Diet by LDL

7. March 2012 William Davis (0)
Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

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

Orange Cream Cookies

5. March 2012 William Davis (5)
If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

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

Preheat oven to 350º F.

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

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

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

Why are heart attacks still happening?

4. March 2012 William Davis (10)
I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

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

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

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

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

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

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

The followers of the Track Your Plaque program who

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

enjoy virtual elimination of risk.

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

8. February 2012 William Davis (7)
The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

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

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

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

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

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

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

60-year old man dies of high cholesterol

1. February 2012 William Davis (12)
Never saw a headline like this? Neither have I. That's because it doesn't happen.

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

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

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

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

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

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

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

Back to basics: Coronary calcium

30. January 2012 William Davis (42)
After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

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

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

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

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

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

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

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

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

But it's the best we've got.

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

Myocardial infraction

15. January 2012 William Davis (45)
I've seen a few heart attacks this past year . . . but none in the people who follow this program.

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

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

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

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

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

Diet is superior to drugs

7. January 2012 William Davis (27)
Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


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

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

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

Isn't that great? Spectacular job, Might!

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

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

Low-carb is heart healthy

4. January 2012 William Davis (88)
Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

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

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

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

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

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

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

Mocha Walnut Brownies

1. January 2012 William Davis (11)
Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

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

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


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


Preheat oven to 350º F.

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

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

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

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

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

11. August 2006 William Davis (0)
The recognition of the metabolic syndrome as a distinct collection of factors that raise heart disease risk has been a great step forward in helping us understand many of the causes behind heart disease.

Curiously, there's not complete agreement on precisely how to define metabolic syndrome. The American Heart Association and the National Heart, Lung, and Blood Institute issued a concensus statement in 2005 that "defined" metabolic syndrome as anyone having any 3 of the 5 following signs:





Waist size 40 inches or greater in men; 35 inches or greater in women

Triglycerides 150 mg/dL or greater (or treatment for high triglycerides)

HDL-C <40 mg/dL in men; <50 mg/dL in women (or treatment for reduced HDL-C)

Blood Pressure >130 mmHg systolic; or >85 mmHg diastolic (or drug treatment for hypertension)

Glucose (fasting) >100 mg/dL (or drug treatment for elevated glucose)


Using this definition, it has become clear that meeting these criteria triple your risk of heart attack.

But can you have the risk of metabolic syndrome even without meeting the criteria? What if your waste size (male) is, 36 inches, not the 40 inches required to meet that criterion; and your triglycerides are 160, but you meet none of the other requirements?

In our experience, you certainly can carry the same risk. Why? The crude criteria developed for the primary practitioner tries to employ pedestrian, everyday measures.

We see people every day who do not meet the criteria of the metabolic syndrome yet have hidden factors that still confer the same risk. This includes small LDL; a lack of healthy large HDL despite a normal total HDL; postprandial IDL; exercise-induced high blood pressure; and inflammation. These are all associated with the metabolic syndrome, too, but they are not part of the standard definition.

I take issue in particular with the waist requirement. This one measure has, in fact, gotten lots of press lately. Some people have even claimed that waist size is the only requirement necessary to diagnose metabolic syndrome.

Our experience is that features of the metabolic syndrome can occur at any waist size, though it increases in likelihood and severity the larger the waist size. I have seen hundreds of instances in which waist size was 32-38 inches in a male, far less than 35 inches in a female, yet small LDL is wildly out of control, IDL is sky high, and C-reactive protein is markedly increased. These people obtain substantial risk from these patterns, though they don't meet the standard definition.

To me, having to meet the waist requirement for recogition of metabolic syndrome is like finally accepting that you have breast cancer when you feel the two-inch mass in your breast--it's too late.

Recognize that the standard definition when you seen it is a crude tool meant for broad consumption. You and I can do far better.
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Low expectations

Low expectations

12. December 2007 William Davis (6)
The Framingham Risk Calculator is a standard method used by many physicians to predict risk for heart attack or death from heart disease over a 10-year period. Low-risk is defined as <10% risk of heart attack or cardiac death over 10 years; high-risk is defined as 20% or more over 10 years; intermediate-risk is in between.

