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.

Cureality | Real People Seeking Real Cures

Blast triglycerides

15. May 2009 William Davis (0)

The conventional answers to high triglycerides levels are generally: low-fat diet, a fibrate drug (Tricor, Lopid), a statin drug, and--most recently--prescription fish oil.

This is the regimen to take if you want the drug industry to get even richer and more powerful than they already are. After all, what CEO of a pharmaceutical company can stand to have his salary and benefits slashed to below $200 million this year? It's outrageous!

If you really want to blast the heck out of your triglycerides and achieve numbers like 50 mg/dl, then the regimen to consider consists of:

--Elimination of sugars, wheat, and cornstarch
--Fish oil--Sam's Club would do fine at $8 for 350 capsules, or the high-potency at $14.99 for 180 capsules (at 680 mg EPA +DHA, nearly the same potency as prescription Lovaza at 842 mg)
--Vitamin D supplementation sufficient to achieve normal blood levels (60-70 ng/ml)

Those three strategies alone can reduce triglycerides far more than any drug combination. In fact, it is rare for someone with triglycerides as high as 900 mg/dl to not reduce them to the <100 mg/dl range.

Cheerios: Prescription required?

13. May 2009 William Davis (15)

Followers of The Heart Scan Blog know my feelings about Cheerios:

Can you say "sugar"?

Cheerios and heart health

There's an interesting tussle going on between the makers of Cheerios, General Mills, and the FDA.

The FDA says that the Cheerios' package claims of:

• "you can Lower Your Cholesterol 4% in 6 weeks"
• "Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is ... clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol."

constitute a medical claim, i.e., trying to promote Cheerios as a drug.

I'm glad that the FDA has come down on General Mills. But I find this entire episode laughable: The debate is over the purported health benefits of what I would regard as pure junk food, no better in my view than claiming that a cupcake has health benefits, or a carton of ice cream.

In my experience, Cheerios does not 1) reduce risk for heart disease, nor 2) reduce cholesterol.

It does, however, cause blood sugar to skyrocket and increase the small type of LDL--you know, the type that causes heart disease.

"Placebos are frequently of value"

12. May 2009 William Davis (1)

The treatment of angina pectoris, generally speaking, is unsatisfactory.

Any procedure that relieves mental tension is valuable. Since patients suffer particularly during the winter, I encourage winter vacations in a southern climate.

I insist that obese patients lose weight, and have found small doses of benzedrine, 10 to 20 mg. daily, helpful in curbing the appetite.

I generally forbid smoking. This is a particularly disturbing task for many patients to carry out. In such cases, I suggest that 3 or 4 cigarettes be smoked daily, knowing full well that regardless of what I say or recommend, the patients is going to continue to smoke.

Innumerable drugs, most of which are of questionable value, have been used to prevent attacks of angina pectoris. In fact, placebos are frequently of value.

Testosterone--The male sex hormone has been effective in my experience. Whether it acts as a vasodilator or merely by promoting a sense of well-being is not known.

Alcohol--Alcohol (whiskey, brandy, rum) has been used for many years in the treatment of angina pectoris. I have prescribed it in moderate quantity--an ounce several times a day--and while I have not made alcoholics of any of my patients, I also have not cured any of them with it. Preparations, such as creme de menthe, are of value in relieving "gas" of which so many patients complain.

From Heart Disease Diagnosis and Treatment

Emanuel Goldberger, MD

1951

Iodine is not salt

12. May 2009 William Davis (3)

I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:

Sodium = iodine

Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"You can't reduce coronary plaque"

10. May 2009 William Davis (9)

"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

Lethal lipids

8. May 2009 William Davis (15)

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself

This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).

If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.

"Get regressive"

6. May 2009 William Davis (0)

This caught my eye:

Niaspan, prescription niacin, now sold by Abbott Laboratories, is now promoting its advantages in regressing coronary plaque:

In patients with a history of coronary artery disease (CAD) and hypercholesetgerolemia, Niaspan (niacin), in combination with a bile acid-binding resin, is indicated to slow progression or promote regression of atherosclerotic disease.

And the new slogan: "Get regressive."

Interestingly, the new marketing campaign is based on relatively old data. They base this new claim on 3 studies:

1) Cholesterol-Lowering Atherosclerosis Study (CLAS)--a 1987

CRP House of Cards

4. May 2009 William Davis (15)

Lew has coronary plaque with a heart scan score of 393. At age 53, that's in the 90th percentile (higher score than 90% of men in his age group).

On our search for causes of his coronary plaque, we identify low HDL of 41 mg/dl, high triglycerides of 202 mg/dl, small LDL (83% of total), calculated LDL of 133 mg/dl, and severe vitamin D deficiency with a starting blood level of 25-hydroxy vitamin D of 19 ng/ml.

His c-reactive protein: 4.1 mg/dl--above the cut-off of 2.0 mg/dl that the pharmaceutical industry is targeting as a mandate for statin therapy, particularly given the JUPITER data.

