cahoots with the hospital?

21. June 2006 William Davis (0)
I got a call from a doctor about a patient we've seen in past.

"I've got Tricia in the office. She's been having some kind of chest and abdominal pain. I think it's esophageal reflux, but just to be safe I'm sending her to the hospital."

I advised this physician that, given Tricia's low heart scan score, she was unlikely to be having a coronary "event" like heart attack or unstable symptoms. It wasn't impossible, but just highly unlikely.

As the patient was without symptoms at the moment and had driven herself to his office, I offered to perform a stress test immediately. (Though stress tests are of limited usefulness in people without symptoms, they can be useful provocative maneuvers in people with symptoms of uncertain significance.)

The doctor declined. Tricia was, after all, in his office and he was responsible for any decisions despite any objections I voiced. Well, Tricia was directed by her doctor to go to a local hospital, though one with an especially notorious reputation for putting virtually anyone they can get their hands on through as many procedures as possible.

As you might guess, this doctor was closely associated with this hospital. He and his colleagues obtain incentives (or are penalized) if they do not generate revenue-producing procedures for the hospital.

So, guess what? Tricia ended up with several procedures, all of which yielded nothing--except $30,000 in revenues from Tricia's insurance company.

I harp on this deplorable state of affairs because it is utterly, painfully, and shamefully TRUE. Just look at the hospital and you'd better brace yourself for a series of tests that could cost you the equivalent of a nice 3 bedroom home. If they were truly necessary after the failure of preventive and other simple efforts, fine. But, all too often, they are driven by profit motives.

Could I have stopped this somehow from occurring? After all, Tricia was reasonably aware of the way we do things around here. I fear that even this failed to serve Tricia well. But I remain hopeful that, as we build broader awareness of these issues, that more and more people and physicians will stand up and refuse to tolerate the status quo.

Where is the Track Your Plaque program going?

21. June 2006 William Davis (1)
I spend a lot of time worrying about how people can be helped to navigate through this program.

Take, for instance, the man in rural Texas who, while traveling in Dallas, got a heart scan on a whim. His score was 990. When he took the report back to his doctor, he got a smirk--and that's all. When he came to the Track Your Plaque program, he lacked a physician advocate to help him.

Or the woman from Florida who sought opinions from two reputable cardiologists for her heart scan score of 377. Both advised her that she needed a heart catheterization--despite her lack of symptoms, her 5-day-a-week exercise program, and normal stress test. She also lacks a physician advocate who acts on her behalf, helping her achieve success, rather than just churning her for money from hospital procedures.

For people like this and for others, I see the Track Your Plaque program evolving in several directions:

1) An online clinic--You enter and we take your "hand" and lead you step by step through the process, not only at the beginning, but over the months and years. This would help clear up some of the confusion and zigzags that some people experience trying to navigate through the program.

2) Develop physician and non-physician partners--The woman in Florida, for instance, could be referred to a doctor nearby who understands the program and is able to assist her. At present, this is virtually impossible because of the bias towards heart procedures, drugs as the sole treatment for heart disease risk, and the superficial physician-patient relationship. The majority of practicing physicians just don't understand the program despite the fact that it is based on sound clinical and experimental data. But it will in time.

Looking back, we've come a long way. I remember first having patients undergo heart scans 10 years ago. My colleagues laughed or called it "silly". The general public didn't know what they meant.

Now we're talking about how to broadcast the most powerful heart disease prevention program available in the world to a larger audience, but making it easier and more accessible. Mass media like Oprah's two hour-long spots helped, but we need to make the next leap. Not just identifying hidden heart disease to feed the hungry cardiovascular hospital procedure monster, but to educate/inform/empower the public on what to do with the scan once they've had it.

Who cares about triglycerides?

19. June 2006 William Davis (0)
Walter's triglycerides were 231 mg. His LDL cholesterol was "favorable" at 111 mg, HDL likewise at 49 mg.

"Everything looks good," his doctor declared.