Let's put it to the test:

Amy is a 53-year old businesswoman. She is 5 ft 4 inches, weighs 150 lbs. Her father had a heart attack in his early 50s followed by the usual list of hospital procedures including bypass surgery at age 60.

What is Amy's risk for heart attack or death from heart disease over the next 10 years? If we enter her data into the Framingham risk calculator, the following result is returned:

Information about your risk score:
Age: 53
Gender: female
Total Cholesterol: 198 mg/dL
HDL Cholesterol: 74 mg/dL
Smoker: No
Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No
Risk Score: 1% Means 1 of 100 people with this level of risk will have a heart attack in the next 10 years.


So, according to the Framingham calculation, Amy has <1% risk for heart attack or death from heart disease over the next 10 years. Most primary care physicians would, at most, prescribe a statin drug and talk about a reduction in saturated fat.

Thankfully, Amy didn't fall for that bit of conventional mis-information. She instead got a CT heart scan, principally because of her father's history. Her score: 117. At age 53, this put her into 90th percentile, in the worst 10% of scores for women in her age group (50-55). By heart scan criteria, her risk for heart attack is probably more like 4-5% per year, or approximately 40-50% over the next 10 years.

Let's do just a bit more math. If Amy hadn't known about her heart scan score and no preventive action was taken, the expected progression of her heart scan scores would likely be:

Start: 117
Year 1: 152
Year 2: 198
Year 3: 257
Year 4: 335
Year 5: 436
Year 6: 567
Year 7: 737
Year 8: 958
Year 9: 1245
Year 10: 1618

In fact, given Amy's starting heart scan score of 117, it is highly unlikely that she survives the next 10 years without heart attack or a fatal heart event. Yet the Framingham risk calculator puts Amy's risk at less than 1%. Could anything be more wrong?

The folly of the Framingham calculator was highlighted by a recent publication from the large Multi-Ethnic Study of Atherosclerosis (MESA), in which 3600 women (45-84 years), all of whom fell into the "low-risk" category by the Framingham calculator--just like Amy--were tracked over approximately 3 3/4 years. This study generated several observations:

1) 30% of the "low-risk" women had positive heart scan scores.
2) 5% of the "low-risk" women had scores of 300 or greater (very significant for a woman). 8.6% of these women experienced a cardiovascular event like heart attack or death over the period. Women with a heart scan score of 300 or greater had a 22-fold greater event risk compared to women with zero heart scan scores.
3) Women with heart scan scores of 1 to 299 had a cardiovascular event risk of approximately 5-fold greater risk over the period.


Across the U.S., 90% of women younger than 70 years old fall into the Framingham "low-risk" category. Yet this fiction is accepted as the prevailing standard, along with LDL and total cholesterol, for determination of risk in women and men.

In my view, using the Framingham risk calculator is a misguided, misleading path, one that will mis-classify a substantial number of women who could otherwise be spared from heart attack and catastrophe.

By the way, Amy is also the Track Your Plaque program record holder (by percentage drop), with a 63% drop in heart scan score over a 15 month period.
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Comments (6) -

  • lungdoc

    12/14/2007 4:21:00 AM |

    I just recently signed up to TYP. My CT score today was 794!
    I am 50 year old diabetic. My LDLs had been <70 and HDLs>50 for years. Recently found vit D was only 25 and now 66 after supplementation. HGB AIC had been 6-7 for years. I have now started concentrating on bringing it down. My most recent HS CRP was 1.3. My small ldl-p was 542 and homocysteine is 15.4
    What's my next step?

  • Dr. Davis

    12/14/2007 12:22:00 PM |

    The next step is to enter your data into the Track Your Plaque program generator to generate basic comments.

    Also, I invite you to participate in the Track Your Plaque Forum for more detailed conversations.

    I assume fish oil is part of your program, an absolute requirement along with with your vitamin D.

    You may benefit spefically from efforts to reduce small LDL.

  • Anonymous

    12/14/2007 5:29:00 PM |

    And perhaps we should do a bit more math in order to prevent terrorizing the readership (something most would not even think about because they're too frightened by the hype). If you do the simple math, you will see that only 15 women out of 3600 had a cardiac event over 3+ years of follow up. That means 4 out of 1000 low Framingham Risk women will have an event. That sounds like a pretty low risk to me.

