Cholesterol effects of carbohydrates

24. mars 2009 William Davis (31)
Let's take a hypothetical person, say, a 50-year old male. 5 ft 10 inches, 160 lbs, BMI 23.0. He's slender and in good health.

Our hypothetical man eats a simple diet of vegetables, some fruit, nuts, and meats but avoids processed industrial foods. By macronutrient composition, his diet is approximately 30% protein, 40-50% fat, 20-30% carbohydrate. His starting lipid panel:

Total cholesterol 149 mg/dl
LDL cholesterol 80 mg/dl
HDL 60 mg/dl
Triglycerides 45 mg/dl

His starting lipids are quite favorable (though I don't often see this kind of starting panel nowadays except in athletes). We begin here because this hypothetical man is going to serve as our test subject.

We ask our hypothetical man to load his diet up on "healthy whole grains." He complies by eating whole grain cereals for breakfast, whole wheat toast; sandwiches made with whole grain bread; dinners of whole wheat pasta; snacks of granola bars, whole wheat pretzels and crackers.

Three months later, his lipids show:

Total cholesterol 175 mg/dl
LDL cholesterol 130 mg/dl
HDL 45 mg/dl
Triglycerides 150 mg/dl


You can see that LDL cholesterol has increased, HDL has dropped, and triglycerides have increased. This wave of change is the hallmark of carbohydrate excess, but more specifically of overreliance on wheat products. Beyond his lipid panel, the man has gained 10 lbs, all concentrated in a soft roll around his abdomen, his blood sugar is now in the "borderline range" of between 110 and 126 mg/dl, i.e., pre-diabetic.

If we were to examine this man's advanced lipoproteins (e.g., NMR from Liposcience, or VAP from Atherotech), we would see that there has been an explosive increase in small LDL particles, along with a shift of large HDL to small, and the appearance of multiple abnormal classes of particles called VLDL and IDL (signalling abnormally slowed clearance of dietary by-products from the blood).

Familiar scenario? The "after-carbohydrate" situation is the rule among the people who I first meet who claim to be eating a "healthy" diet, though their patterns are usually much worse, with higher LDL, lower HDL, and much higher triglycerides, an exaggeration of our hypothetical man's abnormalities.

What if our hypothetical man now goes to his conventionally thinking (read "taught medicine by the pharmaceutical industry") physician? What will likely be the advice he receives? Reduce his saturated fat intake, eat plenty of healthy whole grains, take a statin drug.

Although my illustrative man is hypothetical, I've seen this scenario play out many thousands of times. It happens in real life all the time. It is predictable, it is highly manipulable. Sadly, it is rarely recognized for what it is: the result of excess carbohydrates, or what I call "Carbohydrate Intolerance Syndrome."

The misinterpretation of this condition has created 1) an epidemic of diabetes and pre-diabetes, 2) a nation of frustrated obese Americans, 3) a $27 billion per year statin industry, 4) another growth opportunity for the drug industry in diabetes drugs.

Wheat Belly Revisited

23. mars 2009 William Davis (24)
Do you have a wheat belly?

When I first coined this phrase back in July, 2007, I had witnessed the phenomenal health effects of wheat elimination in several hundred patients.

In the nearly two years that have passed since my original post, I have witnessed hundreds more people who have done the same: eliminate pretzels, crackers, breads of all sorts, bagels, pasta, muffins, waffles, pancakes, etc.

If anything, I am convinced now more than ever that wheat is among the most destructive foods in the human diet. At least 70% of people who eliminate wheat from their diet obtain at least one, if not several, substantial health benefits.

Now, if I were trying to sell you something, say, an alternative to wheat, then you should be skeptical. If I tell you that drug or nutritional supplement X is great and you should take it, only to follow it with a sales pitch, you should be skeptical.

What am I selling? Nothing. I gain nothing by telling everyone to avoid wheat. In fact, I wish it wasn't true. Wheat foods taste good. Wheat flour makes great comfort foods. In years past, I spent many hours sitting at the bagel shop reviewing papers over a cup of coffee and a bagel. No longer.

So here, back by popular demand, the original Wheat Belly post:



Wheat Belly

You've heard of "beer bellies," the protuberant, sagging abdomen of someone who drinks excessive quantities of beer.

How about "wheat belly"?

That's the same protuberant, sagging abdomen that develops when you overindulge in processed wheat products like pretzels, crackers, breads, waffles, pancakes, breakfast cereals and pasta.



(By the way, this image, borrowed from the wonderful people at Wikipedia, is that of a teenager, who supplied a photo of himself.)

It represents the excessive visceral fat that laces the intestines and triggers a drop in HDL, rise in triglycerides, inflames small LDL particles, C-reactive protein, raises blood sugar, raises blood pressure, creates poor insulin responsiveness, etc.

How common is it? Just look around you and you'll quickly recognize it in dozens or hundreds of people in the next few minutes. It's everywhere.

Wheat bellies are created and propagated by the sea of mis-information that is delivered to your door every day by food manufacturers. It's the same campaign of mis-information that caused the wife of a patient of mine who was in the hospital (one of my rare hospitalizations) to balk in disbelief when I told her that her husband's 18 lb weight gain over the past 6 months was due to the Shredded Wheat Cereal for breakfast, turkey sandwiches for lunch, and whole wheat pasta for dinner.

"But that's what they told us to eat after Dan left the hospital after his last stent!"

Dan, at 260 lbs with a typical wheat belly, had small LDL, low HDL, high triglycerides, etc.