"Do you think the triglycerides are okay, too?" Walter asked.

"Well, the guidelines do say that triglycerides should be less than 150, but I believe you're close enough. Anyway, triglycerides don't really cause heart disease."


When I met Walter, I made several comments. First of all, in light of his heart scan score of 713, none of his numbers--HDL, LDL, or triglycerides-- were acceptable. But the triglycerides were glaringly and terribly too high.

Why? What exactly are triglycerides?

Triglycerides are a basic fat particle that, though they do not cause heart disease directly, trigger the formation of an array of abnormal lipoprotein particles in the blood that are among the most potent causes of heart disease known.

These abnormal lipoprotein particles include small LDL, VLDL, and IDL (intermediate-density lipoprotein--a really bad pattern). Excess triglycerides also cause HDL to drop. They also cause a distortion of HDL structure, causing the particles to become abnormally small. Small HDL is also useless HDL, unable to provide the protection that HDL is designed to do.

So Walter's elevated triglycerides are, in reality, a substantial red flag for an entire panel of abnormal particles that contribute to the growth of his coronary plaque.

So, if you get this kind of commentary on your triglycerides, ask for another opinion. (Track Your Plaque Members: Also see Triglycerides: Mother of meddlesome particles at http://www.cureality.com/library/fl_dp002triglycerides.asp.)

Total cholesterol and heart scans

19. June 2006 William Davis (0)
Andy was fearful of heart disease in his life. At age 52, he'd already had four CT heart scans--one each year on or near his birthday.

Yet, when I looked at Andy's scans, his scores had been increasing 20-24% per year. Each and every score was greater by 20% or more over the previous.

So I asked Andy what steps he had taken to stop this relentless progression. "Well, I've always been real health conscious. But ever since my first scan, I really started sticking to a healthy diet, exercising nearly every day, and I take a bunch of supplements."

"What did your doctor advise?" I asked.

"Well, Dr. ---- said that nothing needed to be done, since my total cholesterol was always below 200."



Men's Health magazine's fabulous story about the folly of using total cholesterol to gauge heart disease risk.




Aaaauuuggghhh!! Wrong!

This man was, in fact, at rapidly escalating risk for heart attack. This rate of growth simply can't continue forever without igniting this bomb.

A total cholesterol below 200 is meaningless, as Andy's increasing coronary plaque proved. For instance, you can have a total cholesterol of 165 mg but with an HDL cholesterol of 27 mg. This would constitute very high risk for heart disease despite the low total cholesterol. The low HDL pattern is among the most common reasons for a misleading total cholesterol. Small LDL, high triglycerides, and lipoprotein (a) are other frequent reasons.

Andy, run the other way! Do not heed this doctor's advice! You need a solid answer to the question: Why exactly do I have coronary plaque in the first place?

Then, agree on a treatment program that corrects your specific causes.

Cardiologists out of touch

17. June 2006 William Davis (0)
This weekend, I'm fulfilling some responsiblities I have every so often to some of the local hospitals. It gives me a chance to interact with many of my colleagues who are likewise "on call" for the weekend.

I tried to strike up several conversations with colleagues about how they were managing heart disease prevention. I received blank stares, puzzled looks, indifference. One colleague declared that 80 mg of Lipitor is all you need to know.

These same colleagues are the ones scrambling for the heart attack patients in the emergency room, climbing over one another for consultation in the hospital for patients with chest pain and heart failure. They're consumed with expanding the range of procedures they can perform.

Carotid stenting is hot. So is stenting of the leg arteries. Defibrillators have been a financial bonanza. Opportunities abound on how to add these procedures to a cardiologist's abilities.

But heart disease prevention? How about heart disease reversal?

Frankly, I'm embarassed by my colleagues' lack of interest. Imagine we had a cure for breast cancer--not a palliative therapy that just slows the disease down or prolongs life, but actually cures it once and for all. I would hope that all physicians and oncologists would learn how to accomplish this. What if instead they focused on learning new ways to remove breasts, administer new toxic chemotherapies, etc. but ignored the whole idea of cure?

