No more Lovaza

30. July 2010 William Davis (45)
That's it: I will NEVER ever write another prescription for Lovaza.

I actually very rarely write a prescription for Lovaza, i.e., prescription fish oil. But this was the last straw.

I advised a patient that we've had good success using high-doses of fish oil to reduce lipoprotein(a), Lp(a). 6000 mg per day of the omega-3 component (EPA + DHA) from fish oil reduces Lp(a) in 60% of people after one year. (Recall that Lp(a) is the most aggressive known lipid-related cause of heart disease.)

The two preparations I generally suggest are either the very affordable Sam's Club Members Mark Triple-Strength Fish Oil with 900 mg EPA + DHA per capsule: 7 capsules per day. Another great product (my personal favorite because of its extreme purity--it doesn't even smell like fish oil): Pharmax Finest Pure Fish Oil with 1800 mg EPA + DHA per teaspoon: 3 to 3 1/2 teaspoons per day.

Both preparations work great and are quite affordable, given the high dose. For the Sam's Club preparation, it will cost around $30 per month, while the Pharmax liquid will run around $49 per month.

Well, the woman's husband insisted on a prescription for Lovaza. One Lovaza capsule contains 784 mg EPA + DHA per capsule: 7 to 8 capsules per day.

Here are some prices for Lovaza from online pharmacy discounters:
Prescription Giant: $78.99 for 30 capsules ($2.63 per capsule)
Planet Drugs Direct: $135 for 100 capsules ($1.35 per capsule)

These are lower than the prices I obtained in past by calling local pharmacies in my area, quite a bit lower, in fact.

Filling the Lovaza prescription at Prescription Giant will therefore cost $552.93 to $631.92 per month; at Planet Drugs Direct it will cost $283.50 to $324.00 per month. At local pharmacies, a similar 7 to 9 capsules Lovaza per day will cost upwards of $800 to $900 per month.

The patient's husband insisted on the Lovaza prescription because he knew that his insurance would cover it. When I pointed out that this was a large cost that would have to be borne by others in their healthcare premiums, he said that didn't matter to him.

I hesitated, but ended up writing the prescription for 7 Lovaza capsules per day. As soon as I handed to him, I regretted it. In fact, I am embarassed and angry at myself for having given in.

So I vowed: I will NEVER EVER write another prescription for Lovaza.

I do not believe that we should spread the excessive profiteering of the pharmaceutical industry around on the backs of people who pay their healthcare insurance premiums, just so that a few people, like this selfish couple, can save a few dollars a month.

This is your brain on wheat II

29. July 2010 William Davis (24)
In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia.

These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.)

There's another way that wheat can affect the brain and nervous system: immune-activated damage.

This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies.

The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.

Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.

There's no such thing as a "no-carb" diet

27. July 2010 William Davis (24)
When I tell patients how I advise a wheat-free, cornstarch-free, sugar-free diet on the background of a low-carbohydrate diet, some people ask: "But can I live on a no-carb diet?"

Well, there's no such thing as a "no-carb" diet. Low-carb, yes. No-carb, no.

Here are the carbohydrate contents of various "low-carb" foods:

Gouda cheese--3 oz contains 1.65 grams carbohydrates
Mozzarella cheese--1 cup contains 2.89 grams carbohydrates
Walnuts--4 oz (56 nuts) contains 2.96 grams carbohydrates
Almonds--4 oz contains 1.38 grams carbohydrates
Sour cream--one-half cup contains 3.31 grams carbohydrates
Red wine--3.5 oz glass contains 2.69 grams carbohydrates
Eggplant--1 cup cooked contains 8.33 grams carbohydrates
Green pepper--1 medium-sized raw contains 5.52 grams carbohydrates
Cucumber--1 medium contains 4.34 grams carbohydrates
Tomato--1 medium contains 4.82 grams carbohydrates

(Nutrition data from USDA Nutrient Database)

In other words, foods thought to be "low-carb" actually contain a modest quantity of carbohydrates.

Such modest quantities of carbohydrates may not be enough to trip your blood sugar. But add up all the "low-carb" foods you consume over the course of a day and you can easily achieve 30 grams or more carbohydrates per day even without consuming any higher carbohydrate foods.

Why doesn't your doctor try to CURE diabetes?