I hold the food companies responsible for this state of affairs, selling foods that are clearly causing enormous weight gain nationwide. Unfortunately, the idiocy that emits from Nabisco, Kraft, and Post (AKA Philip Morris); General Mills; Kelloggs; and their kind is aided and abetted by organizations like the American Heart Association, with the AHA stamp of approval on Cocoa Puffs, Cookie Crisp Cereal, and Berry Kix; and the American Diabetes Association, whose number one corporate sponsor is Cadbury Schweppes, the biggest soft drink and candy manufacturer in the world.

As I've said many times before, if you don't believe it, try this experiment: Eliminate all forms of wheat for a 4 week period--no breakfast cereals, no breads of any sort, no pasta, no crackers, no pretzels, etc. Instead, increase your vegetables, healthy oils, lean proteins (raw nuts, seeds, lean red meats, chicken, fish, turkey, eggs, Egg Beaters, low-fat yogurt and cottage cheese), fruits. Of course, avoid fruit drinks, candy, and other garbage foods, even if they're wheat-free.

Most people will report that a cloud has been lifted from their brains. Thinking is clearer, you have more energy, you don't poop out in the afternoon, you sleep more deeply, some rashes disappear. You will also notice that hunger ratchets down substantially. Most people lose the insatiable hunger pangs that occur 2-3 hours after a wheat-containing meal. Instead, hunger is a soft signal that gently prods you that it's time to consider eating again.

You will also make considerable gains towards gaining control over your risk for heart disease and your heart scan score, a crucial step in the Track Your Plaque program.

Thank you, Crestor

20. mars 2009 William Davis (9)
I'm sure everyone by now has seen the Crestor ads run by drugmaker, AstraZeneca. TV ads, magazine ads, and the Crestor website all echoing the same message:

"While I was busy building my life, something else was busy building in my arteries: dangerous plaque."

While previous drug trials with Mevacor, Pravachol, Zocor, and Lipitor have focused mostly on examining whether the drugs reduced incidence of cardiovascular events, Crestor studies have also focused on effects on atherosclerotic plaque volume. The best example is the ASTEROID trial that demonstrated approximately 7% reduction in plaque volume by intracoronary ultrasound.

So the AstraZeneca decision makers took the leap from cholesterol reduction to plaque reduction.

I'm sure this switch wasn't taken lightly, but was the topic of discussion at many meetings before the decision to make plaque reduction the focus of hundreds of millions of dollars of advertising. After all, billions of dollars are at stake in this bloated statin market.

Ordinarily, I couldn't care less about how the drug manufacturers conduct their advertising campaigns. But this one I paid attention to because the Crestor ads are helping fuel a new way of thinking about coronary heart disease: It's not about the cholesterol; it's about the atherosclerotic plaque that accumulates in arteries.

It's not cholesterol that grows, limits coronary blood flow, and causes angina. It's not cholesterol that "ruptures" its internal contents to the surface within the interior of the blood vessel and causes blood clot and heart attack. It's not cholesterol that fragments from the carotid arteries and showers debris to the brain, causing stroke. It's all plaque.

I took the same leap years ago, though not backed by hundreds of millions of dollars of marketing money. When I first called my book Track Your Plaque, some of the feedback I got from editors included comments like "I thought this was a book about teeth!" Even now, the word "plaque" in the book title and website is responsible for confusion.

But AstraZeneca is helping me clear up the confusion. As the word plaque gains hold in public consciousness, it will become increasingly clear that cholesterol reduction is not what we're after. We are looking for reduction of plaque.

If you are trying to develop an effective means to reduce or reverse coronary heart disease, then there are two simple equations to keep in mind:


Plaque = coronary heart disease

Cholesterol ? coronary heart disease


Plaque is the disease, cholesterol is not. Cholesterol is simply a crude risk for plaque.

While I'm no friend to the drug industry nor to AstraZeneca, some good will come of their efforts.

Supermarkets and buggy whips

17. mars 2009 William Davis (17)
Will supermarkets eventually phase out, joining the history books as a phenomenon of the past? Or are supermarkets here to stay, an emblem of the industrialization of our food--easy access to foods that are convenient, suit the undiscriminating masses, stripped of nutritional value despite the prominent health claim on the package front?

Anna left an insightful comment on the last Heart Scan Blog post, Sterols should be outlawed, along with some useful advice on how to avoid this trap for poor health called a supermarket:


I rarely shop in regular supermarkets anymore (farm subscription for veggies, meat bought in bulk for the freezer, eggs from a local individual, fish from a fish market, freshly roasted coffee from a local coffee place, etc.). What little else I need comes from quirky Trader Joe's (dark chocolate!), the fish market, farmer's markets, a small natural foods store, or mail order.

When I do need to go into one of the many huge supermarkets near me, not being a regular shopper there, I never know where anything is, so I have to ramble a bit around the aisles before I find what I'm looking for (and I almost always can grab a hand basket, instead of a trolley cart).

It's almost like being on another planet! There's always so many new products (most of them I hesitate to even call food). It's really a shock to the senses now to see how much stuff supermarkets sell that I wouldn't even pick up to read the label, let alone put in a cart or want to taste. I'm not even tempted by 99% of the tasting samples handed out by the sweet senior ladies in at Costco anymore (only thing I remember tasting at Costco in at least 6 mos was the Kerrygold Irish cheese, because I know their cows have pasture access and it's real food).

