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.

All posts by william-davis

Disease Engineering

20. October 2008 William Davis (0)

Imagine you contract pneumonia.

You have a fever of 103, you’re coughing up thick, yellow sputum, breathing is getting difficult. You hobble to the doctor, who then fails to prescribe you antibiotics. You get some kind of explanation about unnecessary exposure to antibiotics to avoid creating resistant organisms, yadda yadda. So you make do with some Tylenol®, cough syrup, and resign yourself to a few lousy days of suffering.

Five days into your illness, you’ve not shown up for work, you’re having trouble breathing, and you’re getting delirious. An emergency trip to the hospital follows, where a bronchoscopy is performed (an imaging scope threaded down your airway) and organisms recovered for diagnosis. You’re put on a ventilator through a tube in your throat to support your breathing and treated with intravenous antibiotics. Delayed treatment permits infection to escape into the fluid around your lungs, creating an “empyema,” an extension of the infection that requires insertion of a tube into your chest through an incision to drain the infection. You require feeding through a tube in your nose, since the ventilator prevents you from eating through your mouth. After 10 days, several healing incisions, and a hospital bill totaling $75,000, you’re discharged only to be face eights weeks of rehabilitation because of the extreme toll your illness extracted. Your doctor also advises you that, given the damage incurred to your lungs and airways, you will be prone to more lung infections in the future, and similar situations could recur whenever a cold or virus comes long.

A disease treatable by taking a two week, $20 course of oral antibiotics at home has been converted into a lengthy hospital stay that generated extravagant professional fees, testing, and costly supportive care. You’ve lost several weeks of income. You’re weak and demoralized, frightened that the next flu or virus could mean another trip to the hospital.

Such a scenario would be unimaginable with a common infection like pneumonia, or it would be grounds for filing a malpractice lawsuit. But, as horrific as it sounds in another sphere of healthcare, it is, in effect, analogous to how heart disease is managed in current medical practice.

First, you’re permitted to develop the condition. It may require years of ignoring the telltale signs, it may require your unwitting participation in unhealthy lifestyle choices. Palliative treatments that slow, but don't stop, the progression of disease are prescribed like cholesterol drugs. The process then eventuates in some catastrophe like heart attack or similar unstable heart situation, at which point you no longer have a choice but to submit to major heart procedures. That’s when you receive your heart catheterization, coronary stents, bypass, defibrillators, etc. and you're proudly declared a "success" of medical technology.

Of course, none of these procedural treatments cures the disease, no more than a Band Aid® heals the gash in your leg. The conditions that were present that created your heart disease continue, allowing a progressive disease to worsen. At some point, you will need to return to the hospital for yet more procedures when trouble recurs, which it inevitably does.

A coronary bypass operation costs, on average $85, 653 (AHA 2008 Update; based on 2004 data). That doesn't include the $25,433 cost for the heart catheterization performed by a cardiologist to provide the surgical roadmap of your coronary arteries. If there are any complications of your procedure, then your hospital bill may total a substantially higher figure.

$85, 653 is just the upfront financial pay-off. Over the long run, your life is actually worth far more to the cardiovascular healthcare system because no heart procedure yields a permanent fix. In fact, repeated reliance on the system is the rule.

In fact, over 90% of people who enter the American cardiovascular healthcare system do so through a revolving door of multiple procedures over several years. It is truly a rare person, for instance, who undergoes a coronary bypass operation, never to be seen again the wards of the hospital because he remains healthy and free of catastrophe. A much more familiar scenario is the man or woman who undergoes two or three heart catheterizations, receives 3,4, or 6 stents, followed a few years later by a heart bypass, pacemaker, defibrillator, as well as the tests performed for catastrophe management, such as nuclear stress test, echocardiogram, laboratory blood analysis, and consultation with several specialists. Re-do bypass surgeries--a 2nd, 3rd, or 4th bypass--now comprise 25% of all bypass procedures.

The total revenue opportunity is many-fold higher than the initial 80-some thousand dollars, but instead totals hundreds of thousands of dollars per person.

What motivation can there possibly be to 1) identify coronary disease early, when in its asymptomatic stage, then 2) identify its causes, then 3) correct the causes, and finally 4) shut off the disease? You and I can accomplish this with a few hundred dollars of cost, perhaps a few thousand over many years (to cover costs of fish oil, vitamin D, niacin, and whatever else it takes to stop the expression of the disease). Nobody therefore profits substantially from your prevention effort--except you.

