Vitamin D for winter blues?

Winter is now over and spring is in the air, even in Wisconsin.

In this part of the country, winter blues are commonplace. Sometimes called Seasonal Affective Disorder (SAD) when it's severe enough to cause functional impairment, feelings of fatigue, lack of motivation, or the blues are very frequent when days are short and sunlight is in short supply.

I've been seeing many people in the last several weeks who were advised to add vitamin D to their program last fall. Christopher's experience was typical.

"You know, since you told me to take vitamin D, I didn't get sad and tired like I do every winter. This is the first time I can remember that happening. I didn't sleep as much and I didn't get that feeling of always being overwhelmed."

I've felt it myself this past winter. I think there's some real truth to this effect.

Dr. Bruce Hollis has published a small experience in treating people with SAD with vitamin D and showed measurable improvement in depression. (One recent study in older women failed to show any effect, however, when small doses of vitamin D of 800 units were administered. In my experience, this dose doesn't even come close to normalizing blood vitamin D levels.)

The best source for in-depth information on vitamin D is Dr. John Cannell's website, www.vitaminDcouncil.com. If you've read Dr. Cannell's discussion on the Track Your Plaque website, you know that he is an articulate spokesman for the benefits of vitamin D replacement. He also persuasively argues that vitamin D deficiency is rampant in northern climates and in people who don't get frequent sun exposure. Interestingly, we now have two studies of populations in Florida and one in Hawaii, both of which showed substantial percentages of people even in these tropical climates to be deficient in vitamin D (around 50% in Hawaii and 30% in Florida).

The dose we've used with much success is 2000 units per day in females, 3000 units per day in males. This yields normal blood levels of around 50 ng/dl in around 80-90% of people. Occasional people will require more, some less. The best way to do it is to check a baseline blood level and a level on therapy to determine the adequacy of your dose.

Dr. Cannell will tell you that it's very important to have your doctor check the right test: 25-OH-vitamin D3, not 1,25-diOH-vitamin D3. These are two very different tests of two different compounds.

In the Track Your Plaque program, we use vitamin D to reduce pre-diabetic tendencies, reduce blood pressure (vitamin D is an inhibitor of the pressure-raising hormone renin), shut down inflammation, and gain better control over coronary plaque (mechanism uncertain). In the process, you will sharply reduce risk of osteoporosis, colon and prostate cancer.

And maybe you'll be brighter when the winter blues come around again.

$4 per gallon gas is good for your health!

Gasoline is now approaching $4 per gallon in some parts of the U.S. But there's a silver lining in this dark cloud. In fact, I see this as a positive for your health.

How can higher gas prices possbily be good for health?

Imagine this trend continues: Fuel prices climb higher and higher. Driving your car will become increasingly more costly. What will be the fall-out?

Well, there will be a number of implications. But among the developments will be a broad impetus towards rejecting fuel-based sources of transportation. This may come as a shock to you, but humans legs were meant for walking!

Remember way back when, Mom would say "We need some milk"? In 1953, you wouldn't get in your car and zip to and from the supermarket. Instead, you would walk a quarter-mile, half-mile or more to the store. And you would carry your bags back. You might walk a mile or two to school and back. In 2006, this seems incomprehensible.

Higher fuel prices will prompt a gradual return to 1953--As transportation costs climb, your town may try and make it easier to walk as an alternative means of getting places.
Imagine that it was easy to walk three blocks to the grocery store, produce stand, work or school, walk along pleasant paths on the weekend, stroll to the home of friends. Drive or walk? Leave the car in the garage and save you and your family hundreds of dollars a month in gas bills.

In a few years, given the current fuel cost trends, there won't be a choice. But it will be in your favor for health.

Another Ornish casualty

Barry's lipoproteins were nearly all corrected to perfection: LDL 64 mg, HDL 57 mg, triglycerides 45 mg. He was approaching the Track Your Plaque goal of 60/60/60, the levels we find tip the scales heavily in your favor for achieving plaque reversal.

But one problem still prominently persisted: small LDL. Of Barry's 64 mg of total LSL, 90% of his LDL were small.

Barry was already on niacin (Slo-Niacin; Upsher Smith)1000 mg per day and fish oil, 4000 mg per day, both of which contribute to correction of this pattern. He had added occasional raw almonds and oat bran to his daily habits, both of which also help suppress small LDL. "I thought you told me that small LDL should go away if I did all this!" he lamented in frustration.