What's really shocking to me is how large some sections of the markets have become in recent years. While Americans got larger, so did some sections of the supermarket (hint - good idea to limit the consumption of products from those areas). Meat and seafood counters have shrunk, though. Produce areas seem to be about the same size as always (but more of it is pre-prepped and RTE in packaging.

But the chilled juice section is h-u-g-e! And no, I don't think there is a Florida orange grove behind the cases. Come on, how much juice do people need? Juice glasses used to be teeny tiny, for a good reason. To me it looks like a long wall stocked full of sugar water. Avoiding that section will put a nice dent in the grocery expenses.

The yogurt case is also e-n-o-r-m-o-u-s! Your 115 yo Bulgarian "grandmother" wouldn't know what to make of all these "pseudo-yogurts"! Chock full of every possible variety, but very little fit to eat. The only yogurts I'll look at are made with plain whole milk, without added gums, emulsifiers, or non-fat milk solids, and live cultures (I mostly buy yogurt now and then to refresh my starter culture at home). I can flavor them at home if needed. The sterols are showing up in processed yogurts, too, along with patented new strains of probiotic cultures (I'll stick to my old fashioned, but time-proven homemade lacto-cultured veggies and yogurt instead).

I found the same "cooler spread" in the butter & "spread" section. The spread options were just grotesque sounding. Actually, the butter options weren't much better, as many were blended with other ingredients to increase spreadability, reduce calories or cholesterol/saturated fat, etc. A few plain butters were enhanced with "butter flavor" - say what? And on no package could it be determined if the butter came from cows that were naturally fed on pasture or on grain in confined pens.


Well said, Anna.

There's a huge supermarket about 1 mile away from my house similar to the one Anna describes with aisle after aisle of eye-catching cellophane-wrapped foods. I go there about every 3 or 4 months, and then I only go to get something I need in a pinch. Every time I go, I too am reminded just how many products there are that look more like junk food than real food.

But there's no real money in real food. Who gets rich off of selling green peppers, tomatoes, and eggs?

Supermarkets sell these modern industrial foods because people buy it: Look around you. You don't get to be a 250 lb 5 ft 2 inch-woman by eating too many cucumbers.

Like Anna, I drive an additional several miles to Trader Joes', buy at farmers' markets whenever possible, buy some odds and ends like wine and cheese and raw nuts at specialty stores. I grow my own basil in a big pot I keep in the kitchen and we are just about to start turning over the soil in the back yard for our vegetable garden. I don't need nor do I miss having the choice among 40 different chips, 25 brands of ready-made microwavable dinners, an entire aisle of breakfast cereasl (all of which are virtually the same with different names and labels), or 75 varieties of salad dressing.

The supermarket for me--and I hope for many of you--has become a place rarely frequented, and only for the odd forgotten item. Oh, I forgot the dog chewies the grocery does have--my dogs love them. So perhaps they are good for something after all.

Sterols should be outlawed

14. mars 2009 William Davis (10)
While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Texas today, tomorrow . . . the world?

10. mars 2009 William Davis (0)
Texas state representative, Rene Oliveira, has introduced legislation that mandates heart scans for adults in the state of Texas.

Rep. Oliveira

A press release from the SHAPE Society ( Society for Heart Attack Prevention and Eradication) reads:

Assessment of heart attack risk on the basis of traditional risk factors alone such as high cholesterol and high blood pressure and so forth, while useful, misses many who are at high risk and also incorrectly flags some for high risk who are in fact at very low risk of near term heart attack; on the other hand detection of atherosclerosis by non-invasive imaging, as suggested by the SHAPE group, accurately identifies plaque and improves the ability to identify at-risk individuals who could benefit from aggressive preventive intervention while sparing low-risk subjects from unnecessary aggressive medical therapy," said Dr. P.K. Shah, Director of Cardiology at Cedars Sinai Heart Institute in Los Angeles, a leading member of the SHAPE Task Force who is also an active member of the American Heart Association. "Sadly, these vulnerable patients go undetected until struck by a heart attack, because insurance companies don't cover the newer heart attack screening imaging tests."


Rep. Oliveira, whose coronary disease was first uncovered by a heart scan and prompted a bypass operation, states:

"It is about time that we cover preventive screening for the number one killer in Texas, and take action to reduce healthcare costs through preventive healthcare. Right now, we are extending the lives of those who can afford the procedure while hundreds of thousands of Texans with hidden heart disease go undetected because of antiquated thinking. The time has come for this change."


Is this what we've come to? Since practicing physicians are either so entranced by the drug and procedural solutions to heart disease, do we need to resort to heart scan by legislation?

It does indeed appear that we've come to this point. Should this trend catch on, it will surely mean an upfront increase in healthcare costs to cover the expense of heart scans. But in the long run, it will mean reduction in healthcare costs--dramatic reduction--if heart scans prompt effective preventive action.

What your doctor doesn't know about heart disease

9. mars 2009 William Davis (12)
What causes coronary heart disease or coronary atherosclerotic plaque, this thing that we track with heart scans?

Well, here are a few little-publicized facts about heart disease that you are unlikely to hear from your When's-the-next-stent? cardiologist or the What is there besides statins? primary care doctor.

(Since everybody knows that smoking is a modifiable risk for heart disease that can be readily identified, let's focus on the blood tests that reveal heart disease causes.)


What's the number one most common cause for heart disease?