    3600 total low risk

    5% with calcium score of 300 or more=180 women

    8.6% of the 180 women had an event in 3.75 yrs.=15 women in almost 4 years

    15 women out of the entire 3600 low Framingham risk group=0.004 or 4 per 1000 women in 4 years or 1/1000 per year.

    So with low Framingham risk, the calcium  score increases your relative risk but the ABSOLUTE risk remains very low.

  • Dr. Davis

    12/15/2007 12:11:00 AM |

    Yes, you are right: the absolute risk was low in the four year period of observation.

    Actually, there were 18 coronary events (defined as "CHD" in the study) and 24 events if strokes were included ("CVD" events).

  • MAC

    12/15/2007 3:51:00 PM |

    Dr. Davis,
        Do you Have any opinion regarding myeloperoxidase (MPO)?

    http://www.sciencedaily.com/releases/2007/07/070703172506.htm

    "One fascinating aspect of this study is that this marker of inflammation precedes by nearly a decade the development of clinical coronary disease,"

  • Dr. Davis

    12/15/2007 5:05:00 PM |

    Hi, MAC--

    I think myeloperoxidase holds promise as a marker for risk. What we do about it remains an open question.

    We are planning a Track Your Plaque Special Report on unique markers of risk for 2008 that will include a discussion about myeloperoxidase.

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Weight loss: Different causes, different solutions

Weight loss: Different causes, different solutions

1. September 2009 William Davis (8)
Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.
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Comments (8) -

  • vin

    9/1/2009 2:04:41 PM |

    What a lovely story. Shows clearly the importance of listening to your body and taking control of your own health.

    Dr. Davis keep up the good work. I may not follow up on evertyhing you write but I do look forward to your blogs.

  • Anonymous

    9/1/2009 7:22:52 PM |

    I wonder what other people use for soap and shampoo.  I use a vegetable oil soap (yardley).  I find ordinary soap too harsh on my skin.

  • Anne

    9/2/2009 12:50:10 AM |

    Kris, thank you for sharing your story. I am glad to hear that the mosquitoes don't like you anymore. I do ok with the mosquitoes - its the chiggars that love me. I can get chiggars even if I walk on the dirt instead of the grass.

  • Nick

    9/2/2009 4:22:58 AM |

    This is a great story.  I'm really curious about the change in alcohol tolerance.  I removed processed foods, grains, legumes,  limit fructose consumption and eat about 50 carbs a day.  I find that I have a very hard time tolerating much alcohol now and that it interrupts my sleep.  Sometimes it seems to just make me feel ill.  I didn't intend to stop drinking wine, but it seems that my body is telling me something!

    Anyone have thoughts on why this might be, or is it as simple as being more sensitive to toxins?

  • Hans Schrauwen

    9/2/2009 6:43:55 AM |

    Do not use soap or shampoo, it's MUCH to aggressive. I recommend to not put anything on your skin/hair you would not put into your mouth.
    Just rinse and brush dry and afterwards apply a mixture of coconut oil, sea salt and organic apple cider to quickly restore your skin's protective oily/acidic/salty layer.
    Use less coconut oil for your hair.

    Also : do not use plain toothpaste. Brush with a mixture of baking powder, sea salt and coconut oil.

  • baldsue

    9/3/2009 9:02:26 AM |

    Congrats Kris!

    Mosquitos and other bugs don't like me anymore, either.  This is the second summer I've been ignored and the second summer I've been following the same diet.  Coincidence?  I also don't use big-box soaps.  Maybe it's the diet, maybe it's the soap that keeps the bugs away?  Maybe it's the combo.

  • Plamen Ivanov

    9/8/2009 12:39:58 PM |

    Thank you for sharing this.

  • alen mcmilan

    10/11/2010 3:59:10 AM |

    I really glad to read your awesome article on weight loose, I also suffering from this bad weight loose problem so I really enjoyed to read it and I got some nice information from your blog so thanks for sharing nice information.
    Phentermine

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No flush = No effect

No flush = No effect

13. November 2006 William Davis (3)


"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."