Then what if nobody told you that heart disease could be managed this way? That's what I mean by "disease engineering."

Dr. Steven Gundry on The Livin' La Vida Low-Carb Show

20. October 2008 William Davis (4)

I stumbled on a great interview with cardiothoracic surgeon, Dr. Steven Gundry, on Jimmy Moore's Livin' La Vida Low-Carb Show. (Or, cut and paste: http://www.thelivinlowcarbshow.com/dr-steven-gundry-part-1-episode-179/)

Dr. Gundry has some fun ways of looking at eating and health. I found his comments on the activation of genes (discussed at a very light, non-scientific level) useful. He argues that when humans consume sugar-containing foods, the signal received by the body is that winter is approaching and it's time to build up fat stores in anticipation of the food shortages of cold weather. He finds parallels for this phenomenon in other species. Of course, for humans, winter (in the form of extended calorie deprivation) never comes. In fact, you might argue that, given our excessive reliance on grains, corn, and sugars, that we are, in effect, always in anticipation of a winter that never comes.

I've not read Dr. Gundry's books, but I found this light interview a lot of fun.

Does fish oil ADD to statin therapy?

18. October 2008 William Davis (9)

Yet another patient came to my office today saying, "My primary doctor said that I should stop taking fish oil. He say's that I don't need it because I take Crestor."

The woman was in tears, confused and frightened over a potential disagreement between her doctors.

Is this true? If someone takes a statin drug, like Crestor, Lipitor, Zocor (simvastatin), pravachol, or lovastatin, they don't need to take anything else because the statin drug is so powerful that it eliminates risk?

No. Not even close to the truth.

First of all, let's accept that virtually the entire body of statin drug literature--hundreds of studies, billions of dollars spent--was paid for by the drug industry. It's no news that studies paid for by the sponsor are likely to favor the sponsor. Imagine Ford sponsored a study of Ford vs. GM cars vs. Toyota, paying $10 million to fund the effort. Guess who is likely to come out on top? "Studies show that Ford makes the best car in America." (Sorry, I don't mean to pick specifically on Ford. It's just a widely-recognized brand.)

So that means that the statin literature likely overestimates the benefit of statin drugs. Even so, it's clear from the hundreds of studies performed that the best we can hope for by taking statin drugs is a reduction of heart attack and death from heart attack of 30-35%--best case. That doesn't sound like elimination of risk to me.

What are the incremental benefits of adding omega-3 fatty acids from fish oil added to statins? The best data originate with the JELIS Trial (Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis), in which 19,000 Japanese participants (who already have a high omega-3 intake from diet, usually ranging from 1800-3000 mg per day) experienced a 19% reduction (relative reduction) in cardiovascular events.

GISSI Prevenzione demonstrated a 28% reduction in heart attack, 45% reduction in death from heart attack with fish oil.

Omega-3 fatty acids from fish oil also:

--Reduce triglycerides dramatically
--Accelerate after-eating clearance of digestive by-products, i.e., they correct post-prandial abnormalities
--Modify the character (fragmentation potential, structural strength) of plaque
--Raise HDL modestly

If you buy your fish oil from Sam's Club, Costco, or other discounter, a healthy dose of fish oil might cost you $3 per month. Compare that to the $120 per month average cost of a statin agent. Why is there even a discussion over this?

Sadly, the doctor on Main Street, U.S.A, is the unwitting puppet of the pharmaceutical industry. The pretty drug company representative with nice legs and a cute smile promises lunch, dinner and . . who knows what else? Wink. The fifty-something, hairline-receding doctor can't resist. "Of course I'll prescribe your drug!"

Don't kid yourself: The drug industry knows precisely how to manipulate the behaviors of the deliverers of their products.

So, do statin drugs make omega-3 fatty acids from fish oil irrelevant? Absolutely not.

It's all about trying to inch closer and closer--not to reduction--but to elimination of risk for heart disease.

HDL: “H” is for “happy”

16. October 2008 William Davis (10)

What role do emotions play in HDL cholesterol?

I’ve often observed a peculiar phenomenon: People who come to the office or hospital in the midst of a difficult emotional situation-e.g., stress at home, financial struggles, hospitalization (usually an unhappy occasion)- can show dramatic drops in HDL cholesterol. Not uncommonly, HDL drops 20 or more mg/dl.

