Near-fatal brush with nattokinase

14. April 2010 William Davis (0)

Here is precisely why I have spoken out against nattokinase: People may put faith in this "supplement" when there are virtually no data to support its use in such dangerous conditions as pulmonary embolism.

Pulmonary embolism occurs when a large volume of blood clots in the veins of the pelvis, abdomen, and into the legs. A clot breaks off and lodges in the pulmonary arteries of the lungs. This can be fatal within minutes to hours, the victim struggling to breathe, since oxygen is not transferred to the blood and it causes terrible pain in the chest.

The treatments are fairly obnoxious: intravenous anticoagulants (blood thinners), followed by oral blood thinners like warfarin. While they carry risk of bleeding and other long-term risks, it's better than dying.

Would you bet that a "nutritional supplement" manufacturer's vague claims and lack of data are sufficient proof to treat a life-threatening condition? You're a fool if you are.

Anyone reading these pages knows that I am a vigorous supporter of nutritional supplements. I even consult for the nutritonal supplement industry. But I am also an advocate of TRUTH, not BS.

Here is a woman from England who inquired whether she should stop her husband's warfarin in favor of nattokinase. This is precisely the sort of thing that can happen because of the campaign of misinformation behind nattokinase.

Dr. Davis,

Thank you for your very interesting blogs, which I came across searching for natural alternative treatments to warfarin.

My husband has been following the low carb, high fat, real food regime over the past few years. He got off all the blood pressure and cholesterol drugs and never felt better. He even got his blood sugar down from a recorded high that we are aware of 13 nmol/L (234 mg/dol) to 6.1 nmol/L 109.8 mg/dl).

We were on holiday in the Caribbean. Just before our return home, we did a trip to a neighbouring island that included non-alcoholic fruit punches. They tasted great, but were very sweet. I broke my normal refusal to drink these things, but only had a couple of glasses. (After all, we were on holiday!) My husband believes he consumed around 1.5 litres of the stuff and now realises he was feeding his body a very toxic product – fructose. That night, he had an incredible toxic response and we only got him onto the plane with a visit to the hospital and a pain killer injection.

The symptoms of pulmonary embolism only showed 2 weeks later . . . and warfarin treatment was started. We would both like to use an alternative therapy if we can find someone with experience to provide the support.Do you know of any studies that support alternative options?

Do you know of any practitioners in the England who support a non-drug approach with an understanding of nutrition who we may be able to receive advice and support?

FB
York, England

Glucophobia: The Novel

13. April 2010 William Davis (25)

Just kidding: No novel here. However, there is indeed a story to tell that should scare the pants off you.

If you haven't yet gathered that carbohydrates are a macronutrient nightmare, let me recount the list:

Carbohydrates increase small LDL particles
Or, in the cholesterol-speak most people understand, "carbohydrates increase cholesterol." It's counterintuitive, but carbohydrates increase LDL substantially, far more than any fat.

Carbohydrates increase blood sugar
Eggs don't increase blood sugar, nor do chicken, raw almonds, onions or green peppers. But a bowl of oatmeal will send your blood sugar skywards.

Carbohydrates make you fat
Carbohydrates, whether in the form of wheat flour in your whole wheat bread, sucrose in your ice cream, fructose in your "organic Agave nectar," or high-fructose corn syrup in your dill pickles. They all provoke de novo lipogenesis, or fat formation. They also stimulate insulin, the hormone of fat storage.

Carbohydrates cause glycation
High blood sugar, like the kind that develops after a bowl of oatmeal, triggers glycation, or modification of proteins by glucose (blood sugar). This is how cataracts, kidney disease, and atherosclerotic plaque develop. Small LDL is 8-fold more glycation prone than large LDL, providing a carbohydrate double-whammy.

Your glucose meter remains the single best tool to gauge the quality of your diet. Many people have horror stories of the shocking experiences they've had when they finally get around to checking their postprandial glucose.