That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.
Tags :

Comments (3) -

  • Hoop

    7/4/2007 8:38:00 AM |

    Then again it maybe this patient was using too low a dose?
    And what else was the patient ingesting? And there is the issue of which class lipid abnormality this patient had.

    In my comments below I've included some abstracts of some human based studies that suggest inositol hexanicotinate isn't useless for altering serum lipid levels.


    If we assume for a moment the validity of your anecdote,
    I won't call inositol hexanicotinate worthless rather I would suggest it might have has narrower scope of uses not including the altering
    blood lipids.  Not everyone (me) takes large doses niacin for it lipid altering properties. Consider Kaufman's work with niacinamide in patients
    with degenerative arthritis. He used doses of 1.5 to 4 grams and
    claimed increased joint mobility after a couple of months.
    In my experience, niacin also works as well as niacinamide
    against my pains in and around my joints. Its benefits against the pain come about gradually but
    nonetheless are quite effective for me.

    The flush can be pretty nasty if one isn't careful about the dose.
    I know when I mixed niacinamide and niacin in the past I seemed
    to have somewhat more flushing. I took niacin for several years
    until it started to be trigger atrial premature beats.
    I'll comment further in this posting on a way around these adverse effects of niacin.


    Inositol hexanicotinate maybe superior provided one chooses
    the right patients? Please see the second abstract below.
    ----------------------------------------------------


    1: Eur. J. Clin. Pharmacol. 1979 Aug;16(1):11-5.


    Nocturnal inhibition of lipolysis in man by nicotinic acid and derivatives.


    Kruse W, Kruse W, Raetzer H, Heuck CC,
    Oster P, Schellenberg B, Schlierf G.


    The effect of nicotinic acid and several derivatives
    on the nocturnal level of free fatty acids was studied
    in 12 healthy young women and men. Free fatty acids
    are an important precursor of plasma triglycerides
    and their concentration is highest at night.
    The drugs used were nictinic acid, beta-pyridyl-carbinol,
    mesoinositol hexanicotinate and xantinol nicotinate.
    The highest plasma nicotinic acid level was observed
    with beta-pyridyl-carbinol, but significant reduction in
    free fatty acids during the entire night was only
    achieved with inositolhexanicotinate and
    xantinol nicotinate. There was no correlation between
    the plasm levels of free fatty acids and nicotinic
    acid at any sampling time. If prolonged reduction
    in free fatty acid concentration is desired in the therapy of
    hyperlipidemias, the inositol and xantinol esters of
    nicotinic acid appear to be superior to the other preparations.


    PMID: 499296 [PubMed - indexed for MEDLINE]
    ========================================


    Inositol hexanicotinate seems to work to lower some
    blood lipids in this next human study and granted
    another drug is also involved.
    -------------------------------------------------------------
    1: Arzneimittelforschung. 1979;29(10):1621-4.


    [Treatment of various types of hyperlipoproteinaemia with
    a combination of Mg-chlorophenoxy-isobutyrate and
    mesoinositol-hexanicotinate (author's transl)]


    [Article in German]


    Bolzano K, Krempler F, Haslauer F.


    50 patients with different types of hyperlipoproteinaemia
    were treated with a combination of Mg-chlorophenoxyisobutyrate
    (700 mg) and mesoinositol-hexanicotinate (500 mg) (Atroplex)
    twice daily. 7 patients had type IIa, 39 patients type IIb
    or IV and 4 patients type V. After a period of one
    month without any treatment the patients were treated
    during two months. While the effects of this combination
    on cholesterol of type IIa patients was poor, the
    drug had an excellent lipid-lowering effect in the patients
    with type IIb, IV and V. After 14 days' treatment the
    plasma cholesterol and triglyceride levels in
    patients of type IIb or IV were significantly lowered.
    This effect became even more pronounced after
    one-month treatment. There was no significant difference
    between the effect of one-month treatment and
    that of two-month treatment. About two-thirds of the
    patients of type IIb or IV were responders. No serious side
    effects could be observed during our study.


    Publication Types:
        English Abstract


    PMID: 583231 [PubMed - indexed for MEDLINE]
    --------------------------------------------------
    So could it have been that this patient had one of the classes
    of hyperlipidemic disorders such as type 1, type
    2-a or type 3 for which inositol hexanicotinate
    maybe ineffective?


