Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

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

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

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

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

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

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


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

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

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

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

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

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

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

The relationship is especially compelling with schizophrenia:

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


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


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


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

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

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

Why?

Carbohydrates increase small LDL via a multistep process:

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

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

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


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

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

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

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

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

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


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

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


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

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


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


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

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

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

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

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

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

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

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

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

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

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

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

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

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

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

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

Needlessly increased healthcare costs
81 (50%)

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


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

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

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

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

What goes up can't come down

28. November 2009 William Davis (13)
According to conventional wisdom, heart scan scores cannot be reduced.

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

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

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

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

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

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

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


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

Davis W, Rockway S, Kwasny M.

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

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)
Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

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

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

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

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

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

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

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

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

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

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

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



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

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

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

More of Gretchen's thoughts can be found at:

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

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

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

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

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

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

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

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

Addictive Foods

25. June 2007 William Davis (3)
Kraft Foods, Inc. is manufacturer of Kool Aid, Oscar Mayer, Kraft Macaroni and Cheese, Velveeta, Honey Maid Grahams, and hundreds of other processed food products. Post cereals also falls under the umbrella of Kraft with products like Raisin Bran, Post Toasties, and Fruity Pebbles. Annual revenues in 2006 for Kraft: $34.4 billion. A big operation with enormous influence over our eating habits.

Nabisco is manufacturer of Oreos, Ritz Crackers, Chips Ahoy and many others. Like Kraft/Post, it is also a big player.

While Nabisco was owned for several years by tobacco giant RJ Reynolds, in 2000 it was acquired by Philip Morris, another big tobacco manufacturer.

More recently in Spring, 2007, Philip Morris (now called Altria--you'd change your name, too, if it was synonymous with dirt) spun off its Kraft subsidiary for a big profit. However, the management structures remain intertwined.

In other words, despite the shuffling of shares, the two industries, big tobacco and big food, are in many respects one and the same.

Is it any surprise that the same industry that made billions of dollars pushing addictive nicotine products responsible for the deaths of hundreds of thousands of people is now intimately involved with addictive products produced and marketed by the processed food industry?

If you believe that food manufacturers are innocently and honestly conducting their businesses, simply think back to the testimony provided in front of Congress during the tobacco industry hearings. Broad deception, concealed truths, and outright lies were commonplace. There was no conscience involved. This was about money--and lots of it.

Why should the processed food industry, intimate with the tobacco industry, be any different?

If you want control over heart disease and your heart scan score, buy produce and buy local. Spend your time in the produce aisle, not the cereal or chip aisle. Unprocessed food, unadorned by bright labels, cartoon animals, American Heart Association endorsements, that's what we should seek.

Heart Scan Curiosities #7

25. June 2007 William Davis (1)



Here's a situation that crops up once in a while, occurring in perhaps 2% of heart scans.

The white within the circled area represents calcium, and thereby atherosclerotic plaque, situated immediately at the "mouth", or opening, of the the right coronary artery. What is somewhat unusual is that this plaque is not principally coronary, but aortic. That is, the plaque is mostly situated in the large vessel called the aorta. The three coronary arteries arise from the aorta.

In this instance, the aortic plaque involves the mouth of the right coronary artery. (In views not shown, the plaque also extends into the artery as well.) I call this a "double whammy" because the same plaque can post risk for heart attack and stroke.

Generally, aortic plaques pose risk for stroke. When aortic plaque fragments, little bits and pieces can travel upward to the brain and block an artery, thus a stroke.

In the coronaries, disrupted ("ruptured") plaques don't generally shower debris, but permit blood clot formation, resulting in heart attack.

This plaque, however, poses the theoretical risk of both heart attack and stroke because of its strategic location.

Should a plaque like this be handled any differently? I don't think so. But it does provide another reason to take atherosclerotic plaque in any artery seriously.

The nutrition counterculture

23. June 2007 William Davis (2)
When we look back over our American nutritional history over the last 50 years, it's hard not to come to the conclusion that much of the innovation in nutrition did not come from official agencies like the Food and Nutrition Board of the Institute of Medicine, the National Academy of Sciences, the FDA, the USDA, or the AMA.