This is what is happening with coronary plaque reversal. The answer is right in front of them, but the vast majority (99%) of cardiologists choose to ignore it. After all, prevention and reversal simply don't pay the bills.

That means that, in 2006, you simply cannot rely on your cardiologist to counsel you on how to achieve regression or reversal of coronary plaque. How about your internist, family physician, or primary care doctor? Well, they're busy doing pneumovax injections, Pap smears, managing knee and hip arthritis, low back pain, diarrhea, headaches, sinus infections and . . yes, dabbling in heart disease prevention.

And, for the most part, doing a miserable job of it. What you generally get echoes the drug manufacturers pitch: Take a statin drug, cut the fat in your diet.

Until the majority of doctors catch on, you're going to have to rely on sources like the Track Your Plaque program for better information.

What if your lipoproteins are perfect?

16. June 2006 William Davis (0)


Sandy is a 56-year old woman--fit, slender, physically active, with no bad habits. A retired teacher, she has time to devote to her health. She bikes several days per week, mountain bikes, walks, and takes fitness classes. In short, she's the picture of perfect health.

Her heart scan score was not terribly impressive: 41. However, at her age, this modest score placed her in the 77th percentile. This suggested a heart attack risk of around 2-3% per year.

So we measured Sandy's lipoproteins. They were shockingly normal. In fact, Sandy is among the very rare person with absolutely no small LDL particles. All other patterns were just as favorable, including an HDL in the 80s.

This may seem like good news, but I find it disturbing. People are often initially upset by seeing multiple abnormal lipoprotein patterns. But lipoprotein abnormalities are the tools that we use to gain control over coronary plaque.

So what do we do when there are no abnormalities?

There are several issues to consider:

1) Your heart scan score reflects the sum total of your life up until that point. What if you were 20 lbs heavier 10 years earlier and your lipoproteins were abnormal during that period? Or you smoked until age 45 and quit? As helpful as they are, lipoproteins and related patterns are only a snapshot in time, unlike the heart scan score.

2) You have a vitamin D deficiency. This is unusual as a sole cause of coronary plaque. Much more commonly, it is a co-conspirator.

3) The heart scan is wrong--highly unlikely. Heart scans are actually quite easy, straightforward tests. (The only time this tends to happen is when scoring that appears in the circumflex coronary artery is actually in the nearby mitral valve. This really occurs only when there's very minimal calcium in the valve.)

4) There's a yet unidentified source of risk. Probably very rare but conceivable. For instance, there's an emerging sense that phopholipid patterns may prove to be coronary risks. One clinically available measure that we've not found very useful is phospholipase A2, known by the proprietary name "PLAC" test. (See http://www.plactest.com for more information from the manufacturer/distributor of the test.) But there's probably lots of others that may prove useful in future.

How often does it happen that someone fails to show any identifiable source for their coronary plaque? I can count the number of instances on two fingers--very unusual. (Thank goodness!)

Sandy's case is therefore quite unique. How should we approach her coronary plaque? In this unusual circumstance, lacking a cause, we tend to introduce therapies that may regress plaque independent of any measurable lipoprotein parameters. But that's a whole new conversation.

Fly to India for a bypass operation?

16. June 2006 William Davis (1)

In the June 19, 2006 issue of People Magazine, there's an article called "The Doctor is in . . .INDIA". The report talks about how, with health care costs in the U.S. spiralling out of control, more and more Americans are leaving the country to have their procedure performed.

They tell the story of Mr. Carlo Gislimberti of New Mexico and cite these numbers:

Heart Surgery
Cost in U.S.: $200,000

Cost in India: $10,000

Mr. Gislimberti opted to have his coronary bypass operation in India for cost reasons.

