Heart scan gone wrong

Those of you reading the Heart Scan Blog, I hope, have come to appreciate the power in measuring atherosclerotic plaque, the stuff of coronary artery disease, and not relying on indirect potential "risk factors," especially the fictitious LDL cholesterol.

However, like all things, even a great thing like heart scans can be misused. Here's a story of how a heart scan should NOT be used, submitted by a reader.


Dr. Davis,

First of all, let me start out by commending you on all of the work you are doing with your website, blogs, etc. You are truly a breath of fresh air at a time when conventional medicine is no longer making any sense. In the last 3 years or so, I have spent a lot of time using the internet to try and find answers . . . and just about every time, when I find things that make "sense," it coincides which the recommendations you provide. Thank You!!

I am 56 years old, and roughly 5 years ago I bought your book, Track Your Plaque, primarily because I had asked my then Internal Medicine physician about why we weren't more "proactive" about determining the state of our cardiovascular health...since the means to do so existed (scans). He was trying to get me to go on a statin because my cholesterol #'s were a little high and at the time I smoked. Other than that, I was in perfectly good health with no side effects or issues. The following year at my annual physical, we again discussed this and he gave me a few options and I ended up having a calcium score done, which showed some blockage, but again, I never had any pains, sweats, or any other symptoms whatsoever, and I am a very active former athlete. This is when I bought your book to try and set a course of plan that wouldn't just include pharmaceuticals.

At the same time, my father was in his last months of life dealing with prostate cancer and the multiple radiation and chemo treatments, so I was making many trips from my home to be with him . . . a 4 hour drive, and very disruptive to family, as I still have 3 kids at home. At what I thought was going to be my last visit with him, I stopped at the cemetery he had planned on being buried to confirm details and such and then started home.

As I was driving, a symptom hit me which I was unfamiliar with (pretty sure it was an anxiety attack now) and I stopped at a friend's house in Chicago, as I didn't want this to be a heart attack while I was driving. This is when I began thinking about the heart scan and the blockage, and ended up driving back later that night and went right to the ER....not because I had any chest pains, but thought it best to be checked out because I did not want to go before my dad did. I ended up staying the night. In the morning the cardiologist PA [physician's assistant] came in with a copy of my calcium scoring and said it was best to have a heart cath...which I was in total agreement with since it would definitively tell me the current condition of my coronary vessels. As I was getting ready to be wheeled into the cath lab, they approached me with a form that would allow them to treat (stent). This is where I became very uncomfortable, in that I had never even met the cardiologist . . . and I didn't like this. No one ever had asked if I was experiencing pains or anything else . . . but I buckled and signed the form.

Before you knew it, I was awake watching my heart being cathed and the cardiologist angry because they did not have all the right sizes of stents, so he had to use a couple extra and I ended up w/5 total . . . and my life changed forever! In looking back, I can't necessarily argue the need for intervention, but in hindsight, it would have been nice to have tried an alternative method of reversing my plaque, especially since I had never experienced any symptoms and didn't appear to be in any imminent danger.

Upon release from the hospital I was put on a cocktail of drugs that typically follow and I then began to search and research. No one talked to me about lifestyle changes other that smoking....but nothing on diet or other means of cholesterol control, etc....in fact, when I had to pick out my meals in the hospital, they wouldn't let me have cheese....but the rice crispy treat was fine....how stupid! They originally told me the Plavix had to last 6 months....and then 12....and then 2 years....I stayed on it for 1-1/2 years and it was the only thing other than a baby aspirin. I went to another cardiologist out of town and he wanted me back on 5 or 6 medications and said that now I had the stents....I would have to be on these for life.....and he was the expert that talked at several main conferences.....my last trip to him.