Drama with the Dr. Oz Show

11. April 2010 William Davis (27)

A producer from the Dr. Oz show recently contacted my office. They asked whether we could supply them with a volunteer patient from either my practice or the Track Your Plaque program who would be willing to appear on the show and discuss heart disease prevention. They needed someone to commit within 24 hours.

Despite the short notice, we identified a volunteer. He flew to New York the following week where he was interviewed along with several other men and women, all of whom had heart disease (heart attacks, stents, etc.). However, as this young man is very slender and follows most of the Track Your Plaque principles (e.g., vitamin D and omega-3 fatty acid supplementation; no wheat, cornstarch, or sugars, no restriction of fat, etc.), he apparently received less attention than the overweight, I-know-nothing-about-diet interviewees.

Then there was an odd turn of events: Dr. Dean Ornish, apparently a friend of Dr. Oz, will be providing the dietary counseling. The producer had made no mention of Dr. Ornish.

Now that's an odd collision of philosophies: Our Track Your Plaque version of low-carb with the guru of low-fat, Dr. Ornish.

The following week, Dr. Ornish called me and graciously asked whether I was okay with this. I'm not sure just how much he knew about the philosophy I advocate, nor how much I have bashed his program as a destructive approach to diet, nor whether he knew that I gained 30 lbs on the Ornish diet, along with a drop in HDL to 27 mg/dl, increased triglycerides to 350 mg/dl, and type II diabetes that I've talked about on this blog and the Track Your Plaque book and website. I suspect he knew little to none of this.

Anyway, I tried to diplomatically explain that my patient's cause for coronary plaque was small LDL particles that he expressed despite his very slender build, likely from excessive carbohydrates, controlled with carbohydrate restriction. Dr. Ornish maintained his usual arguments: Grains are good, provided they are whole grains, heart disease is "reversed" with his diet program, etc. (I didn't want to challenge him in a phone call and tell him that he never actually reversed coronary plaque, but just reversed endothelial dysfunction. But, as Dr. Ornish is not a cardiologist, I wasn't sure how far his understanding of these issues went.)

We agreed to disagree. This leaves my poor patient in an odd position: Being asked by Dr. Ornish and the Dr. Oz show to follow a low-fat program for the sake of entertainment, or adhering to the advice we follow that has so far served him well, given his small LDL particle size tendencies.

We'll see where this little drama leads.

Response from Nature Made

10. April 2010 William Davis (31)

Here's the response from Nature Made when I emailed them about my concern that there appears to be no vitamin D in their vitamin D gelcaps.

It is the usually CYA corporate-speak that says nothing. The grammatical errors make it clear that this was a "canned" response.

Date: April 9, 2010
From: Marissa Reyes, Consumer Affairs Department
Subject: Reference #346236

Dear William Davis, MD:

We recently received your e-mail regarding Nature Made products. We regret to
hear that the quality standards of our company. [?]

Our company is called Pharmavite, and we manufacture Nature Made nutritional
supplements. We have been in business since 1971. We are committed to quality
control, and have very high quality standards. Our Quality Control personnel
sample and test all raw materials as they enter our plant, and again assay the
finished product, before final packaging.

Dietary Supplements are regulated under the FDA through DSHEA (Dietary
Supplement Health & Education Act of 1994). The United States Pharmacopoeia
(USP) establishes standards for the composition of drugs and nutritional
supplements. This voluntary non governmental organization was set up in 1820
and has officially been recognized by federal law since 1906. Standards
established by USP for products are legally enforceable by the FDA. At
Pharmavite we participate in the USP Dietary Supplement Verification Program
(DSVP). Many of our products have earned the DSVP seal and additional products
are currently being evaluated. Our DSVP certified products will have the DSVP
seal on the product label.

Our Nature Made Vitamin D 400 IU tablets have been reviewed by the USP and bears
the DSVP symbol on the label. Although the USP has not reviewed all of the
Nature Made Vitamin D supplements, all of our products go through the same
rigorous quality testing at Pharmavite. The products which have earned the seal
help us to demonstrate the high quality of our products.