Instead, it came from the popular culture. It came from bold, extravagant claims made by maverick figures like Ancel Keys, Nathan Pritikin, Dean Ornish, and Robert Atkins. Of course, some ideas have now fallen by the wayside, dismissed in a broad American "experiment" as ineffective, impractical, or kooky. But it permitted experimentation on an extraordinary scale with millions of people following a particular strategy at a time.

The advice of the official agencies tended to be reactionary. When nutritional deficiencies (remember those?) of the early 1900s were prevalent, they issued advice on food choices to help alleviate deficiencies. When deficiency transformed into excess after World War II, "smart" food choices from food groups and "sensible eating" became the theme.

Unfortunately, the advice was always adulterated by the enormous influence of various special interests, anxious to protect their national franchise. Powerful groups like the meat industry, wheat producers, and the dairy industry all made sure they had a big hand in crafting and influencing what was told to the American people.

The result: the advice offered by official groups has always represented the compromise of what some agency wished to convey to the people and the very powerful input of industry. What if the government decided to advise us what automobile to buy? Imagine the uproar in the auto industry when Washington tells us to buy Toyota for fuel economy and reliability. How long would that advice last?

That's why almost no knowledgeable adult follows the advice of the USDA, the National Academy of Sciences, or the Food Pyramid. I believe that we all intuitively recognize that the advice is watered-down, sometimes silly, sometimes downright unhealthy.

Nonetheless, the national experiment in diet that has taken place since 1950 has led to a collective wisdom of what is good and what is bad. The most productive conversations on nutrition therefore take place outside of the USDA and Washington. It occurs, instead, in places like bookstores, websites, and the media. Of course, there's lots of misinformation and profiteering in these sectors, as well. But like the enormous force unleashed by the collective wisdom of those contributing to the Wikipedia phemonenon, we've zig-zagged to something closer to the truth than ever uttered by an official agency.

Prescription vitamin D

23. June 2007 William Davis (32)
Niacin:

Over-the-counter: $2-5 per month
Prescription: $120 per month


Fish oil:

Over-the-counter: $3-6 per month
Prescription: $120 per month


Vitamin D:

Over-the-counter: $2 per month
Prescription: $70 per month



With vitamin D in particular, the prescription form is vastly inferior to the over-the-counter preparation. This is because the prescription form is ergocalciferol, or vitamin D2, not the effective human form, vitamin D3 or cholecalciferol.

When you're exposed to sun, what form of vitamin D is activated in the skin? It's all vitamin D3, no vitamin D2 whatsoever. Vitamin D3 is also far more effective than D2. People taking D3 (as long as it's oil-based) easily obtain healthy levels of vitamin D in the blood. People taking 50,000 units per day of D2 (the recommended quantity) remain miserably deficient, with minor increases in vitamin D blood levels. In short, D2 barely works at all. D3 works easily and effectively.

Moreover, D2 is the plant-based form. It is a form not found naturally in humans. D3 is the mammalian form, the same found in humans that exerts all its biologic benefits.

Then why is the prescription form of vitamin D2 (brand names Driscol and Calciferol) more expensive?

It's the same old pharmaceutical industry scam: Look for something patent protectable, regardless of whether it's superior to the non-patent protectable product, then sell it for exagerated profits. Though it is inferior and the science and clinical experience prove that it's inferior, you can still fool lots of people, including prescribing physicians. So what if you only make $50 or $100 million?

Don't fall for it. Prescription doesn't necessarily mean superior. In fact, the prescription form may be significantly inferior, as with vitamin D2. But the pharmaceutical industry carries such power and persuasion, who's going to know?

Nutrition activist Mike Adams

20. June 2007 William Davis (1)












I borrowed the above comic from the website of nutritionist, more properly nutrition activist and author, Mike Adams. His website, www.newstarget.com, was a pleasant surprise.

I was actually looking for some thoughts on pharmaceutical advertising and its pervasive and destructive effects and came across one of Adam's reports, Pharmaceutical television advertising is a grand hoax at http://www.newstarget.com/021526.html. The piece is a rant against the pharmaceutical industry's constant bombardment of the media, who have also been co-opted into their service, enticed by the enormous advertising revenues the drug industry brings.

But I was surprised to find an insightful, informative website on health issues, particularly healthy eating that rejects the manufactured food industry's intensive effort to persuade us to eat their products. While I don't agree with everything Adams has to say, his website provides some great food for thought. He also provides lots of downloadable information.