Now, fast forward to about 6 months ago: I was participating in a father-son soccer scrimmage and was playing goalie. It was wet out and I couldn't catch very well. So being the competitive person I am, I resorted to using my chest on several of the saves and also took a direct blow to my eye ( I wear glasses) and the eye started swelling up pretty good. We then finished and went inside to have pizza and everyone was concerned about my eye. About 30 minutes later I excused myself as i felt some pretty significant sweats and subsequently a pretty severe pain directly in the middle of my chest....I was having a heart attack! Called 911 and went to hospital (2-1/2 years since original stents) and my local cardiologist removed the blockage that was at the anterior portion of my 1st stent causing the blockage. The huge disappointment to me is that I had taken many steps to improve my overall health. But now that I have foreign bodies in my vessels, the chance of further clotting is something that i will most likely always have to live with.

BU, Michigan



This is an example of how heart scans should NOT be used. They should NEVER be used to justify a procedure, no matter how high the score or where the plaque is located. The "need" for procedures is determined by symptoms (BU's symptoms were hardly representative of heart disease), blood findings, EKG, stress testing, and perhaps CT coronary angiography. "Need" for procedures can never be justified simply on the basis of the presence of plaque by a heart scan calcium score.

Unnecessary procedures like the one BU underwent are not entirely benign, as his experience at the soccer game demonstrated.

Heart scans are truly helpful things. But, like many good things, they are subject to misuse in the hands of the uncaring or greedy.

Blood sugar: Fasting vs. postprandial

Peter's fasting blood glucose: 89 mg/dl--perfect.

After one whole wheat bagel, apple, black coffee: 157 mg/dl--diabetic-range.

How common is this: Normal fasting blood sugar with diabetic range postprandial (after-eating) blood sugar?

It is shockingly common.

The endocrinologists have known this for some years, since a number of studies using oral glucose tolerance testing (OGTT) have demonstrated that fasting glucose is not a good method of screening people for diabetes or pre-diabetes, nor does it predict the magnitude of postprandial glucose. (In an OGTT, you usually drink 75 grams of glucose as a cola drink, followed by blood sugar checks. The conventional cut off for "impaired glucose tolerance" is 140-200 mg/dl; diabetes is 200 mg/dl or greater.) People with glucose levels during OGTT as high as 200 mg/dl may have normal fasting values below 100 mg/dl.

High postprandial glucose values are a coronary risk factor. While conventional guidelines say that a postprandial glucose (i.e., during OGTT) of 140 mg/dl or greater is a concern, coronary risk starts well below this. Risk is increased approximately 50% at 126 mg/dl. Risk may begin with postprandial glucoses as low as 100 mg/dl.

For this reason, postprandial (not OGTT) glucose checks are becoming an integral part of the Track Your Plaque program. We encourage postprandial blood glucose checks, followed by efforts to reduce postprandial glucose if they are high. More on this in future.

Diabetes from fruit

Mitch sat in my office, looking much the same as he had on prior visits.

At 5 ft 7 inches, he weighed a comfortable 159 lb, though he did have a small visible "paunch" above his beltline.

I had been seeing Mitch for his heart scan score of 1157 caused by low HDL of 38 mg/dl, severe small LDL (87% of total LDL), and lipoprotein (a).

Part of Mitch's therapeutic program was elimination of wheat, cornstarch, and sugars, the three most flagrant triggers of small LDL particles, and weighing his diet in favor of oils and fats to reduce Lp(a). However, Mitch somehow failed to follow our restriction on fruit, which we limit to no more than two 4 oz servings per day, preferably berries. He thought we said "Eat all the fruit you want." And so he did.

Mitch had a banana, orange, and blueberries for breakfast. For lunch, along with some tuna or soup, he'd typically have half a melon, a pear, and red grapes. For snacks, he'd have an apple or nectarine. After dinner, it wasn't unusual for Mitch to have another piece of fruit for dessert.

Up until Mitch's last visit, he'd had blood glucose levels of 100-112 mg/dl, above normal and reflecting mild insulin resistance and pre-diabetes. Today, on his unlimited fruit diet, his blood sugar: 166 mg/dl--well into diabetes territory.

I helped Mitch understand the principles of our diet better and advised him to reduce his fruit intake to no more than the 2 small servings per day, as well as sticking to our "no wheat, no cornstarch, no sugar" principles.