Small LDL particles. The proliferation and popularity of the snack food/processed food culture, compounded with the "eat more healthy whole grain " propaganda has launched small LDL solidly to first place as the most common reason to have heart attacks, stents, and bypass. All that advice to increase your "healthy whole grain" intake? It increases heart attack risk.


What's the number one most aggressive cause for heart disease?

That's lipoprotein(a), or Lp(a). It's certainly not high cholesterol, though the drug industry loves that you think that. We could argue over whether smoking is more aggressive, but the two are pretty darned close. Combine the two--Lp(a) in a smoker--and the combination is an explosively powerful trigger for heart disease and stroke.


What's the number two cause for heart disease?

After small LDL comes low HDL cholesterol. Ask anyone who has had a heart attack: What was your cholesterol panel like? 9 out of 10 will say "My LDL cholesterol was 135 mg/dl" while knowing little or nothing about HDL, which is commonly in the 30-42 mg/dl range--sufficient to contribute to heart disease risk considerably.


Can "normal" thyroid hormone tests still contribute to heart disease?

Yes. Hypothyroidism is an exceptionally powerful risk factor for heart disease. Many people have been told that their thyroid tests are "normal," when in reality risk for heart disease may be as much as tripled from low thyroid with thyroid blood tests in the "normal" range.


Does a "balanced, healthy diet" prevent heart disease?

No, it does not. In fact, the modern notion of a "balanced, healthy diet" increases risk for heart disease. Of course, the dangers of such diets vary, depending on how you define it. If it's the diet advocated by the USDA Food Pyramid, then it is an enormously destructive diet that causes your health to careen towards both diabetes and heart disease. The American Heart Association TLC diet is little better.


Does eating fish twice a month reduce heart attack risk?

Yes, it does--but just barely. Unfortunately, large studies that show that eating fish as infrequently as twice per month reduce risk for dying from heart attack have led some authorities to suggest that's all you need to do. What they fail to understand is that the benefit is dose-dependent--the greater the intake of omega-3 fatty acids, the greater the benefit (within reason, of course). So, while the effect can be detected by eating fish twice per month, it doesn't mean that full benefits are achieved with this "dose." Full benefits are obtained by mimicking the omega-3 intake of the Japanese.


Do nutritional supplements reduce risk for heart attack?

If you are referring to vitamin D, then, yes, nutritional supplements reduce risk for heart attack . . . enormously. We need more data to validate this phenomenon, though epidemiologic observations strongly bear this out, including the Health Professionals Follow-up Study, the Framingham Heart Study and NHANES, all of which demonstrate a graded effect: the lower the vitamin D blood level, the greater the risk for heart attack.

Over the years, we've experienced more than our share of disappointments in nutritional supplements for heart disease, including vitamin E and B vitamins to reduce homocysteine. But I believe that nothing approaches the solid feel of vitamin D--no other nutritional supplement raises HDL, reduces triglycerides, reduces blood sugar, enhances insulin responses, reduces the inflammatory C-reactive protein, reduces blood pressure like vitamin D. Vitamin D is here to stay--and I'm very grateful.

And don't forget omega-3 fatty acids from fish oil, yet another supplement with unquestioned benefits for reduction of heart attack and death from heart attack.


Why didn't your doctor counsel you on the importance of these issues?

The primary reasons your doctor didn't tell you any of the above:

1) He/she has been persuaded that only drugs are of any real use in health. Nutritional supplements? Hah!

2) Neither the number one cause of heart disease in the U.S.--small LDL particles--nor the most aggressive cause for heart disease--Lp(a)--are corrected by patent-protectable, high profit pharmaceutical agents promoted to your doctor. Instead, these abnormalities can be corrected inexpensively, without prescription. That means no expensive commercials, no media spots, no write-ups in magazines.

3) Your doctor's business is to treat crisis: sore throat, broken ankle, lung tumor, heart attack. Prevent heart disease 10 or 20 years before it shows itself? Heck, no (unless the marketing pull of the drug industry is involved, of course).


It's best that you bear in mind: What your doctor doesn't know can kill you.

Thank you, Dr. Eades

6. mars 2009 William Davis (7)

Thanks to some readers of The Heart Scan Blog, I've become acquainted with Dr. Michael Eades' wonderful blog, Health and Nutrition by Dr. Michael R. Eades, MD.

Dr. Eades is co-author (with his wife, Mary Dan Eades, MD) of Protein Power

In one of his conversations, I stumbled on this exchange between Dr. Eades and one of his readers:



Reader: Regarding EBT scans, I looked up the topic on Google and read an informative 5-page article: EBT (Ultrafast CT) Scans - Godsend, or Scam? Dr. Fogoros says that false positives (where the EBT shows the presence of calcium, but the patient has little coronary artery blockage) occur about 50 percent of the time. The next step, if the EBT is positive, is to do a heart catherterization to find out whether there actually is coronary artery blockage. So the odds are that I’d have to worry!

Dr. Michael Eades: The info you got from Google is one of the reasons one shouldn’t get medical information online. As far as I’m concerned the EBT is the BEST way to determine the presence of plaque. If you have a positive calcium score, you have plaque, and there’s an end on’t (as Samuel Johnson would say). Now you may have a low calcium score for your age or you may have a calcium score that doesn’t change, which means you have stable plaque, but if you have a positive calcium score, you have some amount of plaque in your coronary arteries.

And whoever says that the next step to take if you receive a positive calcium score is a coronary artery cath is a real moron. That’s probably the last thing you would want to do if you are asymptomatic. All the cath procedure does is shows whether or not you have a blockage - you can have huge amounts of plaque (which are a disaster waiting to happen) and have a normal cardiac cath.