    =====================================================
    It may have other uses see next paper.
    -------------------------------------


    1: Clin. Rheumatol. 1988 Mar;7(1):46-9.


    A double blind randomised placebo controlled trial
    of hexopal in primary Raynaud's disease.


    Sunderland GT, Belch JJ, Sturrock RD,
    Forbes CD, McKay AJ.


    University Department of Surgery,
    Glasgow Royal Infirmary, Scotland.


    The peripheral vasospastic symptoms associated
    with Raynaud's disease continue to
    be an unsolved clinical problem. Hexopal
    (Hexanicotinate inositol) has shown
    promise in uncontrolled studies and its use in
    patients with Raynaud's disease may reduce such
    vasospasm. This study examines the effects of
    4 g/day of Hexopal or placebo, during cold weather,
    in 23 patients with primary Raynaud's disease.
    The Hexopal group felt subjectively better and
    had demonstrably shorter and fewer attacks of
    vasospasm during the trial period.
    Serum biochemistry and rheology was
    not significantly different between the
    two groups. Although the mechanism of
    action remains unclear Hexopal is safe
    and is effective in reducing the vasospasm
    of primary Raynaud's disease during the winter months.


    Publication Types:
        Clinical Trial
        Randomized Controlled Trial
        Research Support, Non-U.S. Gov't


    PMID: 3044673 [PubMed - indexed for MEDLINE]
    ====================================================
    : J. Int. Med. Res. 1979;7(6):473-83.


    An experimentally controlled evaluation of the effect
    of inositol nicotinate upon the digital blood flow
    in patients with Raynaud's phenomenon.


    Holti G.


    The vaso-active effects of inositol nicotinate (Hexopal)
    were investigated in thirty patients with primary and
    secondary Raynaud's phenomenon using several
    non-invasive experimental techniques under
    controlled conditions. The earlier formed impression
    that this drug requires a prolonged 'build-up' period was
    confirmed. Recording the time required to induce
    Raynaud's phenomenon as well as assessments of total
    and nutrient digital blood flow showed significant
    beneficial therapeutic effects upon the skin's
    microcirculation by inositol nicotinate. This study
    suggests that the therapeutic effect of this drug is not
    merely due to vasodilation but that other mechanisms
    such as enhanced fibrinolysis and lowering of
    serum lipids may play a significant part in its
    overall effect. Smokers responded slower than non-smokers,
    but even elderly patients with longstanding vasospastic
    disease showed measurably improved digital circulation.
    Unlike some other drugs in this field inositol nicotinate was found
    to be effective orally and to be devoid of unwanted side-effects.
    However, in the majority of patients it failed to
    abolish their increased vascular spasm although
    it diminished it significantly in most. It appears
    to be a safe and well tolerated drug, which,
    together with other symptomatic measures, merits
    to be used in the management of vasospastic
    disease of the extremities even in the
    presence of partial obliteration of the microcirculation.


    Publication Types:
        Clinical Trial
        Randomized Controlled Trial


    PMID: 391622 [PubMed - indexed for MEDLINE]
    =======================================


    Perhaps what is needed is a larger dose in comparison
    to other forms of niacin?

    ---------------------------------------------
    Now to expand the topic to plain old TR niacin and betaine.
    ---------------------------------------------

    Timed release niacin as I recall is twice a effective
    as simple niacin in lowering lipids and twice as toxic.
    So it seems come out about even if one takes a half
    the dose of TR niacin.

    Of course, what I'd love to test is niacin in its various forms
    along with trimethylglycine (TMG) aka betaine. And I won't  
    just consider lipid level effects but also the effects on
    osteoarthritis and other joint pains.