But the People magazine report left out one other option: The Track Your Plaque program: $39.00

Do your part to save ballooning health care costs: Engage in a truly powerful program of heart disease prevention like the Track Your Plaque program. The cost difference is laughably huge. And you won't require a 12-inch chest incision.

Follow conventional guidelines and guess what? You're going to have a heart attack. Follow the American Heart Association diet and you'll have heart disease.

Cut to the chase. The only program that is able to detect, track, and control coronary plaque better than any other process I know of is this program.

Note: I am not proposing that a heart disease prevention program like Track Your Plaque can replace a procedure like coronary bypass when a dangerous situation has developed. The Track Your Plaque program is designed to be implemented in the years before heart surgery is required. That's when you have the greatest control over your fate.

Surprise: Heart scan score reversal

14. June 2006 William Davis (0)
Gene is a jovial, fun-loving railroad worker who didn't take anything too seriously--including his heart scan score of 767.

This score placed Gene solidly in the 99th percentile (in the worst 1%). It came as no surprise to Gene. After all, his father died at age 36 of a heart attack and Gene's brother died at 60 of a heart attack. So Gene took life as it came and long ago decided not to fret about his fate.

But Gene's wife prodded him and prodded him to get the heart scan. That's when I met him.

Of course, Gene had been prescribed Lipitor by his doctor for a somewhat high LDL cholesterol. Our assessment uncovered several additional patterns including lipoprotein (a), small LDL, a pre-diabetic tendency, and a severe deficiency of vitamin D.

At 224 lb and 5 ft 6 inches in height, I felt that Gene was at least 40 lbs overweight.

One year later and with reasonable correction of all his patterns except weight loss and Gene's heart scan score was 590--a reduction of 23%!

Gene was thrilled, as was I. But, frankly, I was also surprised. Dramatic regression of coronary plaque tends to not occur so readily as long as pre-diabetic patterns persist and weight is not controlled.

The lesson: Often the only way to tell if you've achieved control or regression of coronary plaque is to have another heart scan. The tremendous variation in human responses never ceases to amaze me.

Call me when you're having chest pain

13. June 2006 William Davis (0)

I met a patient, Anna, yesterday. She was quite frustrated and frightened.

At age 50, Anna suffered a heart attack and received a stent to her left anterior descending coronary artery. What she found upsetting is that, because several members of her family had suffered heart attacks in their 40s (Dad--heart attack at age 45, paternal uncle--heart attack age 40, and even another uncle with heart attack in his late 20s), she had repeatedly asked her doctor whether she was okay.

She received the usual array of false assurances: "You're feeling fine, right? Then don't worry about it." "Look. Your cholesterol is in the normal range. Even your cholesterol/HDL ratio is fine." "Women don't get heart disease until later in life."

All proved absolutely false. As we talked, Anna exclaimed, "I think what I've been told all along is that we'll take you seriously when you finally have a heart attack!"

She's exactly right. The vast majority of times, heart disease is discovered by accident, usually because of an "event" like heart attack. This is like changing the oil in your car when it finally breaks down--it's too late.

CT heart scan, followed by lipoprotein testing and associated values, then correction of your specific causes. It's that simple.
All posts by william-davis

Why ATP-3 is B--- S---

20. out 2011 William Davis (8)
A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

How far wrong can cholesterol be?

17. out 2011 William Davis (32)
Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

The best artificial sweeteners

13. out 2011 William Davis (23)
Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Sugar Nation

11. out 2011 William Davis (10)


Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.

Track Your Plaque makes Consumer Reports!

8. out 2011 William Davis (27)
. . . but not in a good way.

The September, 2011 issue of Consumer Reports showcases their Protect Your Heart discussion. Third paragraph: "The website Track Your Plaque warns, 'The old tests for heart disease were wrong--dead wrong.' It says heart scans are 'the most important health test you can get.'"

They go on to expose the overuse of heart procedures like angioplasty and stent implantation and offer their advice on how to manage heart disease risk: lower BP, reduce LDL cholesterol, lose weight, stop smoking, take aspirin. They quote Dr. Paul Ridker who declares heart scans are not useful because the "deposits cardiologists worry about are the less stable plaques that CT scans routinely miss."