Take Agnes’s case. Agnes had to go to the hospital for an elective procedure, one she’d been dreading for months. Previously, Agnes had been proud of the fact that she’d incrased HDL from 42 mg/dl range all the way up to 71 mg/dl. She accomplished this dramatic increase by eliminating wheat and cornstarch from her diet (which helped her lose 24 lbs), taking vitamin D and omega-3 fatty acids from fish oil, exercise, 2 oz of dark chocolate per day, and a glass of red wine with dinner.

Although I wouldn’t have bothered checking a cholesterol panel for such a procedure, the hospital had a checklist that included a cholesterol panel regardless of necessity. (Such checklists are common in hospitals, meant to ensure that certain basic issues are not overlooked.)

Agnes’ HDL: 29 mg/dl-a 42 mg drop.

Agnes will recover and her HDL will rebound, but the same effect can occur with other stressful situations, such as death in the family, financial worries, marital stress, etc., as well as physical illness.

Interestingly, the opposite may also hold true: Low HDL may increase risk for depression and stress. A study from Finland of 124 depressed persons, for instance, showed a 240% increased likelihood of depression in those with lower HDL cholesterols.

In other words, there seems to be a curious interdependence between HDL and emotions.

Why? Does it represent the indirect effect of adrenaline, cortisol, or other “stress hormones”? Do factors that relate to low HDL, such as unhealthy diet full of carbohydrates and physical inactivity, also tend to cultivate depression?

It certainly seems to be a chicken-egg situation, with one often leading to the other.

Moral of the story: Maintaining a sense of optimism and engaging in activities that bring you satisfaction and enjoyment can help raise HDL, as can strategies such as those followed by Agnes. Avoiding unnecessarily stressful situations can help. HDL is important, since higher levels are associated with much reduced risk for heart disease . . . and perhaps depression.

Plaquology

13. October 2008 William Davis (3)

Plaquology: A new term.

Plaquology: def: (plaque-: atherosclerotic plaque; -ology: study of.) The study of atherosclerotic plaque, originating in the early 21st century during the time period when the material underlying atherosclerosis gained recognition as a measure superior to "risk factors" for cardiovascular disease. Previous to the plaque concept, blood measures of cholesterol and adverse lifestyle habits, such as smoking and sedentary lifestyle, alone had been used to predict potential for cardiovascular events. With acceptance of the concept of plaque measurement, the concept of risk factors was abandoned.

Look it up in the current Oxford Dictionary of the English Language, or Webster's Dictionary, and I'm afraid that you still won't find plaquology . . . but you should.

I'm currently rewriting many parts of the Track Your Plaque book. The rewriting process has caused me to review just how much we've learned these past few years. One of the phenomena that fascinates me is that we now have non-medical people--teachers, software people, engineers, bankers, bed and breakfast owners, retired businesspeople, etc.--all discussing the finer points of coronary atherosclerotic plaque--plaquology--what constitutes plaque, what triggers plaque inflammation, how to quantify potential for plaque rupture or plaque quiescence, what effect various treatments have on plaque composition and behavior, etc.

We now have a legion of Plaquologists!

I'm very proud of our Plaquologists. Having devoted themselves to the study of plaque, their level of knowledge now exceeds that of 99% of practicing physicians, including my colleagues, the cardiologists. While cardiologists spend their day squashing/cutting/vaporizing plaque, they are no more experts in plaquology than a carpenter is an expert in trees. More often than not, cardiologists view plaque as just something that gets in their way, rather than the quantifiable, modifiable, reversible material that we can exert control over.

One of the software tools currently in the works for the Track Your Plaque website is a certification process. Members will be able to gain a "certification" in various topics relevant to plaquology, such as plaque quantification, lipoprotein testing, and nutritional supplements.

How about a Doctor of Plaquology?

Thyroid perspective update

10. October 2008 William Davis (18)

Since the publication of the extraordinary HUNT Study relating the entire spectrum of thyroid function and heart issues, I have been vigorously and systematically examining thyroid function in numerous patients.

While there's no news in relating flagrant low thyroid function with triggering heart disease in several forms, the cut-off between low thyroid and normal thyroid has been a matter of dispute for decades.