If you want to get a little more information on the validity of EBT than what you find on Google, take a look at Dr. Davis’ blog or get a copy of his book: Track Your Plaque. I’m not crazy about all of Dr. Davis’ dietary recommendations because he comes to diet from a different perspective than I, but the EBT info in his book is terrific.

Cheers–

Dr. Eades "gets" it. He understands that quantification of coronary plaque is a tool for prevention, not something to be subverted into the service of procedures for the financial benefit of my colleagues.

And I think that he is absolutely correct on the diet discussed in Track Your Plaque--it's due for a revision. I wrote the book in 2003, while we were still locked into the low-fat mindset. Much has changed.

Since then, our enormous experience in metabolic manipulation and lipoprotein analysis has shown that there is a far better way to correct the causes of coronary plaque and seizing hold of heart scan scores. In particular, the explosion of small LDL has prompted major changes in the diet, specifically removal of wheat and cornstarch, the foods that trigger small LDL particles.

(I am still in the midst of negotiations for release of a bigger and better Track Your Plaque II. In the meantime, Track Your Plaque Members can refer to the New Track Your Plaque Diet, Parts I, II, and III.)

Can millet make you diabetic?

5. mars 2009 William Davis (10)















If wheat is so bad, what about all the other grains?

First of all, I demonize wheat because of its top-of-the-list role in triggering:

--Appetite--Wheat increases hunger dramatically
--Insulin
--Blood sugar--Wheat is worse than table sugar in triggering a rapid, large rise in blood sugar
--Triglycerides
--Small LDL particles--the number one cause for heart disease in the U.S.
--Reduced HDL
--Diabetes
--Autoimmune diseases--Most notably celiac disease and thyroiditis.

Most other "healthy, whole grains" aren't quite as bad. It's a matter of degree.

Millet, quinoa, oats, sorghum, bulghur, spelt, barley, cornmeal--While they don't trigger appetite nor autoimmune diseases like wheat does (oat can in some people), they still pose a significant carbohydrate load sufficient to generate the other phenomena like excessive insulin and blood sugar responses. The grams of carbohydrate of these grains are virtually identical to wheat: 43.5 grams per 1/2 cup (uncooked). The exceptions are barley, which is especially loaded with carbohydrates: 104 grams per 1/2 cup, while oats are lower: 33 g per 1/2 cup.

It's all a matter of degree. Some people who are exceptionally carbohydrate-sensitive (like me) can have diabetic blood sugars with just slow-cooked oatmeal or quinoa. Others aren't quite so sensitive and can get away with eating them.

People with high blood sugars (100 mg/dl or greater) can be very sensitive to the blood sugar effects of these grain carbohydrates. The best marker of all are small LDL particles measured on a lipoprotein panel, such as NMR. Small LDL particles are exquisitely sensitive to your carbohydrate intake: small LDL gets worse with excessive sensitivity to grain carbohydrates, gets better with reduction or elimination.

Flagrant small LDL, in combination with low HDL, high triglycerides, and pre-diabetic or diabetic patterns all develop from carbohydrate indulgence, along with "wheat belly."

Don't believe it? The prove it to yourself: Go to Walmart and buy an inexpensive glucose meter and check your blood sugar one hour after eating. You can gauge the health of these foods by observing the blood sugar increases. (Small LDL closely parallels blood sugar rises.)

The grain that fails to trigger any of these abnormal patterns? Flaxseed. Flaxseed is entirely protein, fiber, and healthy oils, with virtually no digestible starches. In fact, flaxseed is one of the few foods that reduces the quantity of small LDL particles.

Are you a tree?

5. mars 2009 William Davis (6)
I assume you answered no. Then why would you consider taking the plant form of vitamin D (ergocalciferol)? That's the prescription form of vitamin D, often dispensed as 50,000 unit tablets.

There's nothing wrong with plants. Some of my favorite foods are plants, full of nutritional value.

Then why shouldn't vitamin D2 from plants be every bit as good as the human form of vitamin D?

I believe the issue boils down to taking hormones from non-human sources. (Remember: Vitamin D is a hormone, a very powerful one at that.) Plants can be wonderful sources of flavonoids, fibers, protein, fats, vitamins, minerals, and other healthy components. But hormones?

There are other examples of non-human hormones being given to humans with undesirable or unpredictable effects:

--Xenoestrogens, phytoestrogens, and non-human mammalian estrogens--While non-human estrogens may partially mimic human estrogens, they can also block estrogen effects, or exert altogether novel effects. Non-human mammalian estrogens like Premarin can exert very peculiar (side-)effects, despite their role as prescription estrogen supplementation in humans.

--Progestins--The synthetic versions of human progesterone, like their non-human estrogen counterparts, exert weird effects that are a world apart from real progesterone.

--Sterols--Similar in structure to human cholesterol (while not a hormone, a building block for hormones), sterols have been used to reduce intestinal cholesterol absorption. However, if sterols are absorbed into the blood, they can enormously accelerate growth of atherosclerotic plaque.

--Anabolic steroids--These modifications of the testosterone molecule build muscle, but also cause liver cancer, kidney failure, violent behavior, suicide and homicidal behavior. That's not normal.

Outside of a pharmacologic effect (e.g., prednisone in place of human cortisol), there is no reason to take a non-human hormone in place of a human hormone. For that same reason, there is NO reason to take plant vitamin D2 (prescription or over-the-counter) in place of human vitamin D3.