I thought I'd been transported back to 1995. Not only is it clear that the Consumer Report writers never looked beyond the homepage of Track Your Plaque, but somehow saw our heart disease prevention and reversal program as promoting heart procedures. Incredible.

Of course, the Track Your Plaque program does the exact opposite: Advocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant. That's a critical difference.

And, as I've had to remind my colleagues time and time again, what we are really after is an index of total coronary atherosclerotic plaque. Even in 2011, that index remains the simple coronary calcium score, a gauge of total plaque, not just of "hard," stable plaque. Perhaps in 10 years we will be using a better tool to gauge progression and regression of all the components of coronary atherosclerotic plaque, but today it remains the simple, accessible, mammogram-like coronary calcium score.

Consumer Reports does for the idea of heart disease prevention what food manufacturers do for health and weight loss: Echo conventional wisdom of the sort that generally makes us fatter, more diabetic, leads us to more heart procedures and needless deaths. I might use Consumer Reports to rate MP-3 devices or toasters, but I certainly would not rely on them for insightful health advice.

Paging Dr. Basedow

6. out 2011 William Davis (8)
A 23-year old man came to my office having experienced weeks of extreme anxiety, palpitations, and 19 pounds of weight loss triggered by an overactive thyroid.

It all happened because of a large dose of iodine received during a CT scan using iodine-containing x-ray dye. (X-ray dyes are made visible on x-ray due to the iodine content.) This is a reaction first described in the 19th century by German physician, Karl Adolph von Basedow. (Jod is German for iodine.)[caption id="attachment_4313" align="alignleft" width="217" caption="Dr. von Basedow. Image courtesy Wikipedia"][/caption]

Now, here's the kicker: Jod-Basedow only occurs when there is pre-existing iodine deficiency. Indeed, this young man had an enlarged thyroid, signaling longstanding iodine deficiency (a goiter).

This example is among the more flagrant examples of something I have been witnessing: the return of iodine deficiency. As Americans cut back on their intake of iodized salt and fail to obtain iodine in sufficient quantities from seafood, seaweed, or supplementation, goiters and iodine deficiency are making a return in all its glory, reminiscent of the early 20th century, pre-iodized salt.

This young man's frightening experience is yet another way iodine deficiency can show itself, by the overenthusiastic thyroid response to a large dose of iodine when iodine deficiency has been present for a prolonged period.

Iodine deficiency and goiters have been lost to memory for most people. Even the FDA, in its advice for Americans to reduce salt and sodium intake, have forgotten to remind everyone to obtain iodine from an alternative source. "Those who cannot remember the past are condemned to repeat it."

Get your iodine.

Carb counting

5. out 2011 William Davis (20)
In the recent Heart Scan Blog post, Can I eat quinoa, I discussed how non-wheat carbohydrate sources like quinoa, amaranth, black beans, brown rice, fruit, etc. do not exert the inflammation-provoking, appetite-increasing effects of wheat (since gliadin and gluten are not present), nor do they increase blood glucose as enthusiastically as the amylopectin A of wheat--but non-wheat grains can still increase blood sugar quite substantially.

Of course, any food that triggers blood sugar also trigger hepatic de novo lipogenesis, thereby increasing triglyceride levels and postprandial particles (e.g., chylomicron remnants), which, in turn, triggers formation of small LDL particles.

So these non-wheat carbohydrates, or what I call "intermediate carbohydrates" (for lack of a better term; low-glycemic index is falsely reassuring) still trigger all the carbohydrate phenomena of table sugar. Is it possible to obtain the fiber, B-vitamin, flavonoid benefits of these intermediate carbohydrates without triggering the undesirable carbohydrate consequences?