In the early 20th century, low thyroid function wasn't diagnosed until someone gained 40 lbs, displayed extravagant amounts of edema (water retention) in the legs and huge bags under the eyes, hair fell out in clumps, and often eventually proved fatal. At autopsy, these unfortunates also showed advanced and extensive quantities of coronary atherosclerotic plaque.

Low thyroid is usually diagnosed on the basis of the blood test, thyroid stimulating hormone, or TSH. TSH is a pituitary gland hormone responsible for stimulation of thyroid function. When thyroid function flags, the pituitary increases TSH release. Thus, a high TSH signals lower thyroid hormone levels.

The difficulty is in distinguishing normal thyroid function from low thyroid function judged by TSH levels. As the years have passed, in fact, the cut-off for "normal" TSH has drifted lower and lower.

The HUNT Study, I believe, clinches the argument: A TSH of 1.5 or lower, perhaps even 1.0 or lower, is desirable to eliminate the excess cardiovascular risk provided by an underactive thyroid, not to mention feel better: more energetic, clearer thinking, greater well-being.

Having now applied this renewed appreciation for thyroid, I have come to believe that:

--Low thyroid function, even subtle levels, are rampant and far more common than ever previously thought. In my office practice, the case could be made that several people per day are marginally or mildly hypothyroid (low in thyroid).
--Restoration of optimal thyroid levels facilitates correction of lipid measures, especially LDL cholesterol and, to a lesser degree, lipoprotein patterns dependent on the insulin axis such as triglycerides and small LDL. It's a lot happier way to correct lipids than statins.

I don't discount the value of feeling better. People who feel better--more energetic, more upbeat, clearer thinking--tend to do better in health overall. If thyroid restoration is a part of that equation, then greater attention should be paid to this facet of health on our way to optimal heart health.

Though I sometimes feel like an endocrinologist dispensing desiccated thyroid (rarely the synthetic T4), I believe that this has been a previously neglected and important part of our effort to achieve coronary plaque stabilization and reversal.

Accidental Health

9. October 2008 William Davis (2)

"I shall never have smallpox for I have had cowpox; I shall never
have an ugly pockmarked face."

Such was the idle comment made by a milkmaid to Edward Jenner in 1768 when Jenner was 19, a remark that later prompted his investigations into using isolates of cowpox injected into humans as the first vaccination against the devastations of the European epidemic of smallpox.

(A caricature of Jenner administering cowpox vaccine to people, causing them to sprout bovine appendages. Image courtesy Wikipedia and the Library of Congress.)

When I look back, something similar has happened here.

Although the Track Your Plaque program is intended to stop and reverse coronary plaque using the only available means of tracking coronary plaque, i.e., heart scans, an unintended panel of benefits follow:

--People lose weight, often dramatically
--People gain greater energy
--Thinking is clearer, emotions more stable
--Sleep is deeper
--Bone density increases
--Physical strength and coordination improve
--Winter blues dissipate
--Blood sugar drops dramatically
--Blood pressure drops

Cholesterol (lipid) panels also settle to values that most physicians deem impossible or impractical, given our target of 60:60:60, i.e., LDL 60 mg/dl or less, HDL 60 mg/dl or higher, triglycerides 60 mg/dl or less. And medications are not always necessary to achieve these values. (When I show these values to my colleagues, they declare them flukes, unobtainable only in select people with high doses of medications.)

I didn’t set out to find the next weight loss solution, nor the key to boundless energy. My goal was "simpler": create a program of heart health. I am, after all, a cardiologist.

I was so intently focused on achieving incremental improvements over the steps leading to heart disease prevention that I failed to recognize the profound phenomena that accompanied it: people were quicker, smarter, thinner, and healthier.

In other words, I believe that we have inadvertently created a program of super health and performance.

Ironically, most people don't want to talk about heart disease, let alone reversal of heart disease. They do want to talk about getting thinner, feeling more energetic, living longer, better cholesterol values, etc.

Perhaps there's a lesson in this.

Livin' La Vida Low Carb interview

7. October 2008 William Davis (5)

I recently provided an interview for Livin' La Vida Low Carb's irrepressible Jimmy Moore.

Jimmy runs a fun set of blogs, webcasts, and the like to broadcast this message of reducing carbohydrates in the diet. He credits his 210 lb weight loss to a strict low-carbohydrate and exercise program.

For the interview, just go to The Livin' the Vida Low Carb Show, Episode 185, or click here.