21. July 2010 William Davis (88)
Imagine you have breast cancer. You go to your doctor and she says, "As your pain worsens, we'll help you with pain medication. We'll fit you with a special bra to accommodate the tumor as it grows. That's all we're going to do."

"What?" you ask. "You mean just deal with the disease and its complications, but you're not going to help me get rid of it . . . cure it?"

It would be incredibly shocking to receive such advice. Then why is that the sort of advice given when you are diagnosed with diabetes?

Say you go to the doctor. Lab values show a fasting blood sugar of 156 mg/dl, HbA1c (a reflection of your previous 60 days average glucose) of 7.1%. Both values show clear-cut diabetes.

Your doctor advises you to 1) start the drug metformin, then 2) talk to the diabetic teaching nurse or dietitian about an American Diabetes Association (ADA) diet.

The ADA diet prescribed encourages you to increase carbohydrates and cut fats at each meal and maintain a consistent intake so that you don't experience hypoglycemic (low blood sugar) episodes. You follow the diet, which causes you to gain 10-15 lbs per year, increasing your "need" for diabetes medication. You doctor adds Actos, then Januvia, then injections of Byetta.

Three years and 34 lbs later, you are not responding well to the drug combination with blood sugars rarely staying below 200 mg/dl. You've developed protein in your urine ("proteinuria"), lost 30% of your kidney function, and you are starting to lose sensation in your feet. So the doctor replaces some of your medication with several insulin injections per day.

This formula is followed millions of times per year in the U.S. So where along the way did your doctor mention anything about a "cure"?

Adult diabetes is the one chronic disease that nobody cares to cure. Treat it, maintain control over blood sugars, but cure it? Most physicians say it's impossible.

The tragedy is that diabetes is a curable condition. I've seen it happen many times. Physicians dedicated to curing diabetes like low-carb expert, Dr. Mary Vernon, have cured it countless times. Dr. Eric Westman and colleagues have been building the case for the carbohydrate-restricted cure for diabetes with studies such as this. In this last study, of the 8 participants on insulin + medications at the start of the study, 5 no longer required medications at the close of the study--they were essentially non-diabetic.

I tell patients that diabetes, in fact, is a disease you choose to have or not to have--provided you are provided the right diet and tools. Sadly, rarely are diabetics told about the right diet and tools.

That's why Cadbury Schweppes has been a major contributor to the American Diabetes Association, as are other processed food manufacturers and the drug industry, all who stand to profit from maintaining the status quo.

The cure? Eliminate or at least dramatically reduce carbohydrates, the foods that increase blood sugar.

Note: If you have diabetes and you are taking any prescription agents, such as glyburide, glipizide, insulin, and some others, you will need to discuss how to manage your medications if you reduce carbohydrates. The problem is finding a doctor or other resource to help you do this.

LDL pattern B

18. July 2010 William Davis (17)
Here's a Q&A I stumbled on in the Forum of MedHelp, where people obtain answers from presumed health "experts."

Question:

My VAP test results in July 07 identified an LDL Pattern B.
Overall results:
Total 150
HDL 75
LDL 61
Trig 60
HDL-2 17
LP(a) 6.0
LDL Pattern B

Medications:
Lipitor 10mg
Zetia 10mg
Altace 10mg
Atenolol 50mg
Plavix 75mg
Aspirin 81mg

I had several heart attacks which resulted in CABG performed May 2000. I am a 53 year old white male , 6'1", 190 pounds, exercise every day, watch my diet and feel great. Everything looks OK except my LDL Pattern B. Is there any therapy to improve the Patten B?

Answer from CCF, MD:
Your results indicate an LDL pattern B, which generally indicates small atherogenic LDL particles which may cause increased risk for CAD. However, there are several problems with LDL patterning: 1) its unreliability (of LDL pattern testing ), 2) unclear clinical evidence regarding regarding the usefulness of LDL patterns and particle size. The majority of evidence regarding the progression of atherosclerosis is with LDL lowering and to an smaller extent HDL raising.

All available clinical evidence shows that any particles in the VLDL, IDL, or LDL range are atherogenic, and there is no evidence that whether belonging to pattern A or B one is more atherogenic than others.

Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents.
Thus, current data on LDL subclasses are at best incomplete and at worst misleading, suffering from publication bias, and now given the recent results of the Ensign et al. study, unreliable.

Your LDL, and HDL are at goal. The Lpa level is still not clearly linked as a modifiable risk factor for CAD, although elevated levels are now know to be linked to stroke.

