Do you eat wheat? I thought so.

I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “


Here's some of their starting salvos on their 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.
All posts by william-davis

What's for breakfast?

Breakfast, for some reason, seems to be the toughest meal of the day for many people.

I think it's because the quest for sweet has dominated the American breakfast for so long, with its half-century legacy of cartoon character-festooned breakfast cereals; baked flour products like pancakes, waffles, and English muffins; more recently, "healthy" alternatives like bran muffins and oat waffles.

This breakfast lifestyle has also contributed to the obesity and diabetes ("diabesity") epidemic. Breakfasts of wheat- or corn-based cereals, even those labeled "heart healthy," fruit, and whole grain breads are guaranteed paths to low HDL cholesterol, high triglycerides, flagrant small LDL, increased inflammatory responses, high blood pressure, and higher blood sugar. Such foods also make you tired, make your abdominal fat grow (wheat belly), and increase appetite so that you want more.

So what can you eat for breakfast that doesn't provoke these patterns?

I will never pretend to be terribly clever in creating meal menus, but I can tell you what has worked for me and many of my patients. Be warned: It may require you to suspend your previous notions of what "should" be included in a list of breakfast foods.

Here are some examples that you may find helpful:

--Raw nuts--one or several handfuls of raw almonds, walnuts, pecans, pistachios
--Cheeses--the real, traditional sorts like gouda, goat, Swiss, edam, etc. (not Velveeta, Cheez Whiz, etc.)
--Eggs, Egg Beaters--and "spice" them up with sun-dried tomatoes, salsa, olives, tapenades, olive oil, onions, green peppers, etc.
--Yogurt (real, of course), cottage cheese
--Ground flaxseed, oat bran--as hot cereals or added to yogurt, cottage, or other foods. Esp. helpful for reducing both total LDL and the proportion of small LDL.
--Oatmeal--slow-cooked, not the instant nonsense.
--Soups--great for winter.
--Dinner foods--chicken, beef, fish, green beans, asparagus, tomatoes, etc., most easily added by saving left-overs from dinner. You'll be surprised how filling dinner foods eaten at breakfast can be.

It's really not that tough. It just means selecting from an entirely different list of foods than you might be accustomed to.


Copyright 2008 William Davis, MD

The first lawsuit?


The closing arguments in actor John Ritter's wrongful death lawsuit are over and the two doctors charged with negligence cleared, five years after his death from a dissection (tear of the inner lining) of the thoracic aorta. The family sought $67 million in damages, claiming that the aortic dissection was misdiagnosed as a heart attack and that the enlarged aorta should have been reported to Mr. Ritter two years earlier during a full body scan.

The AP story can be viewed at http://ap.google.com/article/ALeqM5gmv6HnJJPBee2gWgEYResT5m6YkAD8VDF9CO0


Well, perhaps this is the start of a trend. Up until now, it has been commonplace for doctors to ignore many of the important findings on heart scans, full body scans, and similar direct-to-the-public imaging services. For instance, similar to John Ritter's case, enlarged thoracic aortas are commonly ignored. I'd even say that as a rule they are ignored. I have seen many patients in consultation who have had large aortas identified on heart scans, yet nothing--not a thing--was done about it. While the doctors escaped a lawsuit this time, it might not happen a second time.

I truly hope that Mr. Ritter's unfortunate experience and the consequent lawsuit do not trigger the usual defensive medicine response of resorting to major procedural "solutions."

A better response would be to 1) identify the problem--enlarged aorta in this case, 2) identify the causes, then 3) correct the causes. It does not necessarily mean that a major procedure like replacing the aorta (a horrendous surgery, by the way) needs to be pursued each and every time.

It is possible that Mr. Ritter's lawsuit is just the first. Over the next several years, it could trigger an avalanche of lawsuits for all the neglected findings on tests like heart scans, body scans, and other imaging methods that are gaining expanded direct-to-consumer access.


Images courtesy Wikipedia.

The origins of heart catheterization: Part II

On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.)

In 1958, no one had yet injected dye directly into the coronary artery of a living human.


Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:

“It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”


*An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.

Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.

Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.

Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers.

Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery.

Thus was born the modern age of heart catheterization.

Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited.


Copyright 2008 William Davis, MD

The origins of heart catheterization: Part I

The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.



Thus, the very first catheterization of the heart was performed.



An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.


Copyright 2008 William Davis, MD

Conventional therapy vs. alternative therapy

Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl


You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.


Copyright 2008 William Davis, MD

The JELIS Trial

The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

This enormous trial followed a simple design:

Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs.

Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty.

After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%.

There are several features that make the JELIS trial interesting:

--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.

--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events.

--There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females.

--A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit.

--It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations.


One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results.

Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil.


Copyright 2008 William Davis, MD

Omega-3 MUST be from fish oil

Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.


Copyright 2008 William Davis, MD

Osteoporosis and coronary calcium

Several studies over the years have demonstrated a curious paradox:

People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque).

People with more coronary disease and higher heart scan scores tend to have more osteoporosis.



In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related.

I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.

So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic.

The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density).

























The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis.
























It makes you wonder if the disordered metabolism of calcium through vitamin D deficiency allows transport of calcium away from bone and into coronaries. This has, however, been shown to not be the case. Instead, they are separate processes, each under local control, but sharing a common pathophysiology (causative factors).

An intriguing question: Would the 79-year old still look like the 46-year old had he begun increasing his vitamin D intake at, say, age 30?

About comment responses and moderation

Just a brief word about my responses to reader comments:

I appreciate the many often insightful and interesting reader comments I receive to the Heart Scan Blog. However, managing them and responding to them has simply become impossible, due to time demands.

I'm afraid that I am unable to answer questions seeking medical advice; this is for your doctor, who knows you and can diagnose and prescribe. I cannot.

I'm also unable to engage in lengthy debates; I've had commenters become very angry when I was unable to engage in lengthy conversations on some topic. Nor am I able to do Google or literature searches for commenters, or review studies, papers, or other materials.

I would urge any readers who wish to engage in in-depth discussions about these issues, talk about lipoproteins, heart disease reversal, etc. to do so on the Track Your Plaque Forums. Yes, it is a fee-for-membership website, a model that has become necessary to pay for the services we provide (not pay me).

I wish that I could answer all the concerns and questions that come my way, but it's simply physically impossible doing so while maintaining a full-time very busy cardiology practice, developing the Track Your Plaque website (which is becoming an enormous responsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

"Flying in the fog"

I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .













On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.



Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.



Copyright 2008 William Davis, MD