We probed Barry's diet choices more closely. "I eat really healthy foods, just like an Ornish program." Uh oh.

"What do you mean?" I asked.

"For breakfast, I have two slices of whole wheat toast--no butter or margarine, of course! I'll have Shredded Wheat with skim milk. That's it. My typical lunch is low-fat turkey--no mayonnaise!--on whole wheat. I'll add some low-fat whole wheat crackers or pretzels. That's pretty much my habit."

"How about dinner?"

"Dinner varies a lot. I'll usually have a low-fat meat like chicken or turkey, never beef, a vegetable, and a potato. I love rolls but I try to make them whole wheat. I don't use gravy. I love ice cream, so I've been having low-fat frozen yogurt instead. I guess that's about it."

Barry had indeed been counseled on how we approach nutrition. We, of course, do not endorse the low-fat approach of the Ornish program. Low saturated and hydrogenated fat, yes, but not the super-strict low-fat, "all fat is bad" approach of Dr. Dean Ornish.

Barry's diet is typical of someone on a low-fat restriction. When I asked him why he was eating this way, he admitted that he'd seen Dr. Ornish on a TV program in which he persuasively proclaimed that he reversed heart disease in his patients over the past nearly 20 years using this low-fat approach.

That explained it. Barry's nearly pure carbohydrate diet was triggering high blood sugar responses after meals, causing his insulin to skyrocket and magnifying the small LDL pattern.

I advised Barry to dramatically reduce his carbohydates like breads, pretzels, low-fat yogurt, crackers, etc. Instead, he could increase his lean proteins like eggs, egg whites, Egg Beaters, raw nuts and seeds, low-fat (yes, low-fat!) dairy products like yogurt and cottage cheese (both high protein), and healthy oils.

I've seen this happen with many people over the years: A severe low-fat restriction becomes a high-carbohydate diet. It's not uncommon for many people to have more than 70% of calories from carbohydrates on these programs.

The low-fat approach worked in the era of high-fat diets in the 1980s. In 2006, where convenience foods made with carbohydrates, especially wheat, predominate and pack 80% of supermarket shelves, low-fat is now a distorted nutritional mistake that leads to problems like Barry's uncontrolled small LDL, and often pre-diabetic or overt diabetes.

Should you take Plavix?

A question I get fairly frequently nowadays is, "Should I take Plavix?"

For the few of you who've managed to miss the mass advertising campaign for this drug on TV, USA Today, etc., Plavix is a platelet-blocking drug, known chemically as clopidogrel, that "thins" the blood and helps prevent blood clot formation in coronary arteries and carotid arteries, thus potentially reducing heart attack and stroke risk.

What if you have a heart scan score of, say, 450--should you take Plavix?

In general, no. First of all, aspirin and Plavix (generally taken together, since the effect of Plavix is incremental to that of aspirin) only block blood clot formation. They have no effect whatsoever on the rate of plaque growth. Aspirin and Plavix will neither slow it or increase it.

What they do is when a plaque ruptures like a little volcano and exposes its internal contents (inflammatory cells, fat, etc.--like a raw wound), a blood clot forms on top of the ruptured surface. If the clot is big enough, it can occlude the vessel and causes heart attack. Or, if it's a carotid artery, debris from the clot can break off and find its way headward to the artery controlling your speech or memory center. Aspirin and Plavix simply help inhibit clot formation once a plaque ruptures. That's it.

Interestingly, if you view any of Sanofi Aventis' commercials for Plavix, you'd think they came up with a cure for heart disease. It ain't true.

When is Plavix helpful? It's clearly an advantage after someone receives a coronary stent, drug-coated or uncoated;, after coronary bypass, particularly if certain metal punch devices are used to create the grafts in the aorta; and during and after heart attack. These are all situations in which blood clot formation is a forceful process. Blocking it helps.

In general, in asymptomatic people with positive heart scan scores at any level, we do not recommend taking Plavix. The Plavix people are extremely aggressive pushing their drug (hang around any medical office and see!) and, I believe, have gone overboard in promoting its benefits. Rarely, in someone with a very high heart scan score, say 2000 or more, we'll use Plavix for a period of a few months until lipids/lipoproteins and other risk measures are addressed, just as an added safety measure. But, in general, the great majority of people with some heart scan score or another do not receive it and I don't believe that they should.