Continue with your present treatments: aspirin, plavix, ateonol and altace are all essential medications.


Wow. The extent of ignorance that pervades the ranks of my colleagues is frightening.

Contrary to the response, LDL particle size assays are quite reliable and accurate. I've performed many thousands of lipoprotein assays and they yield reproducible and clinically believable results. For example, eliminate wheat, oats, cornstarch, and sugars and small LDL drops from 2400 nmol/L to 893 nmol/L (NMR)--huge drops. If repeated within a short period of time, the second measure will correspond quite closely.

The data are also quite clear: Small LDL particles (i.e., "pattern B") are a potent predictor of cardiovascular events. What we lack are the treatment trials that show that reduction of small LDL results in reduced cardiovascular events. The reason for this is that small LDL research is not well-funded, since there is no prescription drug to treat small LDL, only nutritional means. Niacin (as Niaspan) is as close as it comes for a "drug" to reduce small LDL. But diet is far more effective.

Given the questioner's fairly favorable BMI of 25.1 and his history of aggressive heart disease, it is virtually certain that he has what I call "genetic small LDL," i.e., small LDL that occur on a genetically-determined basis (likely due to variants of the cholesteryl-ester transfer protein, or CETP, or of hepatic lipase and others).

Ignoring this man's small LDL will, without a doubt, consign him to a future of more heart attacks, stents, and bypass. Maybe by that time the data supporting the treatment of small LDL will become available.

What increases blood sugar more than wheat?

15. July 2010 William Davis (38)
Take a look at these glycemic indexes (GI):


White bread 69
Whole wheat bread 72
Sucrose 59
Mars bar 68
White rice 72
Brown rice 66


I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.

With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:


Kidney beans 29
Chick peas 36
Apple 39
Ice cream 36
Snickers Bar 40


Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food.

While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list.

Take a look at this list:

Cornflakes 80
Rice cakes 80
Rice Krispies 82
Rice pasta, 92
Instant potatoes 83
Tapioca 81



Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100.

Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.

So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.

China fiction?

10. July 2010 William Davis (39)
Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk.

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

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

Her comments on the relationship of wheat to heart disease:

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

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

Carbohydrate-LDL double whammy

9. July 2010 William Davis (14)
Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles.

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

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

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

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

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


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

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

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

To lose weight, prick your finger

8. July 2010 William Davis (45)
We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day.

So how can you stop triggering insulin?

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

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

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

To do this, you will need:

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

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

Iodine update

2. July 2010 William Davis (30)
As the iodine experience grows, I've made several unique observations.

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

Among the phenomena I've observed:

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

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

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

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

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

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

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


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

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

Why do the Japanese have less heart disease?

24. April 2011 William Davis (49)
We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

20. April 2011 William Davis (52)
Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0

18. April 2011 William Davis (0)

Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

12. April 2011 William Davis (67)
Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

9. April 2011 William Davis (30)
In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

7. April 2011 William Davis (37)
Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

7. April 2011 William Davis (17)
I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

5. April 2011 William Davis (0)
Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

4. April 2011 William Davis (5)
The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

3. April 2011 William Davis (13)
While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.

Green coffee bean extract in AGF Factor I

7. June 2012 William Davis (16)
Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

Endogenous glycation, discussed at length in a recent Track Your Plaque Special Report, makes LDL particles (especially small LDL particles) more prone to oxidation and thereby more atherogenic, i.e., more likely to contribute to atherosclerotic plaque. Endogenous glycation also exerts unhealthy effects on long-lived proteins in the body, such as the proteins in the lenses of your eyes (cataracts), the lining of arteries (hypertension), and the cartilage cells of joints (brittle cartilage and arthritis).

Endogenous glycation is reduced by slashing carbohydrates in the diet, especially the most offensive carbohydrates of all, the amylopectin A of wheat, sucrose, high-fructose corn syrup and other fructose sources. Endogenous glycation can also be blocked by using blockers of the glycation reaction, such as benfotiamine (lipid-soluble thiamine), pyridoxal-5'-phosphate (a form of vitamin B6 with greater glycation blocking effect), and chlorogenic acid from green coffee beans, all components of AGF Factor I, which also contains Portulaca oleracea (Portusana), or purslane, for reduction of glucose.