    Why do I mention betaine? I know from personal experience
    high doses of betaine along with niacin pretty well blocks
    the flushing effect as well as completely
    blocking the atrial premature beats (AVB) that I would get
    when taking either high dose niacin or niacinamide.
    I had taken niacin at a rather high doses for about 5 or 6 years
    back a couple of decades ago and then I started
    to get the AVBs when I tried to
    resume the use of doses above 100 milligrams.
    Now of course provided I take the betaine I don't have
    this problem. However, I do get AVBs if I don't use the
    betaine and only take the niacin.
    Granted some suggest niacin lowers the lipid levels
    by "stressing" the liver so if betaine blocks
    this effect it maybe contraindicated for the purpose
    of changing lipid levels.
    Here are Pubmed ID numbers, for some papers that
    reflect similar thinking using betaine to reduce
    the toxicity of high dose B-3.
    PMID: 10985907
    PMID: 17156888

    --------------------------------------------

    I'd be interested in your comments on the points of
    theory and science. I am not looking for personal
    advice. A number of people including myself
    are discussing the niacin topic on the
    Usenet forum....sci.life-extension (which
    is also available by way of the Google Group
    Archive for free provided you have a throw away email address).
    Someone else referred to your blog comments and yet
    another person proposed contacting you for a comment.
    I was elected Wink to contact you.
    The group/forum members were interested as to whether there is
    more to your anecdote concerning the possible ineffectiveness
    of inositol hexanicotinate as a lipid lower agent.

    Thank You.

  • Dr. Davis

    7/4/2007 1:36:00 PM |

    Thanks for your insightful comments.

    My experience is based on the experiences of about 10 patients on the no-flush preparation in doses of 1000-4000 mg per day.

    If the rationale for the no-flush preparation is that it provides niacin in such a way as to avoid the flush, we should see rises in HDL, reductions in triglycerides, small LDL, and lipoprotein(a), regardless of the type of hyperlipidemia present (IIa, IIb, III, etc.).

    After using no-flush for up to one year, I have seen absolutely no effect, accepting my relatively small experience.

    Please also understand that my focus is prevention and reversal of coronary heart disease, something that the Track Your Plaque approach does exceptionally well, so I try not to stray off too far from our focus. But why would no-flush have any beneficial effects on arthritis, etc.,as an alternative method of delivering niacin when niacin itself does not possess these effects? I'm not sure I follow the rationale. To be included in a program of coronary atherosclerotic regression, we would have to see substantial effects, as we do with plain old niacin.

    Nonetheless, I encourage your continuing interesting thoughts.

  • buy jeans

    11/3/2010 12:29:51 PM |

    Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

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Even mummies do it

Even mummies do it

20. November 2009 William Davis (16)

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

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

But why would people of that age have developed atherosclerosis?

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

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.
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Comments (16) -

  • Jim Purdy

    11/20/2009 8:52:23 AM |

    "hunger-gatherers"?

    The original article said hunter-gatherers.

    However, I like hunger-gatherers better.

    Hunger is certainly quite a motivator to go seek food.

  • Peter

    11/20/2009 11:05:33 AM |

    As a person who can't figure it out, the mummy scans are interesting.

    It's not clear to me if saturated fat or grains and sugar are largely to blame for heart disease, or something else.

    It made an impression on me that Jimmy Moore (low carb blogger who eats mostly meat) and Dean Ornish (who eats mostly grains and vegetables) both scored zero on their heartscans.  They both avoid flour and sugar, that might be a point of agreement and a possible explanation.  I wish I was privy to the nutritional studies that come out a hundred years from now: long-term studies of different diets.

  • bronkupper

    11/20/2009 11:45:39 AM |

    On what ground are they basing their assumption that meat is the culprit?

    It is just blatant and annoying!

  • billye

    11/20/2009 12:18:34 PM |

    Dr. Davis, I love the way your mind works.  Which only proves once again, that the advent of agriculture produced diseases of the metabolic syndrome, even in ancient Egypt.  Wheat, Beer, and date consumption indeed.  If the ancient Egyptians avoided all starch, grains, legumes, and sweet fruit in excess, particularly high fructose types, it is quite apparent that they would have been healthier and lived longer, even in those ancient times.  We should all take heed, and throw out the so called and wrong "healthy diet", the diet that advcates eating low fat and high carbohydrates. This is the dogma that for the last 60 years pervades all medical decisions.  For the sake of our good health we must,MUST all switch to the very healthy low carbohydrate and high saturated fat diet that our ancient genes crave.  If this is not true, how did we all get here?

  • renegadediabetic

    11/20/2009 1:55:47 PM |

    Yep, the always ASSUME it's the meat or fat.  It just couldn't be all those "healthy whole grains."  Smile

    It seems to me that the Egyptian diet was a nutritionist's dream.