As always, look beyond the marketing. The purpose of marketing is to increase profits, not to educate.

Dr. Ornish goofed

"I don't think I need the Track Your Plaque program. I've been doing the Ornish program, so I think that my plaque has already regressed."

So proclaimed Bruce, a recent patient I saw in consultation. Having suffered a heart attack three years earlier, he was thoroughly convinced that he was now cured following the Ornish program.


Indeed, back in the 1980s, many of us existed on greasy, high-fat diets of cheeseburgers, French fries, fried chicken, plenty of butter or margarine, mayonnaise, and the like.

Along came Dr. Dean Ornish, who wrote a book called "Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery". This book struck a chord during this era and has been a hot-seller ever since it was published.

Does it work? In my experience, no, it does not.

Dr. Ornish claimed that sharply curtailing fat intake reverses heart disease. Closer to the truth is that, in people who start with high fat intakes, a low-fat restriction is indeed an improvement. This will lead to a modest improvement in blood flow in the coronary arteries due to a phenomenon called "endothelial dysfunction." This means that arteries will dilate modestly when specific changes are made. Thus, you will see minimal improvements in the measures he used (stress testing with nuclear imaging.)

What it does not mean is that plaque has regressed, certainly not "reversed".

In fact, our experience (over 10 years ago, when we first used the Ornish approach) was that the majaority of people did worse on this low-fat program: HDL dropped, triglycerides increased, blood sugar increased, inflammatory measures like C-reactive protein increased. Some people even magnified diabetic or pre-diabetic patterns.

It's almost certain that Bruce has not reversed his coronary plaque. In fact, I would bet that his plaque has grown substantially. Bruce started three years earlier from a diet high in unhealthy fats. If the expected rate of coronary plaque growth is 30% per year, perhaps he slowed it--to 20% or so. Since he didn't have a heart scan score at the time of his heart attack, we'll never know if he truly did reduce the quantity of coronary plaque he had.

But when I met him on his Ornish program, Bruce showed disturbing patterns that included an HDL cholesterol of 38 mg, 70% of all LDL particles were small, triglycerides measured 209 mg, and C-reactive protein was high at 2.8 mg/l. In other words, Bruce's plaque causes were far from corrected. Perhaps they were worse.

The Ornish program, despite it's ambitious claims, has outlived its usefulness. In 2006, it is an antiquated relic of a time past when lifestyle habits and technology were different.

Warning: This product may contain wheat!

Jerry experienced a peculiar sensation in his chest one evening while watching TV with his wife and kids. He squirmed in his chair and experienced a little breathelessness. But he kept it to himself and didn't say anything to his wife.

Fortunately, the feeling passed. But it concerned Jerry enough that he called a local heart scan center and scheduled a CT heart scan.* Minutes later, Jerry had a heart scan score of 112. At 46 years old, this placed him in the 90th percentile compared to other men in his age group.

Jerry came to my office for consultation. Among the first steps we took was to perform lipoprotein testing. Jerry showed striking abnormalities that included an HDL cholesterol of 38 mg, triglycerides of 210 mg, an unimpressive LDL of 133 mg but comprised of 99% small LDL, and excessive IDL (meaning that he was unable to clear dietary fats after eating).

At 5 feet 10 inches, Jerry weighed 190 lbs. He showed a slight excess bulge at the tummy, but hardly obese.

Jerry's history was remarkable, however, for the amount of carbohydrates he ate. "I'm addicted to bread. I love it! If I smell a loaf of fresh baked bread, I sometimes eat the whole loaf!"

Jerry also admitted to over-indulging in bagels (whole wheat), pretzels, low-fat snack chips, Raisin Bran cereal, Cheerios, and noodles. In fact, many days he'd have 5 or 6 servings of any of these foods. He also complained of an extraordinary amount of bowel gas and cramping. "Sometimes, I'm afraid to go to a group function. I might embarass myself."

I suggested an experiment: For a 4 week period, completely eliminate wheat-containing products--breads, pretzels, breakfast cereals, pasta, etc. In their place, increase intake of protein foods like eggs, raw almonds and walnuts, low-fat yogurt, cottage cheese, chicken, fish, and use healthy oils (olive, canola, grapeseed, flaxseed) more liberally.