While fruit is certainly better than, say, a half-cup of gummy bears (84.06 g carbohydrates, 50.12 g sugars), fruit is unavoidably high in carbohydrates and sugars.

Take a look at the carbohydrate content of some common fruits:

Apple, 1 medium (2-3/4" dia)
19.06 g carbohydrate (14.34 g sugar)

Banana, 1 medium (7" to 7-7/8" long)
26.95 g carbohydrate (14.43 g sugar)

Grapes, 1 cup
27.33 g carbohydrate (23.37 g sugar)

Pear, 1 medium
25.66 g carbohydrate (16.27 g sugar)

Source: USDA Food and Nutrient Database

Fruit has many healthy components, of course, such as fiber, flavonoids, and vitamin C. But it also comes with plenty of sugar. This is especially true of modern fruit, the sort that has been cultivated, hybridized, fertilized, gassed, etc. for size and sugar content.

When you hear such conventional advice like "eat plenty of fruits and vegetables," you should hear instead: "eat plenty of vegetables. Eat a small quantity of fruit."

The sniff test

It is well established that omega-3 fatty acids from fish oil are free of mercury, PCBs, furans, and other pesticide residues. Several independent analyses have all agreed: little to none are contained in fish oil. In the Consumer Lab series of assessments, for example, no fish oil supplement failed because of any heavy metal or pesticide residue.

However, oxidative byproducts are a problem. Just as fish that sits on the store shelf or your refrigerator too long starts to smell "fishy," so will fish oil. When fish or fish oil becomes rancid, smelling like rotten fish at its worst, it means that

Is there something fishy about fish oil?

To be sure, there's plenty of misinformation out there about fish oil. Take a look at the swill that passes for health information on Woman's Day: On Call with Dr. Sandy: Fish Oil and Mercury:



Reader Question: My doctor recommended that I take a fish oil supplement, but I'm concerned about mercury. Is there any way to tell which brands are lowest in mercury content?



On Call Response: When it comes to OTC supplements, the answer is no. Though most fish oil supplements sold by major brands are probably safe, there's really no way to tell what's in the bottle or how much mercury it might contain.




Perhaps Dr. Sandy should read the many independent analyses performed on nutritional supplement fish oil, including those at Consumer Lab and Consumer Report before she offers her blind criticisms.

Lovaza vs fish oil supplements?

Lovaza is the FDA-approved form of fish oil that is available only by prescription. It contains 842 mg of the omega-3 fatty acids, EPA and DHA, per capsule.

The FDA application for Lovaza is viewable here on the FDA website. Interestingly, while there is plenty of the usual regulatory gobbledy-gook about toxicology, dose escalation, and efficacy in the extensive documentation, there is little said about the issue of contamination.

In other words, critics of nutritional supplement fish oil harp on the possibility of contamination with mercury and pesticide residues, like dioxin and PCBs (polychlorinated biphenyls). Yet there is virtually nothing about these same issues in the FDA application for Lovaza.

Let's take a look at a sample over-the-counter fish oil product. Our friends at PharmaNutrients (a new Track Your Plaque partner for nutritional supplements) have a fish oil product called PharmaNutrients" Cardio. Here's an independent analysis of the Cardio product (per 1000 mg fish oil capsule):

EPA content: 566.1 mg
DHA content: 216.6 mg
(Total EPA + DHA 782.7 mg)

Cardio passed all tests for peroxides, PCBs, dioxin, furans, dioxin-like PCBs, and heavy metals (arsenic, cadmium, lead, mercury) using criteria at least 60% more stringent than European Commission (EC) standards (EC standard <2 picograms/gm for dioxins and furans, PharmaNutrients <1 picograms/gm; EC standard <10 picograms/gm for dioxin-like PCBs, PharmaNutrients <3 picograms/gm). PCBs levels in particular are less than 0.009 ppm, 90% below the industry-wide purity standard of 0.09 ppm. Likewise, mercury is >90% lower than European Commission standards.