Yes, by using small portions. Small portions are tolerated by most people without triggering all these phenomena. Problem: Individual sensitivity varies widely. One person's perfectly safe portion size is another person's deadly dose. For instance, I've witnessed many extreme differences, such as 1-hour blood sugar after 6 oz unsweetened yogurt of 250 mg/dl in one person, 105 mg/dl in another. So checking 1-hour blood sugars is a confident means of assessing individual sensitivity to carbs.

Some people don't like the idea of checking blood sugars, however. Or, there might be times when it's inconvenient or unavailable. A useful alternative: Count carbohydrate grams. (Count "net" carbohydrate grams, of course, i.e., carbohydrates minus indigestible fiber grams to yield "net" carbs.) Most people can tolerate around 40-50 grams carbohydrates per day and deal with them effectively, provided they are spaced out throughout the day and not all at once. Only the most sensitive, e.g., diabetics, apo E2 people, those with familial hypertriglyceridemia, are intolerant to even this amount and do better with less than 30 grams per day. Then there are the genetically gifted from a carbohydrate perspective, people who can tolerate 50-60 grams, occasionally somewhat more.

People will sometimes say things like "You don't know what the hell you're talking about because I eat 200 grams carbohydrate per day and I'm normal weight and have perfect blood sugar and lipids." As in many things, the crude measures made are falsely reassuring. Glycation, for instance, from postprandial blood sugars of "only" 140 mg/dl--typical after, say, unsweetened oatmeal--still works its unhealthy magic and will lead long-term to cataracts, arthritis, and other conditions.

Humans were not meant to consume an endless supply of readily-digestible carbohydrates. Counting carbohydrates is another way to "tighten up" a carbohydrate restriction.

One hour blood sugar: Key to carbohydrate control and reversing diabetes

2. out 2011 William Davis (27)
Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Wheat Belly coming to bookstores!

31. zilye 2011 William Davis (18)
Anyone following the conversations on these pages know that I have some very serious concerns about this thing being sold to us called "wheat"--cause it ain't wheat! It is the result of incredible genetics shenanigans inflicted on this plant, mostly in the name of increased yield per acre.



I now classify wheat as "Public Enemy #1," the prime nutritional culprit underlying obesity, heart disease, "cholesterol" abnormalities, hypertension, arthritis, psychiatric illness, and on and on. Once you read the full story, I believe that you will agree: Modern Triticum aestivum, the plant that now serves as the source for virtually all the wheat flour products now consumed--organic, whole grain, multigrain, sprouted . . . it makes no difference--does not belong in the human diet. So many people, searching for solutions for their fatigue, weight gain, leg edema, incurable rashes, joint pain, etc., will find their answers here.

Wheat Belly: Lose the wheat, lose the weight and find your path back to health will be on bookstore shelves including Barnes and Noble August 30, 2011 or is available for preorder here at Amazon. Wheat Belly will also be available as a downloadable Kindle book and as unabridged audio CDs.

You can also follow the Wheat Belly conversations on my Wheat Belly Blog. One of my recent posts discusses the herbicide-resistant semi-dwarf wheat strain, Clearfield, that is now making its way to more and more supermarket shelves.

You'll also find more conversation on the Wheat Belly Facebook pages.

The exception to low-carb

31. zilye 2011 William Davis (60)
I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.
Small LDL: Simple vs. complex carbohydrates

Small LDL: Simple vs. complex carbohydrates

4. May 2010 William Davis (17)
Joseph is a whip-smart corporate attorney, but one who accepts advice at his own pace. He likes to explore and consider each step of the advice I give him.

Starting (NMR) lipoprotein panel on no treatment or diet change:

LDL particle number 2620 nmol/L (which I would equate to 262 mg/dl LDL cholesterol)
Small LDL 2331 nmol/L--representing 89% of LDL particle number, a severe dominance of small LDL

I advised him to eliminate wheat, cornstarch, and sugars, while limiting other carbohydrate sources, as well. Joseph didn't like this idea very much, concerned that it would be impractical, given his busy schedule. He also did a lot of reading of the sort that suggested that replacing white flour with whole grains provided health advantages. So that's what he did: Replaced all sugar and refined flour products with whole grains, but did not restrict his intake of grains.