There's also some great laughs at his poke at the pharmaceutical industry with his Disease Mongering Engine at http://www.newstarget.com/disease-mongering-engine.asp, in which you get to create your own diseases. I got a real kick out of this.

CT scans and radiation exposure

19. June 2007 William Davis (8)


The NY Times ran an article called

With Rise in Radiation Exposure, Experts Urge Caution on Tests at

http://www.nytimes.com/2007/06/19/health/19cons.html?_r=1&adxnnl=1&oref=slogin&adxnnlx=1182254102-vQpytpx6W/Z9gvAaNPDZvA



“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”


Where do CT heart scans fall?

Let's first take a look at exposure measured for different sorts of tests:



Typical effective radiation dose values

Computed tomography Milliseverts (mSv)

Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv

Non-CT Milliseverts (mSv)

Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv

Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN


If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

A heart scan on a 16- or 64-slice multidetector device, your exposure is around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 chest x-rays or 20 mammograms. Now that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legimate medical questions. They are not screening tests to be applied broadly and used year after year.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.



Detail on radiation exposure with CT coronary angiograms on multidetector devices can be found at Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305-1310, one of several studies on this issue.

Mediterranean diet vs. American Heart Association Diet

18. June 2007 William Davis (4)
In 1994, the Lyon Heart Study demonstrated a 50-70% reduction in coronary events in participants who followed a diet rich in vegetables, olive oil, fish, nuts, red wine, and enjoyed meals as a family activity. Various other studies have documented similar phenomena with less metabolic syndrome, better lipid patterns, less obesity with the Mediterranean lifestyle.

There are two fundamental differences between the Mediterranean diet and the diet advocated by the American Heart Association (AHA) for people with heart disease: the Mediterranean diet uses olive oil more liberally, such that fat calories can reach 40% of total; and, unlike the AHA diet, processed foods are not a part of the Mediterranean diet. Greeks, for instance, are far less likely to eat Count Chocula cereal for breakfast, or snack on Healthy Choice Premium Caramel Swirl Sandwich (ice cream sandwiches) or Malt-O-Meal Honey Nut Scooters. All three of these foods on listed on the AHA Heart-Check Mark heart-healthy program.

In other words, remove all the processed foods, and the AHA diet pretty closely resembles the Mediterranean diet. There are differences but they tend to be relatively small. If the only major difference is the presence of processed foods, wouldn't you therefore expect the AHA to embrace the Mediterranean diet?

Here's what their official stand on the Mediterranean diet states:

Does a Mediterranean-style diet follow American Heart Association dietary recommendations?

Mediterranean-style diets are often close to our dietary recommendations, but they don’t follow them exactly. In general, the diets of Mediterranean peoples contain a relatively high percentage of calories from fat. This is thought to contribute to the increasing obesity in these countries, which is becoming a concern.



The AHA is actually lukewarm towards the diet that was the first to show a dramatic decrease in heart attack and death. Why?

The answer is obvious, once cast in this light. To wholeheartedly endorse the Mediterranean diet might be seen as an indirect rejection of American processed foods. You know, the foods that have caused an extraordinary and unprecedented epidemic of obesity in the U.S., the foods that are manufactured by ConAgra, General Mills, Kelloggs--all also major financial contributors to the AHA, according to the AHA Annual Report.

I tell my patients: If you want heart disease, follow the American Heart Association diet. In my view, it is a diet founded on politics and money, not on health. How else could Cocoa Puffs be regarded as heart healthy?

Track Your Plaque in 50,000 BC

16. June 2007 William Davis (3)
Imagine we could send you back in a time machine to 50,000 BC.

However, our agreement: no modern tools or equipment. Just your brain, hands, and legs. And your landing spot will be tropical or semi-tropical, the same climate that humans spent much of their evolutionary time in.

Not only might you rub elbows with contemporaries like homo erectus and neanderthalensis, you'd also have to fend for your life and survival.

To eat, you will have to chase and kill wild game, all with your bare hands or crude tools crafted from sticks and stones. You will have to learn what wild berries, roots, and plants are edible and distingusih them from those that make you retch, make your bowels run, or kill you. You won't be able to cultivate grain, at least for a good long time, since you don't have a community that makes such an undertaking easier.