We would like to look into the product(s) your patients have been using. If you
could provide the UPC and lot numbers of the product(s), we will be happy to
review our records. In addition, if you would like us to test the product(s)
that you currently have, we will be pleased to send a prepaid postage mailer so
you may return the product(s) to us so that our Quality Control Department can
examine it. Please let us know if you would like us to send you the prepaid
postage mailer.

We thank you for contacting us and hope that you will continue to use and enjoy
Nature Made products with complete confidence.

Sincerely,
Marissa Reyes
Consumer Affairs Coordinator
Pharmavite, LLC
MR:346236-10

Patients who come to the office do not provide me with the bottles nor lot numbers. In past, when I've gone to the trouble of doing this (with other companies, not Nature Made), it has come to nothing helpful. The information gets passed on to the company and we hear nothing and never learn if there was a problem, or receive some more corporate-speak letter saying everything was fine. This is obviously a liability-avoidance tactic: Admitting that something was wrong would open them up to legal risk. So, frankly, I can't be bothered.

So we are left with the unsatisfying experience of relying on street-level experiences.

For now, my advice: Avoid Nature Made vitamin D. Too many people have had blood tests demonstrating that they are not obtaining any vitamin D.

By the way, the Nature Made brand of fish oil is among the very few problem brands of fish oil we've encountered. Fish oil should be only mildly fish in smell and generally should not cause stomach upset and excessive belching if properly purified. Nature Made is excessively fishy when you smell it, suggesting oxidation. We've had repeated (dozens) of patients who have experienced difficulties with this brand. Rather than dealing with the frustrating gobbledy-gook of this company, just avoid their products.

What to Eat: The diet is defined by small LDL

9. April 2010 William Davis (15)

I approach diet from the perspective of small LDL particles.

Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)

Small LDL particles are:
--More likely to persist in the bloodstream longer than large LDL particles.
--More likely to adhere to components of atherosclerotic plaque.
--More likely to gain entry to plaque.
--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque.
--More likely to be oxidized.
--More likely to be glycated (8-fold more likely than large)

To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging.

So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.

Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely.

So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:

1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation.
2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose.

Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.

Is it or isn't it vitamin D?

7. April 2010 William Davis (63)

Jackie takes 10,000 units of vitamin D(3) per day as a gelcap.

Her starting 25-hydroxy vitamin D blood level was 18.1 ng/ml. Severe deficiency, no surprise.

On her 10,000 units per day, Vitamin Shoppe brand, her 25-hydroxy vitamin D level was 76.2 ng/ml--perfect. It stayed in this range for about two years.

She then changed to the Nature Made brand gelcaps she picked up at Walgreen's. Repeat 25-hydroxy vitamin D level: 23 ng/ml.

This has now happened with five different people, all taking the Nature Made brand.

If you are taking this brand of vitamin D, please be on the alert. You might consider a 25-hydroxy vitamin D blood level to be sure it actually has the vitamin D it's supposed to have.

Or, change brands.

What to eat: Part I

6. April 2010 William Davis (0)

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

4. April 2010 William Davis (16)

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

4. April 2010 William Davis (0)

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

3. April 2010 William Davis (1)

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.

The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

All posts by william-davis

Be patient with niacin

19. January 2007 William Davis (0)

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

18. January 2007 William Davis (6)

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

17. January 2007 William Davis (1)

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

16. January 2007 William Davis (0)

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)

Some recent samples:

Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.

Heart attack kills groom at reception

A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.

Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.

Heart-attack victim to return to Hamburg stage

Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.

That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.

Watch your weight plummet:Be a super vegetarian

14. January 2007 William Davis (0)

Here's a neat trick for losing weight: Become a strict vegetarian for 3 days.

Before you yawn or say "Yecchhhh!", let me elaborate.

Pick some time period. It doesn't have to be 3 days. It could be 2 days, or 5 days, or two weeks. But, for the period you choose, eat only vegetables. No meat, cereals, breads, milk, cookies, etc.

Vegetables alone could get monotonous, so make them interesting. Possibilities include:

--Hummus--add a little bit of olive-oil, chopped garlic, paprika, red pepper.