If the non-human hormone is identical to the human form, then there is no difficulty. The best example of this are thyroid hormones from pigs. That's what Armour Thyroid is, a thyroid hormone replacement that works wonderfully well.

You will notice that virtually all of the examples of non-human hormones substituted for human hormones share one common motivation: profit. Synthetic or modified versions are more readily patent-protectable, unlike their natural counterparts which are not.

Vitamin D2 is an anemic facsimile of the real human hormone, vitamin D3 (cholecalciferol). Stay away from it.

The Framingham Crap Shoot

22. November 2008 William Davis (2)
The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.


Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

At what score should a heart catheterization be performed?

21. November 2008 William Davis (2)
That's easy: NONE.

(Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)

In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms.

This question is a common point of confusion.

In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur.

However, EVERY heart scan score above zero is a reason to engage in a program of prevention.

"It's genetic"

17. November 2008 William Davis (17)
At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.


There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

Tim Russert Revisited

16. November 2008 William Davis (7)
A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention.

Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life.

Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.

What exactly could Mr. Russert have done to prolong his life? Several basic strategies:

--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half.

--Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.

Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end.

Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"

In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely.

Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.

Water: Bottled vs. tap

16. November 2008 William Davis (4)
The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water.

The full text of the study from the EWG can be viewed here.

They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified."

"EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."


For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.

Can CRP be reduced?

13. November 2008 William Davis (17)
The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.

CRP and Jupiter

11. November 2008 William Davis (15)
What is C-reactive protein (CRP)?

It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

In other words, many, many conditions, from trivial to serious, trigger increased inflammatory markers like CRP.

A recent analysis (Genetically elevated C-reactive protein and ischemic vascular disease of persons with genetically elevated levels of CRP) suggests that CRP does not, by itself, cause atherosclerotic disease. CRP is therefore simply a marker for conditions that heighten inflammatory responses.

The AstraZeneca people sponsored the enormous JUPITER study of the statin drug, Crestor, that has been causing a stir, mostly glowing pronouncements of how the world would be a better place if everyone took Crestor.

In JUPITER, nealry 18,000 people (men 50 years and over, women 60 years and over) took 20 mg per day Crestor for two years. Participants all had starting LDL cholesterols in the "normal" range of no higher than 130 mg/dl and elevated CRP of 2 mg/dl or greater.

Crestor treatment resulted in 44% reduction in nonfatal heart attack, nonfatal stroke, hospitalization for unstable angina, revascularization (bypass surgery, stents) and death from cardiovascular causes. The reduction in nonfatal heart attack was most marked at 55%.

Admittedly, these are impressive results. Benefits held true for both males and females. At the very least, JUPITER should put to rest some of the fringe arguments that statins do not reduce cardiovascular events. They do. There is no sense in arguing against that. While we might argue about the value of statins in various subsets of people, there is no doubt that they do indeed exert a significant effect.

However, contrary to the hype and broad pronouncements of my colleagues, my concerns are:

1) Rather than shotgun the inflammatory response with a statin drug regardless of cause, doesn't it make more sense to ask why a specific individual has an increased CRP in the first place? For instance, if the answer is vitamin D deficiency, doesn't correction of the deficiency make more sense? (Vitamin D by itself reduces CRP around 60%--more than statin drugs.) Not to mention you obtain all the extraordinary benefits of vitamin D restoration, such as reduced cancer risk, increased bone density, relief from winter "blues," rise in HDL, etc. How about junk foods, obesity, and unrelated inflammatory conditions? Would we therefore indirectly be treating obesity with Crestor?

2) Crestor 20 mg per day, contrary to the study and to many statin studies, will not be tolerated for long by the majority. Muscles aches are not common--they are inevitable, sometimes incapacitating. While JUPITER showed 15% of both treatment and placebo groups experienced muscle effects--no different--this is wildly contrary to real life.

3) While there was a 55% reduction in the number of heart attacks, there continued to be a substantial number of heart attacks in the Crestor treatment arm. Clearly, reduction of CRP with Crestor, while helpful, is not a cure.

I view studies like JUPITER as simply an interesting piece of semi-scientific evidence, tainted to an unknown degree by commercial interests (including those of Dr. Paul Ridker, one of the principal investigators). It is not a mandate to use Crestor carte blanche in people with elevations of CRP.

My interpretation of these data in a practical sense is that Crestor 20 mg per day as sole therapy is useful in a disinterested, non-compliant patient who is unwilling to make substantial changes in lifestyle and nutrition. Helpful? Yes, but hardly an invitation for the world to take Crestor.

I believe that doesn't include any of the readers of this blog.

Nutritional approaches: Large vs. small LDL

11. November 2008 William Davis (13)













It is now a rare person who does not have at least some proportion of their LDL cholesterol as small particles. I estimate that, of the people who come to the office or report their data on the Track Your Plaque website, 90% have at least 40-50% small LDL particles. Some people have 100% small LDL particles. The sample NMR lipoprotein report shows the result for someone with a severe small LDL pattern (the tallest red bar labeled 1354 nmol/L, compared to the 74 nmol/L of the tiny red bar of large LDL.)

The nutritional approach for small vs. large LDL differs. Small LDL particles are most sensitive to carbohydrate intake; large LDL particles are more sensitive to saturated fats.