Instead, you are constantly on the run, from the moment you awake until you finally settle back as the sun sets, hopefully with a full stomach, but often empty and growling, anticipating the hunt and forage of tomorrow.

You are outdoors all day, except for the period when you hide in your cave or self-made shelter. You wear what little clothing you can make yourself from your kills, a skin or two. Your skin becomes a dark brown, a 5 foot 10 inch male will weigh 140 lbs, a 5 foot 5 inch woman 95 lbs. There are obvious downsides: your teeth will rot, you will be prone to infections, and predators view you as fair game.

But the result will be that many chronic diseases of modern life will no longer be worries for you. Heart disease? Highly unlikely. Do you need vitamin D? No, because you are outdoors virtually all day with most of your body surface area exposed to sun. Omega-3 fatty acids? You get those from the wild game you eat, since they have higher omega-3 content feeding in the wild, not eating corn like modern livestock. Since your body fat is minimal, just enough for survival, you don't need niacin.

In other words, many of the strategies of the Track Your Plaque program are modern necessities, responses to the "deficiencies" of modern life. Of course, I don't really have a time machine. I also doubt that you wish to hunt wild game every day, forage for plants and roots, run nearly-naked in the sun. You probably also have become accustomed to brushing your teeth and not viewing every animal as a potential threat to your life.

Nonetheless, I find this an interesting exercise for understanding the role of all the tools we use in the Track Your Plaque program for plaque control.

When pessimism wins

15. June 2007 William Davis (3)
When I first met Hank, I immediately sensed it: anger, hostility, fear. His heart scan score of 685 just made it worse.


He didn't want to be there talking to me. His wife was giving him a hard time. Work was a constant source of irritation. The receptionist at the front desk screwed up his paperwork. Our office charges were too much.


In short, Hank was a pessimist. A bad one.


All the nutrition information out there is bunk. Only he knew how he should eat right. It's stupid to take a lot of fish oil. "You want me to grow gills?"


Among the parameters we use in the Track Your Plaque program is blood pressure during exercise, which provides a surrogate measure of blood pressure during emotional stress, anxiety, etc. "No, I don't need that. I already exercise." No amount of justification could change his mind. "A guy at work had a stress test. They said everything was fine, then Bang! He drops dead. What good is that?"


Hank did go along with a few pieces of advice.


A repeat heart scan 12 months after the first: 870, a 27% per year rate of increase. That's about what would happen if Hank had done nothing, had taken no action to try and stop or reduce his heart scan score.


I don't know if Hank will ever succeed in dropping his score. In fact, I suspect that he will fail, meaning that plaque will grow and he will eventually, perhaps in a year, two or three, require several stents, heart bypass, or have a heart attack. In other words, Hank's pessimism is a self-fulfilling phenomenon: If he believes he will fail, he will. If he believes the world is a rotten place, it is.


Is it possible to "cure" someone like Hank of his deeply-rooted pessimistic attitudes? I don't know of any easy solutions for someone with attitudes as deeply-ingrained as Hank's. (See my prior post, "Cure for pessimism?" at http://heartscanblog.blogspot.com/2007_05_01_archive.html.)

I believe it does help to make someone aware of their attitudes and that it does indeed exert ill health-effects--if they will believe it. But this is a very tough nut to crack.

Bad news on CoQ10?

13. June 2007 William Davis (8)
A review of the effects of Coenzyme Q10 (CoQ10) on the muscle aches and weakness (myopathy) of statin drug therapy was just published in the Journal of the American College of Cardiology.

(Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy. J Amer Coll Cardiol 2007;49(23):2231-2237.)

This is not a study, but a review of the existing scientific and clinical data available on this topic. The study authors conclude with a lukewarm statement:

". . .there is insufficient evidence to prove the etiologic [causal] role of CoQ10 deficiency in statin-associated myopathy and that large, well-designed clinical trials are required to address this issue. The routine use of CoQ10 cannot be recommended in statin-treated patients. Nevertheless, there are no known risks to this supplement and there is some anecdotal and preliminary trial evidence of its effectiveness. Consequently, CoQ10 can be tested in patients requiring statin treatment, who develop statin myalgia, and who cannot besatisfactorily treated with other agents. Some patients may respond, if only via placebo effect."