Just four weeks later, Jerry came to the office a new man: 8 lbs lighter, brighter, with bursts of energy he hadn't had in years. And no gas!

Lesson: Wheat-based carbohydrates can be the culprit behind many lipoprotein patterns, especially low HDL, high triglycerides, small LDL, and others. Wheat can also be responsible for a myriad of abdominal symptoms, even joint pains and rashes. In its most extreme form, it's called "celiac disease". But experiences like Jerry's are quite common--not as obvious and dramatic as full-blown celliac disease, but smouldering and destructive, nonetheless.

Track Your Plaque expert, Dr. Loren Cordain of Colorado State University, tells us that, in his reconstruction of the history of human illness, there was an extraodinary surge in disease just about the time when humans began cultivating wheat around 8000 B.C. (Track Your Plaque members: Read Dr. Cordain's fascinating interview at http://www.cureality.com/library/fl_04-005cordaininterview.asp.)

Do you need to eliminate wheat products entirely from your diet? It's something to think about, particularly if you share any of the difficulties that Jerry had.


*In general, I do not recommend heart scanning as a self-prescribed tool for chest pain or other symptoms. Symptoms should always be discussed with your doctor.

Hospital Administrators' Wish List

I've known enough hospital administrators over the years to understand what most of them want.

Of course, most of them want to deliver high quality care to patients in a safe, efficient setting. They want to comply with national standards of performance, attract quality physicians to use their facilities, and appeal to patients as a desirable place to obtain care.

But one fact is hard for many administrators to ignore: 30% of a hospital's revenues and 50% of their profits come from heart services.

So, if your hospital administrator had a wish list, I believe that among their wishes would be:

--More heart catheterizations, angioplasties, stents, and bypass surgery.
--More pacemaker and defibrillator implantations.
--More heart attacks.
--More heart failure with need for intravenous infusions, defibrillators, and bi-ventricular pacemaker implantations.
--More heart valve surgery.

Highly successful hospitals do more of these procedures than less successful hospitals.

Are you getting the picture? Heart care is a business. It's not very different than Target, Home Depot, or McDonalds--businesses eager to sell more of their product. Yes, there is attention to detail, quality, and competitiveness, but the bottom line is "sell more product, make more profit."

Keep this in mind the next time you catch one of the many TV or newspaper ads, radio spots, physician "interviews", or other media pitches in your town. Does Target run ads for the public good or to generate profitable sales? Does your hospital run ads to broadcast its contribution to public welfare or to generate profitable "sales"? Pretty clear, isn't it?

Poor, neglected vitamin D!

We now routinely check blood levels of vitamin D in all our patients. I am reminded everyday that, if you're a resident of a northern climate (as we are in Wisconsin and similarly in Michigan, Washington, New York, Pennsylvania, Ohio, etc.), the overwhelming likelihood is that you are deficient in vitamin D. And not just a little deficient, but severely deficient.

As humans, we're meant to obtain vitamin D through exposure to sunlight. This was how humans evolved. We are all ill-equipped to get vitamin D through nutritional sources. The average (Wisconsin) patient we see has vitamin D blood levels of 17-30 ng/dl. Most authorities would agree that a level of 30 ng or less would constitute severe deficiency. An ideal level is probably around 50 ng, what many (but not all) residents of southern climates like Florida, Texas, and Hawaii have if they get frequent sun exposure.

When vitamin D levels are normal, bone health is maximized (inhibiting osteoporosis); prostate, uterine, breast, and colon health is heightened and cancer risk diminished; pre-diabetic and diabetic patterns are suppressed and blood sugar reduced; blood pressure drops 10 mgHg, on average;and inflammatory measures like C-reactive protein are substantialy reduced. But, of greatest interest to us, coronary plaque is easier to regress.

Although our experience in the last several hundred people is still anecdotal, I believe that I'm seeing a dramatic increase in the amount and rapidity of coronary plaque regression. People we've struggled with are suddenly regressing. People with higher heart scan scores (e.g., >500) are regressing more readily.