  • caphuff

    11/20/2009 3:11:22 PM |

    Thanks for blogging on this fascinating topic, doc.

    Unfortunately, the media reports seem to emphasize meat consumption as if that was the conclusion of the researchers.

    I'm betting they don't actually go that far in the JAMA article.

  • Dr. William Davis

    11/20/2009 3:50:34 PM |

    Ooops!

    Yes, hunter-gatherers, not hunger-gatherers.

  • LPaForLife

    11/20/2009 4:55:44 PM |

    I have been reading about the wealthy ancient Egyptian diet. It is interesting that they used many types of vegetable oils. Many were high in omega 6. They often fried foods. The rich ate meat, bread and some dairy products. They used Honey(fructose) as a sweetner. So I ask the qestion. Was their diet much different than the modern diet?

  • Anonymous

    11/20/2009 7:49:57 PM |

    I understand the McTut burger, although quite unhealthy, was all the rage.
    This could explain it.

  • Dan

    11/20/2009 10:15:46 PM |

    I love how the LA Times summed things up in their article about this study.

    "Both groups, however, share some risk factors. The high-status Egyptians ate a diet high in meat from cattle, ducks and geese, all fatty.

    And because mechanical refrigeration was not available, salt -- another contributing factor in heart disease -- was widely used for food preservation."

    Sigh...

  • Helen

    11/21/2009 5:01:13 PM |

    It occurs to me that the atherosclerosis could have been at least partially due to a vitamin D deficiency resulting from eating grain, which depletes the body of vitamin D.  

    Dr. Davis, are you familiar with the theory that Europeans lost their skin pigment in part as an adaptation to eating grain?

    If this was the dawn of grain-eating, it could also have been the dawn of selecting for lighter (not to say white, necessarily) skin pigments in grain-eating peoples.  (I think the same vitamin D depletion may hold true for eating dairy, so if they ate this, too, even more so.)  

    I wonder if this was also the dawn of largely indoor living for some members of the population - like the wealthy and their servants - and if this could have contributed to a vitamin D deficiency.

  • Anonymous

    11/21/2009 5:22:27 PM |

    but here we are again; Peter points out that there was no difference in calcium score between the veggie and meat diets, yet those of the paleo-diet religion will summarily dismiss this and continue to believe a meat diet is the healthy true diet for humans.  What was the life expectancy of Paleolithic man.... under 20 years maybe?  It wasn't until the diversification of diet that life span increased.... but maybe that is irrelevant if your point is to justify one's own choices

  • Dr. William Davis

    11/22/2009 2:46:42 AM |

    Hi, Helen--

    No, I wasn't aware of that particular theory. I am aware of the notion that northern Europeans lost dark pigmentation as they settled in sun-poor regions. I was not aware that grain had added to it.

  • Allen

    11/23/2009 7:22:15 PM |

    @Anonymous who claims that food diversity was the chief cause of the increase in life expectancy. First, ancient hunter-gatherers had a life expectancy of around 35 years. This dropped to under 20 years AFTER the advent of agriculture. Ask ANY anthropologist who can tell at a glance whether the bones they've found are pre or post agriculture (pre are strong, straight and healthy with no dental decay. Post are small, brittle, and diseased with plenty of dental decay.)

    As to food diversity. It is estimated that hunter-gatherers had hundreds of different food choices ranging from animals great to small, insects, and hundreds of indigenous plants/nuts/seeds/fruits. Early agriculturists primarily ate the grains that could be cultivated locally, and their food choices dropped perilously.

    As for mummies, only Egyptian royalty were mummified and ancient Egyptian royalty were known for their high-carb food depravity, where meals included plenty of honey, grains, starches, and beer. The feasts were frequent and included ritual bulimia so that the eating could continue indefinitely. That these people had heart disease should be no surprise to anyone.

    As a final note, life expectancy is much less about living long, and more about infant mortality. Infant mortality did not go down significantly until the advent of modern medicine and birthing techniques in the 19th and 20th centuries (at least for western societies.)