--Tabouleh--I get mine from Trader Joe's and it's delicious.

--Salsa--Low in calories, rich in lycopene and other flavonoids, with no nutritional downside. Also, pico de gallo--chopped tomatoes, onions, jalapeno chiles, cilantro, cucumbers.

--Mustards--hot, yellow, brown, spicy, gourmet, horseradish, etc.

--Cocktail sauce--i.e., ketchup and horseradish. Use the low-carb ketchup made without high fructose corn syrup.

--Tapenades--e.g., olive tapenade made with chopped olives, capers, and olive oil.
--Pesto-made with basil, garlic, and olive oil.

--Spices and herbs--basil, arugula, peppers, mustard powder, garlic, cilantro, ginger, etc.

--Vinegars--wine, Balsamic, rice, apple cider.

--Infused olive oils--infused with garlic is especially delicious,e.g., added to hummus.

--Bean dips--white bean dip, roasted bean dip, etc.

With the varieties of ways to jazz up your vegetables, you couldn't possibly be bored.

For example, for breakfast on day 1, eat sliced cucumbers and green peppers dipped in garlic-infused olive oil hummus and a handful of almonds. For a snack, some walnuts, sunflower seeds, sliced zucchini dipped in salsa. For lunch, a salad with an olive oil and balsamic vinegar dressing. For dinner, tablouleh, a cucumber and tomato salad, celery sticks dipped in pico de gallo.

All vegetables can be eaten without restricting portion size, since calorie content of vegetables are so low compared to other calorie-dense foods. (See The Heart Scan Blog from a few days back, "One bit or many mouthfuls?" at http://heartscanblog.blogspot.com/2007/01/one-bite-or-many-mouthfuls.html.)

This approach works nearly as well as fasting. A half-pound per day weight loss or more is common and painless. You'll also feel great living on low glycemic index foods.

(Photos courtesy Wikipedia.)

Dr. Agatston to the rescue

12. January 2007 William Davis (0)

Dr. Arthur Agatston, author of wildly successful South Beach Diet, has just released a new book titled The South Beach Heart Program. Dr. Agatston has started on a media speaking circuit to promote his book and concepts.

A reporter from Time, who interviewed Dr. Agatston, commented:

". . .not enough doctors prescribe niacin for their heart patients, even though the medicine is a proven treatment for raising 'good' cholesterol. Physicians are reluctant, Agatston suggests, because niacin requires diligent follow-up to watch for side effects, taking time that most primary-care practices cannot afford. On the other hand, he says, too many doctors are performing heart operations that represent a financial windfall for hospitals. Bottom line: there isn't as much money to be made in prevention as in treatment."

Amen.

Dr. Agatston echoes many of the concepts that the Track Your Plaque program advocates. His notoriety is going to help disseminate the idea that 1) CT heart scans are the #1 method to identify hidden atherosclerotic coronary plaque, 2) taking control of your heart scan score is the best way to seize hold of your future, and 3) the present-day popularity of heart procedures like stents and bypass is intolerable, inexcusable, and needs to be reined back.

Agatston also brings great credibility and fairness to the conversation and his comments will gain tremendous attention in the press and with the public.

When is a vitamin not a vitamin?

12. January 2007 William Davis (0)

When it's a hormone.

That's the stand that several researchers in vitamin D have taken and I think they're right. Dr. John Cannell has made a fuss over this in his www.vitamindcouncil.com website.

Structurally, vitamin D is most closely related to testosterone, estrogen, and cortisol. You wouldn't call testosterone vitamin T, would you?

Vitamins are also meant to be obtained from food. Yes, vitamin D is in milk but only because humans are required to put it there to prevent childhood rickets. Otherwise, the only substantial food source of vitamin D is in oily fish like salmon and then only a modest quantity.

Vitamin D is cholecalciferol, a hormone. Deficiencies of hormones can have catastrophic consequences. Imagine that every winter your thyroid gland shuts down and produced no thyroid hormone. You'd get very ill, gain 30 lbs, lose your hair, feel awful.