Next lipoprotein panel with whole grains replacing white refined flour:

LDL particle number 2451 nmol/L
Small LDL 1998 nmol/L--representing 81.5% of LDL particle number.

In other words, replacing white flour products with whole grain products reduced small LDL by 14%--a modest improvement, but hardly great.

I explained to Joseph that any grain, complex, refined, or simple--will, just like other sugars and carbohydrates, still provoke small LDL. Given the severity of his patterns, I suggested trying again, this time with full elimination of grains.

Next lipoprotein panel with elimination of whole grains:

LDL particle number 1320 nmol/L
Small LDL 646 nmol/L--48.9% of total LDL particle number, but a much lower absolute number, a reduction of 67.6%.

This is typical of the LDL responses I see with elimination of wheat products on the background of an overall carbohydrate restriction: Big drops in precisely measured LDL as LDL particle number (i.e., an actual count of LDL particles, not LDL cholesterol) and big drops in the number of small LDL particles.

You might say that wheat elimination and limitation of carbohydrate intake can yield statin-like values . . . without the statin.
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Comments (17) -

  • medeldist

    5/4/2010 8:26:52 AM |

    Interesting. I'm looking through my screening results (I'm in Europe) and there is no mention of LDL, but I have two other values, P-Apo A1 (1.77 g/L) and P-Apo B (1.09 g/L). Is there a relation between these and LDL/HDL?

  • tom

    5/4/2010 1:02:12 PM |

    It is good to have positive feedback via blood testing to show changes one is making to their body. I wonder what is a good interval between tests to show cholesterol changes?

    On a similar note, I have been eating low carb for 4 months using my blood meter to reduce both blood sugars and insulin resistance for pre-diabetes. I am still thinking about your slo-niacin suggestions and how the bad increase in blood sugar and insulin resistance vs the good cholesterol effects would affect me. I am waiting to get results from my first NMR lipoprofile to make a decision.

  • Ned Kock

    5/4/2010 3:49:58 PM |

    Indeed, restricting carbohydrates is more similar to taking statins than many people think. With the advantage that it does not have the side effects of statins, and is not costly at all.

    Many people do not know that carbohydrates stimulate the production of VLDL, suppressing the production of free fatty acids and ketones. Our liver then pumps out small VLDL particles at a high rate, and these end up as small-dense LDL particles. The potentially atherogenic type, in the presence of other factors (e.g., chronic inflammation).

    Low carbohydrate dieting stimulates the production and release of free fatty acids and ketones, suppressing the production of VLDL. Our liver then pumps fewer VLDL particles into the bloodstream (since FFAs and ketones are already doing a good job at feeding muscle and brain tissue), and when it does it lets out big VLDL particles, which end up as large-fluffy LDL particles prior to re-absorption by the liver.

    If anyone wants to see what these particles look like, the figure in the post below may be useful:

    http://healthcorrelator.blogspot.com/2010/02/large-ldl-and-small-hdl-particles-best.html

    Ketones are not shown because they are water soluble:

    http://healthcorrelator.blogspot.com/2010/04/ketones-and-ketosis-physiological-and.html

  • Anonymous

    5/4/2010 4:01:31 PM |

    Do you have any comments on oatmeal? I've noticed that for me personally, it doesn't significantly spike my blood sugar, and I've heard a lot about how oatmeal can improve cholesterol -- but of course this is often just focused on total cholesterol or general LDL amount.

  • Anonymous

    5/4/2010 5:05:47 PM |

    Hi Dr. Davis
    I'm really hoping to hear your opinion on this study:
    http://www.pnas.org/content/early/2009/08/21/0907995106.abstract?sid=

  • Dr. William Davis

    5/5/2010 1:38:40 AM |

    Hear, hear, Ned!