  • Yelena

    11/24/2009 10:35:56 PM |

    @Allen - There's no evidence that ancient Egyptian royalty engaged in ritual vomiting during feasts. Perhaps it may have happened right at the end of the last dynasties when Rome's influence was strong, as purging during a Roman feast was not uncommon. BTW, feasting Romans would just vomit right at the table and a slave would clean it up. A vomitorium is not for vomiting, it's a kind of passageway.

    Talking about an 'Ancient Egyptian diet' is a little silly anyway. Which kingdom/era? We're talking over thousands of years here with influences from many cultures and changing weather and environmental conditions. Modern analysis of residue in beer jars over various times shows that the ancient Egyptian beer was actually almost opaque and had a relatively high protein content, interestingly.

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Oat vs. wheat

Oat vs. wheat

17. August 2007 William Davis (7)
Here's a fascinating 2002 study by Dr. Brenda Davy and colleagues at Colorado State University that examined the NMR lipoprotein differences between a diet enriched in oats and one enriched with wheat. (Davy BM, Davy KP, Ho RC et al. High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J Clin Nutr 2002; 76:351-358.)

36 sedentary, overweight men (average BMI around 30--obese), aged 50-75 years, were given a diet enriched with either oat bran (as oatmeal and oat bran, providing 5.5 grams of beta-glucan) or wheat (as a hot cereal or Frosted Mini-Wheats), with equivalent calories in each group. All underwent baseline NMR lipoprotein analysis.

Three months later, there were no differences in "anthropometrics" like weight, waist size, or BMI (though there was a trend towards larger waistlines in the wheat group). The NMR lipoprotein analysis was repeated.



Comparison of the lipoprotein changes revealed:

--LDL cholesterol: Down 2.5% with oats, up 8.0% with wheat.

--LDL particle number: Down 5% with oats, up 14.2% with wheat.

--Small LDL: Down 17.3% with oats, up 60.4% with wheat.

--Triglycerides: Down 7.6% with oats, up 22.0% with wheat.



The across-the-board differences between the wheat and oat effects were astounding. In particular, note the extraordinary effect on small LDL particles: wheat triggered a 60% increase.

Similar studies yielding similar results have been conducted elsewhere, including Dr. Ronald Krauss' group at University of California-Berkeley.

Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet.

What a wonderfully graphic representation of the undesirable effects of wheat products. When you see Mini-Wheats, Shredded Wheat, whole grain bread, whole wheat bread, whole wheat crackers, Raisin Bran, and the thousands of other wheat-containing products that promise health, run the other way. Grab some oat bran on the way out.
Tags :

Comments (7) -

  • Anonymous

    8/17/2007 8:07:00 PM |

    Dr Davis,

    I can highly recommend Nairns Oatcakes if you want another, and its quite a tasty  way,  way to eat oats. They replace english muffins and crackers in my diet.

    Best,
    Jim

  • mill

    8/21/2007 10:58:00 PM |

    Dr Davis
    I took fish oil (6/day) and red rice yeast for several months and my cholestral score went up a few points tp 278. I had a CTScan done and have palque (stage 2). I really don't want to take Lipitor etc because of side effects. any suggestions???

  • Dr. Davis

    8/22/2007 2:05:00 AM |

    The Track Your Plaque website, www.trackyourplaque.com, is devoted to answering that question. You're welcome to take a look and see if it's right for you.

  • Anonymous

    11/15/2007 3:55:00 PM |

    My husband and I are both in our
    50's and have incorporated lots of wheat in our diets, which we thought was wonderful for us but now we have our doubts, we feel we had been getting too much! We have switched to oats and reduced our
    gluten intake by 75%. We feel less gasy, bloated and more energy. Any other baby boomers bloated?  
    overwheated in Wisconsin.

  • Kym

    10/11/2008 10:27:00 AM |

    Regardless, both oats and wheat are healthy. One should not stick to just one. Smile

  • Peter

    9/9/2009 9:20:29 AM |

    I started adding lots of oat bran to my oatmeal after you pointed out that it's an excellent cholesterol lower.  I became anemic.  I read that oat bran can interfere with iron absorption, so I discontinued the oat bran and the anemia went away.

  • buy jeans

    11/2/2010 8:45:39 PM |

    Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet.

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