That's what happens when you're sun deprived and thereby deficient in cholecalciferol--you're deficient in a hormone. And it happens to most of us every year for many months.

I continue to witness spectacular effects by bringing 25-OH-vitamin D3 blood levels to 50 ng/ml with supplementation, including an apparent surge in success dropping heart scan scores.

An epidemic of heart disease reversal

10. January 2007 William Davis (3)

Heart disease reversal is nothing new in my office. However, I have to admit that it's not something that generally happens each and every day.

As our approach is refined, we are witnessing an unprecedented frequency of plaque reversal. Since Monday (today is Tuesday), I've seen four people who have regressed their coronary plaque and dropped their heart scan score.

Pat was the most recent addition to this list. At age 53, I was honestly surprised at the ease of dropping her heart scan score from 128 to 42 in the space of a year. I was surprised because among her lipoprotein patterns was the dreaded combination of lipoprotein(a) and small LDL, probably the most aggressive risk for heart disease I know of and also among the most difficult to gain control over. She also suffered a deep personal tragedy in her family, an emotional convulsion that can sometimes wipe out any hope of plaque reversal.

I'm hopeful that this virtual epidemic of heart disease reversal continues. And I hope that you participate in it.

Second heart scan and heart attack risk

9. January 2007 William Davis (0)

At first, Joe felt disappointed, defeated, and frightened. After his heart scan, a radiologist at the center told him that his score of 264 was moderately high. He told Joe that he was at moderate risk for heart attack and that a nuclear stress test was going to be required.

This left Joe feeling confused. After all he'd had a heart scan 18 months earlier and his score was 278, 5% higher.

I reassured Joe that the radiologist had not been aware that Joe had a prior heart scan. The radiologist didn't know that Joe's heart scan score had actually been reduced.

In fact, Joe's risk for heart attack was not moderate--it is now very low, since his score was 5% lower. While growing plaque is active plaque, shrinking plaque is inactive plaque and thereby at far less risk for heart attack.

I wrote about this phemonenon in a previous Blog: When is a heart scan score of 400 better than 200? at http://heartscanblog.blogspot.com/2006_09_01_archive.html. When you've had more than one scan, the risk for heart attack suggested by the score takes a back seat to the rate of change of your score. In other words, even though Joe's score of 264 represented a moderate risk (of approximately 3% per year, roughly 30% over 10 years), this no longer held true, since it actually represented a 5% decrease over a previous score.

Joe's risk for heart attack is probably close to zero. ALWAYS view your second (or any subsequent) heart scan score in the context of your previous score, not in isolation.

Track Your Plaque newsletter subscribers: We will detail more of Joe's story in the coming January 2007 newsletter. If you'd like to read or subscribe to the newsletter, go to http://www.cureality.com/f_scanshow.asp.

Heart scan curiosities #5

8. January 2007 William Davis (1)

Despite the controversy over drug-coated stents, I maintain that the best stent is no stent at all.

Yes, there are indeed times when such things are necessary, but not with the frequency that they are implanted nowadays.

Another reason why stents are an undesirable phenemenon is that they muck up your heart scan. Take a look:

The long white object in the center is a stent in the left anterior descending artery of this 60 year old man. Just beyond the stent (at about 1 o'clock from the stent) is a plaque that could be scored. However, you can see that, with the presence of the stent, the bulk of this artery is no longer "scorable". If this man wishes to "track his plaque", he will have to be content with tracking only the circumflex and right coronary arteries, the other two arteries without stents.

The stainless steel or similar metallic materials of current stents simply prevent us from seeing through them for plaque scoring purposes. It's best if you can simply avoid getting one for this and other reasons.

Track Your Plaque Members: Watch for the upcoming editorial by our Heart Hawk on drug-eluting stents.

Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)

I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."

Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."

Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984

Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.

Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)

Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)

http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal

one-on-one video teleconferencing

to discuss your heart health issues.

You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil

Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.

The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)

The results of the latest Heart Scan Blog poll are in.

DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)

Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

28. November 2009 William Davis (13)

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)

Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.

Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.

This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)

In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.

Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.