Lew instead eliminates wheat and other small LDL-provoking foods and, as a result, loses 28 lbs in 3 months; adds omega-3 fatty acids from fish oil; supplements vitamin D sufficient to increase his blood level to 70 ng/ml.

Along with dramatic correction of his starting abnormalities, his c-reactive protein: 0.4 mg/dl--no statin drug.

In my view, increased CRP is nothing more than a surrogate for the inflammatory phenomena that arise from high-carbohydrate diets, overweight, and small LDL. Correct those and CRP drops off a cliff. In fact, it is exceptionally rare for CRP to not drop to very low levels following this formula.

I believe that CRP is one more item on the list of reasons--the house of cards--the pharmaceutical industry is building to persuade us to take more and more statin drugs. LDL not low enough? Take more statin. Diabetic with low cholesterol? Take a statin. Inflammation? Take a statin.

Enough already.

At-home blood tests

2. May 2009 William Davis (6)

Our at-home blood tests are proving a hit.

So far, vitamin D is the number one most popular test, no surprise.

Second--to my surprise--is DHEA. I would have predicted it would have been thyroid testing.

Our male and female hormone panels are also proving popular.

I've personally been using the thyroid and vitamin D testing to monitor my levels. I increased my Armour thyroid based on a low free T3 value, while my vitamin D was perfect at 77 ng/ml on 8000 units vitamin D3 (cholecalciferol) per day.

The process of performing the blood spots is straightforward. The finger pricks are virtually painless using the automatic spring-loaded finger stick devices:

The number of blots to make depends on how many tests you'd like. Just a vitamin D test requires 2 blots. If 6 or more tests are ordered at a time, then all 12 blots should be made. (Two spring-loaded lancets are provided in each kit.)

If you are interested in any of our at-home blood tests, go here.

Our own Heart Hawk has posted an editorial on about blood spot testing on Health Central:

Simple, affordable home blood testing is a real game-changer in the arena of informed, self-directed healthcare. For the first time broad access to home blood testing, on a scale similar to that enjoyed by persons who routinely test their blood sugar, is available to virtually everyone and it removes doctors as the gatekeepers of these tests. Even private insurance companies and Medicare are beginning to understand the potential for improving healthcare and decreasing costs and are slowly beginning to expand coverage of home blood testing much as they do for diabetics or persons taking anti-coagulants.

"Help keep your family goiter free"

1. May 2009 William Davis (10)

People ask, "If I need iodine, should I go back to iodized salt?"

First of all, how did this notion of iodized salt originate?

In 1924, J. Edgar Hoover was appointed head of the FBI, Marlon Brando and Doris Day were born, and Calvin Coolidge was elected President of the United States. Half of American households had a car, while 1 in 4 Americans were illiterate.

In the 1920s, cities were a fraction of their current size and a third of the U.S. population, or 36 million people, lived in small rural communities.

Goiters were also wildly prevalent in 1924. Up to a third of the population in some areas of the country, particularly the Midwest, suffered from goiters, thyroid glands that enlarged due to lack of iodine.

Goiters were not only unsightly, but sometimes grotesque, causing a visible bulge in the front of the neck. Occasionally, they would grow so big that it compressed adjacent structures, like the trachea, and would have to be surgically removed. Goiters were commonly associated with thyroid dysfunction, especially low thyoid or hypothyroidism, that resulted in low IQ's in schoolchildren, debilitation in adults. Women of childbearing age delivered retarded children.

So iodine deficiency in early 20th century America was a big problem. How to solve this enormous public health problem in a large nation without television, few radios, no internet, with a largely rural and often illiterate population?

Thus was iodized salt born, a simple, technologically available solution that could be implemented on a large scale nationwide at low cost. The FDA chose this route in 1924, figuring that it was the best way to ensure that most Americans could obtain sufficient iodine through liberal use of iodized salt. Public health officials urged Americans to use salt. Morton's salt label proudly bore the slogan "Help keep your family goiter free!"

It worked. Goiters largely became a thing of the past.

How about today? The American Heart Association recommends limiting salt, recently announcing that they would like to limit intake to 1500 mg per day. The American Medical Association has been lobbying the FDA to set lower salt limit guidelines. The FDA has been clamping down on food manufacturers to reduce the quantity of salt in processed foods.

Why limit salt? The concern is that there are segments of the population (not all) that are salt sensitive, particularly African Americans, people with certain genetic forms of high blood pressure, conditions that cause water retention, and any degree of heart or kidney failure. Salt in these peoplem, in fact, can be disastrous.

So adding iodine to salt was the solution to epidemic goiter. And it worked.

But salt is not a perfect solution, just one that served its purpose back in 1924. What we need is a 21st century solution.
You will find that in the various iodine supplements at your health food store. My favorite is kelp--inexpensive, available, and a form that mimics the way Japanese people obtain iodine (though by eating seaweed, rather than with tablets).

Image of kelp courtesy Wikipedia