And click here for Part 2

For more of Jimmy Moore's spin on the entire low-carbohydrate diet experience, he maintains several popular blogs, including Carb Wire and The Livin' La Vida Low-Carb Blog.

Wheat withdrawal: How common?

5. October 2008 William Davis (11)

In response to the recent Heart Scan Blog poll,

Have you experienced fatigue and mental fogginess with stopping wheat, i.e., "wheat withdrawal"?

the 104 respondents said:

Yes, I have experienced it: 26 (25%)

No, I stopped wheat and did not experience it: 65 (62%)

I'm not sure: 3 (2%)

I haven't tried it but plan to: 7 (6%)

I haven't tried it and don't plan to: 3 (2%)

So 25% of respondents reported experiencing the fatigue and mental fogginess of wheat withdrawal. This is similar to what I observe in my practice.

I counsel many patients to consider the elimination of wheat, as well as cornstarch products, in an effort to regain control over:

--Weight
--Appetite
--Low HDL
--High triglycerides
--Small LDL
--High blood sugar
--High blood pressure

All of these issues respond--often dramatically--to elimination of wheat and cornstarch.

Why would there be undesirable effects of eliminating wheat?

One clear issue is that elimination of wheat and other sugar-equivalents deprives your body of glucose. Your body then needs to resort to fatty acid metabolism to generate energy. Apparently, some people are inefficient at this conversion, having subsisted on carbohydrates for the last few decades of their lives. However, as fatty acid metabolism kicks in, energy generation improves. That is my (over-)simplified way of reasoning it through.

However, are there other explanations behind the mental fogginess, drop in energy, and overwhelming sleepiness? Some readers of this blog have suggested that, since opioid-like sequences (i.e., amino acide sequences that activate opiate receptors) are present in wheat, perhaps withdrawal from wheat represents a lesser form of opiate withdrawal. I find this a fascinating possibility, though I know of no literature devoted to establishing a cause-effect relationship.

Whatever the mechanism, I find it very peculiar that this food widely touted by the USDA, American Heart Association, and other agencies actually triggers a withdrawal syndrome in approximately 25% of people. Spinach does not trigger withdrawal. Nor does flaxseed, olive oil, almonds, and countless other healthy foods.

Then why would whole wheat grains be lumped with other healthy foods?

Treat the patient, not the test

5. October 2008 William Davis (0)

"Treat the patient, not the test."

That is a common "pearl" of medical wisdom often passed on during medical training.

It refers to the fact that we should always view any laboratory or imaging test in the context of the live, human patient and not just treat any unexpected value that doesn't seem to make sense.

I raise this issue because it recently came up on a discussion on the Track Your Plaque Forum. A Member with a high heart scan score of around 1100 was advised by his doctor that it should be ignored, because he'd prefer to treat the patient, not the test. The patient is apparently slender, physically active, and entirely without symptoms, with favorable cholesterol values as well. The high heart scan score didn't seem to jive with the appearance of the patient, as viewed by this doctor.

This common phrase is meant to impart wisdom. It is a reminder that we treat real people, not just a jumble of laboratory values.

But the unspoken part of the equation is that judgment needs to be applied. A well looking person who shows an unexpected rise in white blood cell count could just have a screwy result, or could have leukemia. Liver tests (AST, ALT) that top 400 could represent a fluke, or dehydration incurred during a long workout, or hepatitis from a long ago blood transfusion.

Yes, treat the patient. But don't be an idiot and entirely dismiss the signficance of an unexpected laboratory or imaging test. A heart scan score of 1100 should be as readily dismissed as discovering a white blood cell count of 90,000 (normal is less than 12,000), or a 5 cm mass in the lung. The absence of symptoms or the failure of conventional risk factors to suggest causation is insufficient reason to dismiss the concrete findings of a test.

In this particular person, dismissing the significance of the heart scan finding by suggesting that the doctor should treat the patient, not the test, is tantamount to:

--Colossal ignorance
--Malpractice
--A certain sentencing of the hapless patient to future major heart procedures, heart attack or death (20-25% likelihood every year, or a virtual certainty over the next 5 years).

There is an ounce of wisdom in this old medical pearl. But there's also plenty of room for a knuckleheaded doctor to misconstrue and abuse its meaning for the sake of covering up his/her ignorance, laziness, or lack of caring.