Green coffee bean extract, and thereby chlorogenic acid, is receiving increased attention, most recently due to a study demonstrating substantial weight loss with 750-1050 mg green coffee bean extract, providing approximately 325-500 mg chlorogenic acid per day. Participants lost 15.4 pounds over 8 weeks at the higher dose (500 mg chlorogenic acid per day), while participants lost 8.8 pounds over 8 weeks at the lower dose (325 mg chlorogenic acid per day).

AGF Factor I was not formulated for weight loss but, taken twice or three times per day, does indeed mimic the dose of chlorogenic acid from green coffee bean extract used in the weight loss study. If you wish to take advantage of this application of chlorogenic acid/green coffee bean extract, while also maximizing protection from endogenous glycation, our AGF Factor I is one excellent choice to do so.

Lessons learned from the 2012 Low-carb Cruise

14. May 2012 William Davis (13)
I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.

The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!

Among the most important lessons provided:

Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.

Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."

Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.

Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.

Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.

Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.

Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.

Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.

All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!

Chili Sesame Crackers

3. May 2012 William Davis (0)
Looking for something hot and crunchy?

These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.

This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.

For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.

Makes approximately 30 chips

2 cups raw sesame seeds
1 cup shredded Parmesan cheese
2 tablespoons extra-virgin olive oil
1 tablespoon chili powder
½ teaspoon cayenne pepper
2 teaspoons onion powder
1 teaspoon garlic powder
1 teaspoon dry mustard
1 teaspoon sea salt
1 teaspoon Tabasco sauce
1¼ cups water

Preheat oven to 350º F.

In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.

Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.

Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.

Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.

Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.

Remove and allow to cool. Cut with pizza cutter to desired size.

Opiate of the masses

18. April 2012 William Davis (22)
Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:

Modern wheat is an opiate.

And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive.

Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone.

But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry.

This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant.

Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat.

Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:

"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."

In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.

Jelly beans and ice cream

23. March 2012 William Davis (6)
What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."

That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?

Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:

1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation).

2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.

3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.

I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:

rice starch, tapioca starch, potato starch, and cornstarch?

These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.

The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.

So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.

This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!

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

Low thyroid: What to do?

8. February 2009 William Davis (25)
I've gotten a number of requests for solutions on how to solve the low thyroid issue if either 1) your doctor refuses to discuss the issue or denies it is present, or 2) there are government mandates against thyroid correction unless certain (outdated) targets are met.

Oh, boy.

While I'm not encouraging anyone to break the laws or regulations of their country (and it's impossible to generalize, with readers of this blog originating from over 30 countries), here are some simple steps to consider that might help you in your quest to correct hypothyroidism:

--Measure your body temperature--First thing in the morning either while lying in bed or go to the bathroom and measure your oral temp. Record it and, if it is consistently lower than 97.0 degrees (Fahrenheit), show it to your doctor. This may help persuade him/her.(You can still be hypothyroid with higher temperatures, but if low temperatures are present, it is simply more persuasive evidence in favor of treatment).

--Supplement with iodine 150 mcg per day to be sure you are not iodine deficient. This is becoming more common in the U.S. as people avoid iodized salt. It is quite common outside the U.S. An easy, inexpensive preparation is kelp tablets.

--Show your doctor a recent crucial study: The HUNT Study that suggests that cardiovascular mortality begins to increase at a TSH of only 1.5 or greater, not the 5.5 mIU usually used by laboratories and doctors.

--Ask people around you whether they are aware of a health practitioner who might be willing to work with you, or at least have an open mind (sadly, an uncommon commodity).

Also, see thyroid advocate and prolific author, Mary Shomon's advice on how to find a doctor willing to work with you. Yes, they are out there, but you may have to ask a lot of friends and acquaintances, or meet and fire a lot of docs. It shouldn't be this way, but it is. It will change through public pressure and education, but not by next week.

Another helpful discussion from Mary Shomon: The TSH Normal Range: Why is there still controversy? You will read that even the endocrinologists (a peculiarly contentious group) seethingly debate what constitutes normal vs. low thyroid function.

Also, you might remind a resistant health practitioner that guidelines are guidelines--they are not laws that restrain anyone. They are simply meant to represent broad population guidelines that do not take your personal health situation into consideration.

Which statin drug is best?

8. February 2009 William Davis (7)
I re-post a Heart Scan Blog post from one year ago, answering the question: Which statin drug is best?