    I agree: Carbohydrate restriction is the unsung hero of VLDL and LDL reduction, though actual measurements are required to appreciate this effect.

  • Dr. William Davis

    5/5/2010 1:40:35 AM |

    Oatmeal anonymous--

    It's all about individualizing your food choices.

    Checking postprandial blood sugars is an excellent way to know if these issues apply to you or not, or to what degree.

  • Jeff

    5/5/2010 11:56:35 AM |

    What are your thoughts on Amlamax for the reduction of LDL?

  • Lucy

    5/5/2010 3:41:11 PM |

    OK, so here's my question... I am young (late twenties), thin (BMI: <20.2), and active (run, bike).  However, I still have almost all small, dense LDL.   I'm an ApoE 3/4, which I understand means I need to limit the amount of fat in my diet.  However, if grains also contribute to small LDL, what am I supposed to eat?   I don't eat much wheat as it is (my husband is celiac), but I do enjoy oats, rice, and the occassional piece of bread when we eat out, etc.  Would cutting all grains from my diet and living on only vegetables, some fruits, and lean meats be acceptable? Sounds like a boring and sad diet...

  • pjnoir

    5/5/2010 9:58:04 PM |

    Oatmeal reducing Cholestral is a joke. If I eat Oatmeal for breakfast( even a 1/2 cup) my BG numbers stay HIGH all day. Oatmeal is not a food I have on my breakfast table ever.

  • Anonymous

    5/9/2010 3:08:36 PM |

    Over what time period were these
    panels taken or in other words, how many weeks or months in-between test?
    Love the blog!
    CB

  • Conrad

    5/11/2010 2:28:43 PM |

    Who knows where to get an (NMR) lipoprotein panel in Toronto/Mississauga?

  • holym

    5/12/2010 6:36:06 PM |

    You say, "LDL particle number 2620 nmol/L (which I would equate to 262 mg/dl LDL cholesterol)"

    Why would you equate 2620 nmol/L to 262 mg/dl? The conversion factor given at http://jama.ama-assn.org/content/vol295/issue1/images/data/103/DC6/JAMA_auinst_si.dtl is roughly 1mmol/l = 39mg/dl.

  • Dr. William Davis

    5/12/2010 10:21:43 PM |

    Holym--

    I believe you are confusing Friedewald calculated LDL in nmol/L and LDL particle number--two entirely different things.

    My simple conversion is meant to yield a "Friedewald-like" LDL cholesterol from LDL particle number.

  • Dolly.G

    5/14/2010 3:34:18 AM |

    I do agree!!

  • Anonymous

    5/22/2010 11:06:37 PM |

    Where can I find the peer reviewed research upon which you base your advice? Thanks

  • David M Gordon

    6/15/2010 1:18:55 AM |

    My lab results are in, and they are,  on balance, not much improved. I think.

    The changes I effected since my prior panel panel 3 months ago:
    1) Lost 20 lbs
    2) Ingest 6,000mg of fish oil for a total of 1200mg (total) of DHA and EPA/day
    3) Ingest 500mg of Slo-Niacin/day (with 125oz of water/day)
    4) Ingest 6,000mg of Vitamin D/day (Changed to the proper Vitamin D soy capsule from the powdered tablet)
    5) Eat a large handful of almonds/day
    6) Exercise hard (weight training and cardio intervals for a minimum of 90 minutes/day).

    The (worsened) numbers:
    1) Total Cholesterol: 269 (from 267)
    2) LDL Cholesterol: 186 (from 175)

    The (improved) numbers:
    3) Triglycerides: 201 (from 280)
    4) HDL Cholesterol: 43 (from 36)

    Unfair to ask you, I know, but I am frustrated. What do I do wrong? What can I do more? I am VERY reluctant to take a statin, as I have tried many, all with terrible side-effects. And, fwiw, I started today on my wheat-free diet.

    Thank you for your guidance,
    David

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