In other words, this over-the-counter "pharmaceutical grade" fish oil has virtually nothing but omega-3 fatty acids.

Interestingly, the PharmaNutrients fish oil capsule also contains the third omega-3 fatty acid, docosapentaenoic acid (DPA), a neglected form that some authorities have proposed has superior cardiovascular protective properties over eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). If DPA is included in the analysis, PharmaNutrient's Cardio contains a total of 900 mg omega-3 fatty acids per capsule.

At some point, I'd like to see a head-to-head comparison not just on purity grounds, since I am convinced that high-quality products like Cardio can match or exceed the purity of prescription fish oil, but on efficacy in raising omega-3 blood levels, the omega-3 index. (The omega-3 index is a predictor of heart attack and sudden cardiac death--the higher, the better.) My prediction: High-quality fish oil supplements will match or exceed prescription fish oil.

More on blood sugar

Take any of the following foods:

One chicken breast
Quarter-pound ground beef
6 oz salmon steak
½ cup raw almonds
3 eggs scrambled in olive oil

How much is blood sugar increased by any item in the above list?

If you said virtually zero, you’re correct. Eat any of these foods, regardless of portion size, and blood sugar won’t change substantially. If you started with a blood sugar of, say, 90 mg/dl, 1-2 hours later it would be 90 mg/dl. It might go up or even down a few milligrams, but for all practical purposes it remains substantially unchanged.

How much is blood sugar increased by the foods in this list:

2 slices multigrain bread
1 whole wheat bagel
4 oz high-fiber breakfast cereal
2 whole grain pancakes, 2 oz maple syrup

The foods in this list are a different story from the first. Depending on your body weight, exercise habits, and other factors, a typical blood sugar response in an otherwise healthy non-diabetic person would be 120 mg/dl to 160 mg/dl. In someone with diabetes, it could easily exceed 200 mg/dl.

That isn’t good. Large blood sugar excursions to 140 mg/dl have been clearly associated with greater risk for heart attack, progression to diabetes, inflammatory responses, and other adverse health effects. In fact, blood sugars as low as 100 mg/dl after eating have been associated with increased cardiovascular risk.

Then why are the USDA, American Heart Association, the American Dietetic Association, and the American Diabetes Association telling us to eat more of the foods that shoot blood sugar up to such high levels? “Eat more healthy whole grains”?

To see how much the issue of exaggerated blood sugars after eating applies to you, a simple blood sugar check 1-2 hours after eating can show you. Either your doctor can have the test drawn or you can purchase your own inexpensive glucose meter (e.g., Walmart, Wagreens).

My prediction: You will be very surprised at blood sugar responses after common foods, including “healthy whole grains.” And, by the way, keeping blood sugar excursions to a minimum will facilitate weight loss.

Postprandial blood sugar: Almonds vs. whole wheat bread

Here's my postprandial (after-eating) blood glucose demonstration.



I tested raw almonds vs. 100% whole wheat bread, matched for calories. (Full nutritional composition below.)



Blood sugars:

Raw almonds

Start:

One-hour after eating:





2 slices 100% whole wheat bread

Start:

One-hour after eating:





100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384





23 almonds, raw



Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

Food sources of vitamin K2: Reprint

For some reason, my December, 2007, Heart Scan Blog post, Food sources of vitamin K2, has been receiving a lot of traffic.

I therefore reprint the vitamin K2 post below.





Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.















Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Green coffee bean extract in AGF Factor I

Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

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

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

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

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

urner&utm_medium=feed&utm_campaign=Feed%3A+sixservings+%28SixServings.org%29">Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly explodes on the scene!



Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.



Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

Good fat, bad fat

No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D or . . .

You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

More lipoproteins zero!

A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!


Diet: One size does NOT fit all

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.


This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


Why ATP-3 is B--- S---

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

How far wrong can cholesterol be?

Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

The best artificial sweeteners

Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Sugar Nation



Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.

The Framingham Crap Shoot

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?

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"

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

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

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?

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

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














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

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

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.