Should the media get hold of this report, be prepared for the usual "Nutritional supplement no help for drug toxicity" headlines, or "Yet another nutritional supplement shows no benefit" with parallels drawn to vitamin C or E.

There are several issue that need to be factored into the discussion:

1) This is not a study, just a review. Thus, any biases of the authors are more likely to exert themselves.

2) The understanding of CoQ10 absorption among different preparations may be an issue. I just received a mailing from Life Extension that made extravagant claims about the superior absorption of ubiquinol, to be distinguished from ubiquinone, the more common form. They claim that eight-fold increased absorption and blood levels of CoQ10 are achievable with ubiquinol. Unfortunately, virtually all the supportive data are unpublished, proprietary observations, i.e., generated by companies who make or sell it. This is as reliable as drug manufacturers who publish glowing reports on their own drugs--perhaps it's true, but it requires unbiased corroboration.

3) Despite the lack of a large, well-funded clinical trial (all are small), the issue continues to live and breathe because of the powerful anecdotal experience.

In our experience, CoQ10 does work. It doesn't work all of the time, perhaps just 80-90% of the time. It does generally require higher doses (100 mg per day, occasionally more). It very clearly must be an oil-based gelcap (just like vitamin D) to work; capsules containing powder do not work.

It's difficult to doubt when someone starts a statin drug, develops the muscle aches and weakness, begins CoQ10 and obtains distinct relief, stops CoQ10 and aches and weakness return, then only to go away again with resumption of CoQ10 . I've seen this countless times.

We do need better information on CoQ10. There's no doubt about it. For people who obtain benefit from statin therapy, I think CoQ10 remains a useful solution. A better solution would be to get rid of the offending drug. But that's not always possible--e.g., LDL cholesterol 190 mg/dl despite the best diet and "adjunctive" food effort. Then CoQ10 can be very useful.

And you thought gasoline was expensive

2. June 2009 William Davis (5)
In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

31. May 2009 William Davis (18)
Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.


Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

30. May 2009 William Davis (20)
Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

26. May 2009 William Davis (17)
What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

25. May 2009 William Davis (17)
Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

22. May 2009 William Davis (7)
I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Lipoprotein(a): 205 nmol/L


The atherogenicity, or plaque-causing potential, of this pattern was reflected in Ed's heart scan score of 2133.

You can readily see that, of this combination, only HDL cholesterol would be adequately identified through conventional lipid testing. Small LDL and lipoprotein(a) need to be specifically measured via lipoprotein testing.

And, contrary to the drug industry's "statin drugs for everybody" motto, this pattern, while improved with statin therapy, is not shut off.

Specific correction of each abnormality is required. For instance, niacin addresses all three: increases HDL, reduces small LDL, and (usually) reduces lipoprotein(a). A standard low-fat diet makes this pattern worse by reducing HDL, increasing small LDL, and (usually) increasing lipoprotein(a).

"You've got 10 minutes"

20. May 2009 William Davis (0)
There's a new trend in office healthcare in Milwaukee: Time-restricted office visits.



I'm told by several physicians who are employed by a major healthcare system here in town that they are peridically watched--physically watched by an administrator--to make sure that they do not exceed the allotted 10 minutes of time. My cardiologist colleagues, I gather, were at first incredulous at such intrusions into their practices, but apparently had no choice: They were employees.



Goiter, goiter everywhere

20. May 2009 William Davis (25)
The results of the recent Heart Scan Blog poll are in.

The question:

Do you used iodized salt?

The responses:

Yes, I use iodized salt every day
94 (28%)

Yes, I use iodized salt occasionally
56 (16%)

No, I do not use any iodized salt
41 (12%)

No, I use a non-iodized salt (sea salt, Kosher)
126 (37%)

No, I use a non- or low-sodium substitute
15 (4%)


Thanks for your responses.

If only 28% of people are regular users of iodized salt, that means that the remainder--72%--are at risk for iodine deficiency if they are not getting iodine from an alternative source, such as a multivitamin or multimineral.

Even the occasional users of salt can be at risk. The common perception is that occasional use is probably sufficient to provide iodine. This is probably not true and not just because of the lower quantity of ingestion. Occasional users of salt tend to have their salt canister on the shelf for extended periods. The iodine is then lost, since iodine is volatile. In fact, iodine is virtually undetectable four weeks after a package is opened.