I still get this question from patients in the office and online, nearly always prompted by a TV commercial. So let me re-express my thoughts from a year ago, which have not changed on this issue.


The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.

Dr. Nancy Sniderman, heart scans on Today Show

5. February 2009 William Davis (6)
While shaving this morning, I caught the report by NBC medical expert, Dr. Nancy Sniderman, about her coronary plaque and CT coronary angiogram.

Visit msnbc.com for Breaking News, World News, and News about the Economy




Those of you in the Track Your Plaque program or who follow The Heart Scan Blog know that we should tell Dr. Sniderman and her doctor that:

She has done virtually nothing that will stop an increasing heart scan score! In fact, Dr. Sniderman is now following the "prevention program" that is eerily reminiscent of Tim Russert's program! We all know how that turned out.

It is pure folly to believe that a combination of Lipitor, exercise, and a "healthy diet" (usually meaning a low-fat diet--yes, the diet that promotes heart disease) will stop the otherwise relentless increase in heart scan score.

Dr. Sniderman, please consider:

1) Having the real causes of your coronary plaque identified. (It is highly unlikely to be just LDL cholesterol, though the drug industry is thrilled that you believe this.)

2) Ask yourself (or, if your doctor knew what she was doing, ask her): Why do I have heart disease? LDL cholesterol is insufficient reason--virtually nobody I know has high LDL cholesterol as the sole cause. LDL cholesterol is, at most, one reason among many others, but is insufficient as a sole cause.

3) What is your vitamin D status? Crucial!

4) What is your thyroid status?

5) Fish oil--a must!

6) Do you have lipoprotein(a)? Small LDL?

Just addressing the items on the above checklist would put you on a far more confident path to stop your heart scan score from increasing.

If you were to repeat your heart scan score, my prediction: Your score will be higher by 18-24% per year.

My personal experience with low thyroid

3. February 2009 William Davis (31)
Something happened to me around October-November of last year.

I usually feel great. Ordinarily, my struggles are sleeping and relaxing. As with most people, I have too many projects on my schedule, though I find my activities stimulating and fascinating.

I blasted through a very demanding November, trying to meet the needs of a book publisher. This involved sleeping only a few hours a night for several days on end, all after a full day of office practice and hospital duties.

But it was getting tougher. My concentration was becoming more fragmented. Getting things done was proving an elusive goal. Exercise became a real chore.

Although I usually force myself to go to sleep, I was starting to fall asleep before my usual bedtime, and I was sleeping longer than usual.

It's been a tough winter in Wisconsin. Let's face it: It's Wisconsin. But it's been tough even for this region, with weeks of temperatures consistently below 10 degrees. Even so, I was having a heck of a time keeping warm. Extra shirts, socks, soaking my hands in hot water--none of it worked and I was freezing.

So I had my thyroid values checked:

Free T3: 2.6 pg/ml (Ref 2.3-4.2)
Free T4: 1.20 ng/dl (Ref 0.89-1.76)
TSH: 1.528 uUI/ml (Ref 0.350-5.500)

Normal by virtually all standards. I measured my first morning oral temperature: 96.1, 96.3, 95.9. Hmmmm.

My experience coincided with the Track Your Plaque and Heart Scan Blog conversations about low thyroid being enormously underappreciated, with the newest data on thyroid disease suggesting that a TSH for ideal health is probably 1.5 mIU or less. (More about that: Is normal TSH too high? and Thyroid perspective update .

Could this simply be a case of medical student-oma in which every beginning medical student believes he has every disease he learns about?

Despite the apparently "normal" thyroid blood tests, I took the leap and started taking Armour thyroid, beginning at 1/2 grain (30 mg), increasing to 1 grain (60 mg) after the first week.

Within 10 days, I experienced:

--Dramatic restoration of the ability to concentrate
--A boost in mood. (In fact, the last few blog posts before I replaced thyroid reflect my deepening crabbiness.)
--Large increase in energy, now restored to old levels
--Need for less sleep
--I'm warm again! (It's still <20 degrees, but I get easily stay warm while indoors.)

I am absolutely, positively convinced of the power of thyroid. I am further convinced from the clinical data, patient experiences, and now my own personal experience, that low levels of hypothyroidism are being dramatically underappreciated and underdiagnosed.

I shudder to think of what my life would have been like 6 months or a year from now without correction of thyroid hormone.