The conventional "heart healthy" diet that restricts saturated fat reduces large LDL but exerts no effect on small LDL. Thus, a diet that is restricted in saturated fat and weighed more heavily with "healthy whole grains" triggers small LDL particles. Followers of the conversations here recognize that small LDL particles are flagrant triggers for coronary plaque; they have, in fact, become the number one most common cause for heart disease in the U.S.

When you have lipoproteins tested, you can therefore gauge the likely result obtained when specific dietary changes are made. Follow the low saturated fat advice, large LDL will drop modestly, but small LDL skyrockets.













(Image courtesy Liposcience, Inc.)


Eliminate sugars, wheat, and cornstarch and you will see small LDL plummet (along with total LDL).

As an aside, my personal observation is that the "need" for statin cholesterol drugs can be reduced dramatically by paying attention to this important LDL size distinction.

Factory hospitals

8. November 2008 William Davis (8)
Twenty years ago, the American farming industry experienced a dilemma: How to grow more soybeans, corn, or wheat from a limited amount of farmland, raise more cattle and hogs in a shorter period of time, fatter and ready for slaughter within months rather than years?













(Image courtesy Wikipedia)

The solution: Synthetically fertilize farmland for greater crop yield; “factory farms” for livestock in which chickens or pigs are crammed into tiny cages that leave no room to turn, cattle packed tightly into manure-filled paddocks. As author Michael Pollan put it in his candid look at American health and eating, The Omnivore’s Dilemma:


“To visit a modern Concentrated Animal Feeding Operation (CAFO) is to enter a world that for all its technological sophistication is still designed on seventeenth-century Cartesian principles: Animals are treated as machines—“production units”—incapable of feeling pain. Since no thinking person can possibly believe this anymore, industrial animal agriculture depends on a suspension of disbelief on the part of the people who operate it and a willingness to avert one’s eyes on the part of everyone else. . .”


Pollan goes on to argue that the cultural distance inserted between the brutal factory farm existence of livestock and your dinner table permits this to continue:


“. . .the life of the pig has moved out of view; when’s the last time you saw a pig in person? Meat comes from the grocery store, where it is cut and packaged to look as little like parts of animals as possible. The disappearance of animals from our lives has opened a space in which there’s no reality check on the sentiment or the brutality . . .”


The same disconnect has occurred in healthcare for the heart. The emotional distance thrust between the hospital-employed primary care physician, the procedure-driven cardiologist, the crammed-into-a-niche electrophysiologist (heart rhythm specialist) or cardiothoracic surgeon whose principal concerns are procedures—with an eye always towards litigation risk—mimics factory farms that now litter the landscape of the Midwest. The hospitals and doctors who deliver the process see us less as human beings and more as the next profit opportunity.

The “factory hospital” has allowed the subjugation of humans into the service of procedural volume, all in the name of fattening revenues. Never mind that people are not (usually) killed outright but subjected to a succession of life-disrupting procedures over many years. But whether livestock in a factory farm or humans in a factory hospital, the net result to the people controlling the process is identical: increased profits.

The system doesn’t grow to meet market demand, but to grow profits. The myth that allows this growth is perpetuated by the participants who stand to gain from that growth.

See hospitals for what they are: businesses. Despite most hospitals retaining "Saint" in their name, there is no longer anything saintly or charitable about these commercial operations. They are ever bit as profit-seeking as GE, Enron, or Mobil.

Medicare and The Law of Unintended Consequences

5. November 2008 William Davis (6)
This post carries on the line of conversation begun in The Origins of Heart Catheterization: Part I and Part II.



While Dr. Sones labored in the relative obscurity of his catheterization laboratory, the American public was experiencing a crisis in healthcare availability, particularly among the over-65 age group. The population of elderly in the U.S. was growing rapidly. Between 1950 and 1963, their ranks grew from 12 million to 17.5 million. The cost of hospital care was also increasing 6.7% annually, several times the rate of increase in the cost of living of the time. From 1950 to the day of Dr. Sones’ discovery, the average cost for a day in the hospital jumped from $29 to $40. As a result, private health insurance carriers were forced to increase rates, driving premiums higher and farther out of reach for many. Half of all elderly were uninsured. Many feared that, while the sophistication of medical services advanced, healthcare was becoming increasingly unavailable to many, perhaps most, Americans.

The pivotal contribution that ignited wide dissemination of healthcare technology didn’t come from a physician, nor someone in healthcare. It was spurred by a nearly-forgotten bureaucrat. Without the behind-the-scenes laboring of this one man, the present healthcare system might be quite different.

It was largely the work of Nelson H. Cruikshank, an ordained Methodist minister with a Master of Divinity degree and veteran of battling for rights of the elderly and poor deprived of health care. For 10 years, Cruikshank served as director of the AFL-CIO's Social Security Department and had been instrumental in getting the Social Security Disability act passed. Working on the side of organized labor but maintaining the public demeanor of a church pastor, Cruikshank gained a reputation as a fighter for the working man, one who didn’t back down from a political brawl. In an interview regarding the question of corporate-retained earnings for capital investment, he blasted the practice, calling it "taxation by corporation without representation. Through prices paid for consumer goods, buyers are providing capital for industries over which they have no control and from which they receive no dividends” (Time Magazine, Dec. 20, 1948).