In my office, now that I'm looking for them much more systematically and carefully, I am finding about 2 people with goiters every day. They are not the obvious grotesque goiters of the early 20th century (when quack therapies like the last post, the Golden Medical Discovery, were popular). The goiters I am detecting are small and spongy. Yesterday alone I found 5 people with goiters, one of them visible to the eye and very distressing to the patient.

It seems to me that iodine deficiency is more prevalent than I ever thought. It is also something that is so simple to remedy, though not by increasing salt intake. Kelp tablets--cheap, available--have been working quite well in the office population. My sense is that the Recommended Daily Allowance of 150 mcg per day for adults is low and that many benefit from greater quantities, e.g., 500 mcg. What is is the ideal dose? To my knowledge, nobody has yet generated that data.

Thyroid issues being relatively new to my thinking, I now find it incredible that endocrinologists and the American Thyroid Association are not broadcasting this problem at the top of their lungs. This issue needs to be brought to the top of everyone's attention, or else we'll have history repeating itself and have goiters and thyroid dysfunction galore.

For more on this topic, see the previous Heart Scan Blog post, "Help keep your family goiter free."

Goiter and the Golden Medical Discovery

17. May 2009 William Davis (19)

Thick neck, or goitre . . . consists of an enlargement of the thyroid gland, which lies over and on each side of the trachea, or windpipe, between the prominence known as "Adam's apple" and the breast bone. The tumor gradually increases in front and laterally, until it produces great deformity, and often interferes with respiration and the act of swallowing. From its pressure on the great blood vessels running to and from the head, there is a constant liability to engorgement of blood in the brain, and to apoplexy, epilepsy, etc.

The causes of the affection are not well understood. The use of snow water, or water impregnated with some particular saline or calcareous matter, has been assigned as a cause. It has also been attributed to the use of water in which there is not a trace of iron, iodine, or bromine. . . The disease is often due to an impeded circulation in the large veins of the neck, from pressure of the clothing, or from the head being bent forward, a position which is often seen in school children.


Treatment

We have obtained excellent results in many cases, not too far advanced, by a method of treatment which consists in the employment of electrolysis. . . Many cases at the present time are operated upon with entire success.

Those who are afflicted with this disease and unable to avail themselves of special treatment cannot do better than to take Doctor Pierce's Alterative Extract, or Golden Medical Discovery, and apply over the skin around the tumor, night and morning, the following, which may be prepared at any drug store:

Resublimed Iodine--One dram
Iodide of Potassium--Four drams
Soft Water--Three ounces 


Apply to the tumor, twice daily, with feather or camel hair pencil.


From The People's Common Sense Medical Adviser by R.V. Pierce, MD; 1918.

Magnesium and you-Part I

15. May 2009 William Davis (11)
If this were 10,000 B.C., you'd get your drinking water from streams, rivers, and lakes, all rich in mineral content. Humans became reliant on obtaining a considerable proportion of daily mineral needs from natural water sources.

21st century: We obtain drinking water from a spigot or plastic bottle. Pesticides and other chemicals seep into the water supply. Municipal water purification facilities have intensified water purification in most communities to remove contaminants like lead, pesticide residues, and nitrates. (For a really neat listing of the water quality of various cities, the University of Cincinnati makes this data available.)

But intensive water treatment also removes minerals like calcium and magnesium.

Many people have added water filters or purifiers to their homes,, like reverse osmosis and distillation, that are efficient at extracting any remaining minerals, converting “hard” into “soft” water. In fact, manufacturers of such devices boast of their power to yield pure water free of any “contaminant,” minerals like magnesium included. The magnesium content of water after passing through most commercial filters is zero.

Modern enthusiasm for bottled water has compounded the problem. Americans consumed a lot of bottled water, nearly 8 billion gallons last year. In the U.S., nearly all bottled water has little or no magnesium.

The result is that we can no longer rely on drinking water to provide magnesium. The Recommended Daily Allowance (RDA)—the amount required to prevent severe deficiency—for magnesium is 420 mg per day for men, 320 mg/day for women. In cities with the highest magnesium water content, only 30% of the RDA can be obtained by drinking two liters of tap water per day. In most cities, only a meager 10–20% of the daily requirement can be obtained. That leaves between 70–90% that needs to come from other sources. As a result, the average American ingests substantially less than the RDA.