Now, the tough question: Why the heck is this happening to so many people?

Speaking availability

3. February 2009 William Davis (5)
Just a quick announcement:

If you would like to hear more about the concepts articulated in The Heart Scan Blog or in the Track Your Plaque program, I am available to speak to your group.

Among the possible topics:

Return to the Wild: Natural Nutritional Supplements That Supercharge Health
Why this apparent "need" for fish oil and other heart-healthy supplements? I discuss why some nutritional supplements make perfect sense when we are viewed in the context of primitive humans living modern lives, while other supplements do little.


Shrink Your Tummy . . .or, Why Your Dietitian is Fat!
Weight loss doesn't have to involve calorie counting, deprivation, or hunger pangs. But the conventional "rules" for weight loss and health have to be broken.

The Politically Incorrect Guide to Extraordinary Heart Health
Heart health is something that you can seize control over, something identifiable, correctable, and . . . reversible. Much of this can be achieved with little or no medication, nor procedures. I detail all the enormously empowering lessons learned through the Track Your Plaque program.


I can also present in-depth yet entertaining discussions on the power of vitamin D, natural cholesterol control, screening for heart disease, and similar topics covered in the blog.

To learn more, just e-mail us at contact@trackyourplaque, or call my office at 414-456-1123.

Learn how to eat from Survivorman

31. January 2009 William Davis (22)

Look no farther than Discovery Channel to learn how humans were meant to eat.

The Survivorman show documents the (self-filmed) 7-day adventures of Les Stroud, who is dropped into various remote corners of the world to survive on little but ingenuity and will to live. Starting without food or water, the Survivorman scrapes and scrambles in the wilderness for essentials to survive in habitats as far ranging as the Ecuadorian rainforest to sub-arctic Labrador.

What does Survivorman have to do with your nutrition habits?

Everything. The lessons we can learn by watching this TV show are plenty.

Survivorman plays out the life we are supposed to be living: slaughtering wild game with simple handmade tools and his bare hands, identifying plants and berries that are safe to eat, trapping fish, scavenging the kill of other predators. He's even resorted to eating bugs and caterpillars, particularly following several days of unsuccessful hunting and scavenging.

What is notable from the Survivorman experience is what is absent: In the steppe, desert, tundra, or jungle, you will not find bread, fruit drinks, or Cheerios. You won't find farm-fattened, corn-fed livestock with meat marbled with fat.

Imagine the result of such an experience for us, drawn out over 6 months. Even an obese, diabetic, gluttonous, XXX dress size 350-lb woman would return a lean 105 lbs, size 0, non-diabetic, fully able to run miles in the wild tracking game.

Survivorman's quiet desperation of living in the wild, preoccupied with worries over where his next meal might be found, is a stark contrast to the bloated, shelves stacked floor-to-ceiling supermarkets, and our modern society's all-you-can-eat several times per day lifestyle.

Am I advocating selling the car and house and chucking modern society for the "safety" of the jungles of Borneo?

No, of course not. I am advocating taking a lesson from the clever experiment conducted by Mr. Stroud, a return-to-the-wild experience that should teach us something about how perverse our modern nutritional lives have become.

CIS: Carbohydrate intolerance syndrome

28. January 2009 William Davis (28)
Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl
BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl


In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.

Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.

CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.

The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)

The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.

Making sense out of lipid changes

27. January 2009 William Davis (9)
Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:

Total cholesterol: 149 mg/dl
LDL cholesterol: 67 mg/dl
HDL cholesterol: 73 mg/dl
Triglycerides: 43 mg/dl

The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.

Maggie returned to the office 6 pounds heavier with these values:

Total cholesterol: 210 mg/dl
LDL cholesterol: 124 mg/dl
HDL cholesterol: 57 mg/dl
Triglycerides: 144 mg/dl

In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.

What happened?

At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.

Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:

--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood.
--Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.
--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.

The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.

I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.

How to Give Yourself Hashimoto's Thyroiditis: 101

25. January 2009 William Davis (18)
I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog.


How to Give Yourself Hashimoto's Thyroiditis: 101

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)


If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.


We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.

Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.

I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?

I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.

Framing

24. January 2009 William Davis (0)
Heart health without a 12" incision



Heart health for less than $44,483 (Cost of a coronary stent according to the American Heart Association 2008 Update)



Track Your Plaque: A drug-free zone