For years, Cruikshank lobbied tirelessly on behalf of American unions to bring the new national healthcare bill, known as Medicare, to a vote on the floor of Congress. Numerous efforts at a national program had languished for a decade before Medicare was drafted, and the Medicare legislation remained bottlenecked for years in committees. Cruikshank’s relentless and forceful persuasion was instrumental in finally bringing the bill to a vote. Among the most vocal opponents Cruikshank parried was the American Medical Association (AMA), terrified that the new program would lead to loss of control over healthcare delivery and reimbursement. The AMA labeled Medicare "the most deadly challenge ever faced by the medical profession."

Cruikshank proved how tough he was when he faced off with Dr Morris Fishbein, then president of the AMA, in a radio debate. Oscar R. Ewing, attorney and Democratic political organizer under the Truman administration, offered these reminiscences of the debate:

“Dr. Fishbein described the horrible confusion that existed in the [government-run] British Health Service that had recently been established in Britain. He told of the utter confusion that he found existed when he was in England a few weeks previously; that there were long queues in every doctor's office, that doctors were overburdened with paper work; that a mother who wanted an extra allowance of milk for her sick child had to get a doctor's prescription for it and then go to the Health Department for permission to buy the milk. Dr. Fishbein painted a picture of complete confusion.

“After Dr. Fishbein had described all these horrible details he found existing when in England a few weeks earlier, Mr. Cruikshank pulled out this particular diary [published in a nationally-syndicated column called “Dr. Fishbein's Diary” ] of Dr. Fishbein in which he described his last visit to London. He had arrived in London Friday morning and that afternoon had gone out to spend the weekend with Lord and Lady so-and-so at their country place; that he'd come back to London Monday morning, had stopped by the Health Department to pick up some papers, and had gone on to catch the noon plane for Paris. So the questioner then asked, "Well, is your appraisal of the British Health Service based on those few hours in London?" The question was a stinger and pretty much discredited Dr. Fishbein.”

(Interview by Mr. J.R. Fuchs, April 29, 1969; Harry S. Truman Library Archives)



Cruikshank went on to point out that Dr. Fishbein had indeed never visited the offices of British general practitioners and had spent his brief stay in the company of British aristocracy, attending the Olympics, then making the rounds of Parisian night clubs. Fishbein stumbled through the remainder of the interview, trying unsuccessfully to cover up his gaff. Dr. Fishbein was forced out of his post as AMA president by his peers shortly following the humiliating episode.

Largely due to the years of behind-the-scenes maneuvering by Mr. Cruikshank, on July 30, 1965, President Lyndon Johnson signed the Social Security Amendment that enacted the Medicare program. The legislation that survived into law included Medicare Part A, the portion of the program providing payment for hospital-based diagnostic and treatment services, and Medicare Part B, allowing payment for office-based services and outpatient diagnostic tests.

Finally, after decades of political battles, a national healthcare bill had been passed. Although benefits were restricted to only those eligible for Social Security benefits, it represented a start, a first step toward greater access to healthcare for the broader American public.

At first, the full implications of the Medicare program were not apparent. But as healthcare technology advanced, including that sparked by Sones’ innovation in coronary imaging, Medicare, much as engineered in large part by Nelson Cruikshank, proved a bonanza of payment for heart procedures. Medicare also set the pace for the payment for procedures by non-government, private health insurance.

Thus the stage was set. Thanks to Medicare, over the next 40 years cardiovascular healthcare services, yielding generous revenue for practitioners and hospitals, exploded on the scene, much to the surprise of many, including the AMA. When then president of the American College of Cardiology, Dr. Charles Fisch, was asked how the passage of Medicare affected cardiology, he replied, “It made cardiologists rich, as simple as that” (American Cardiology: The History of a Specialty and Its College, W. Bruce Fye, MD). Indeed, from its introduction in 1965 to 1980, Medicare payments for health claims ballooned 10-fold from $9.6 billion to $105.7 billion, a substantial portion of which went to pay for cardiology claims.

Little did Nelson Cruikshank, ministerial defender of the working man, anticipate that the Medicare he helped engineer would prove to be the catalyst for explosive growth of the modern cardiovascular healthcare system. Ironically, the program of healthcare-for-all that Cruikshank envisioned has, over the last 40 years, soured into a self-serving system that has been corrupted by the profit motive.

In too many instances, it’s a system that uses the working man as its victim, rather than its beneficiary.
All posts by william-davis

When MIGHT statins be helpful?

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

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

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

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

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

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

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

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

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

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

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

Advanced topics in nutrition

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

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

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

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

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

The New Track Your Plaque Guide now available

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

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

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

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

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

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

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

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


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

Don't wet yourself

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

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

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

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

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



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

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



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

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

Wheat brain

30. March 2011 William Davis (52)
Among the most common effects of wheat are those on the brain.

Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.)

It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.)

Here is Heart Scan Blog reader, Nicole's, mental fog story:

I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.

I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!

In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!

And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!

Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.

Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.

The Westman Diet

27. March 2011 William Davis (71)
Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Handy dandy carb index

25. March 2011 William Davis (21)
There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.

Battery acid and oatmeal

23. March 2011 William Davis (38)
Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

What'll it be: Olive oil or bread?

21. March 2011 William Davis (0)
We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category.

But what's the worst of all? Combining fats with carbohydrates.

Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods.

John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):

LDL particle number 1800 nmol/L
Small LDL 923 nmol/L


(The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)

Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.

We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:

LDL particle number 2200 nmol/L
Small LDL 1378 nmol/L

Note that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)

John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:

LDL particle number 2400 nmol/L


Let's

Chocolate peanut butter cup smoothie

19. March 2011 William Davis (18)
Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.