We're accumulating our data and it will take a couple more years to develop it in a scientifically-useful format. But, in the meantime, adding vitamin D to your program or having your vitamin D level checked may be among the most important steps you can take to gain control over coronary plaque. Be sure to ask your doctor to get the right blood test: it must be 25-OH-vitamin D3. (The wrong test is the 1,25-OH2-vitamin D3; though they look and sound the same, they measure very different parts of the vitamin D pathway.) Also, Track Your Plaque members: read Dr. John Cannell's tremendous summary of the vitamin D experience on the Track Your Plaque website.

Leave the greatest legacy to your children

Phyllis was dumbfounded when she learned of her heart scan score of 995. At age 56, this placed her solidly in the 99th percentile--a score that grouped her with the worst 1% of scores for women her age. Track Your Plaque followers know that scores of 1000 (just days away, given the expected 30% increase in score per year!) pose a risk of heart attack, symptoms leading to stent or bypass, or death of 25% per year.

But after Phyllis gathered her thoughts and thought it over, her first question was "What about my children?"

A natural response for a mother. Phyllis' "children" actually ranged in age from 26 to 37. We talked about how, given her high score, she'd probably been creating plaque in her coronary arteries for 20 years. This triggered her mother's concern for her kids.


This is probably the #1 most useful lesson for all of us. If we learn of our own risk for heart disease, we can pass our concerns on to our children. Imagine how much more well-equipped you could be if you started out with the advice and experience of a parent who'd identified and then conquered their heart disease risk.

Pass your awareness and knowledge on to your children, particularly if they are 30 years old or more.

Interestingly, my own personal experience with my 14-year old son taught me a lesson or two. I had previously assumed that, at age 14, how could he be even remotely interested in these issues? (I have a terrible family history of heart disease and I have a high heart scan score myself.) When my son asked that we check his lipid values (I talk about this more than I'd like to admit!), we did a fingerstick lipid panel in my office. Lo and behold, his HDL (good) cholesterol was a shocking 31 mg--exceptionally low for a teenager. His risk for heart disease over the long-term is very high.

Much to my surprise, this awareness has triggered a genuine interest in healthy eating. It's not uncommon to see him examine food labels and to report to me that "Hey, Dad. Can you believe that this yogurt has 43 grams of carbohydrates?"

Pass on the lessons you've learned to your children and to the important people in your life. This is probably the most crucial lesson you can take from the Track Your Plaque experience.

Half effort will get you half results

Greg walked into the office.

"Just back from a 10-day Caribbean cruise, Doc. It was fabulous."

"Yes, but I see you're 14 lbs heavier. What happened?"

"Well, you know, a 24-hour a day open brunch. Anything and everything you wanted. But I only had dessert twice."

"Did you exercise?"

"Come on, Doc! It was vacation!"

With this serious indiscretion, Greg gained 14 lbs in 10 days. That's a total surplus of 49,000 calories Greg put in his body over that period. 49,000!

Greg had started the cruise 40 lbs overweight. Now, he's 54 lbs overweight. The pre-diabetic tendency he showed earlier was now full diabetes. All associated lipoproteins blossomed with it--small LDL, a drop in HDL of 5 points, triglycerides skyrocketing to 320.

He blew it.

Can Greg turn back? Yes, he most likely can, given a serious and rapid effort to lose the weight he gained on the cruise and more.

But can he do it? I doubt it.

Someone who allows himself to gain an extraordinary quantity of weight, completely neglects exercise, then blows it off as having some fun will never succeed.

In all honesty, this is someone who shouldn't waste his time in the Track Your Plaque program. He will fail--period. By failure I mean he will experience explosive plaque growth over the next few years and then end up with stent(s), heart attack, bypass surgery. Some people will die. He will also--should he survive--experience the long-term complications of diabetes, such as retinal disease, kidney impairment, loss of sensation to his feet and legs, and on and on. His life will be substantially abbreviated.

To me, there's no choice. But Greg and many people like him are fooling themselves if they believe that a half-hearted effort will allow them to succeed in controlling or reversing heart disease. Maybe we'll come up with some magic supplement or prescription medication that will erase his heart disease in a few days.

Don't count on it. I'll make no bones about it. Controlling and reversing heart disease requires a commitment--a full commitment to eat and live healthy, to follow the advice we give, and not engage in serious indiscretions that erode your efforts. If you believe that taking 40 mg of Lipitor is all you're going to need to regress heart disease, plan on your first stent or heart attack within a few years. And you'll hobble to the doctor's office in the meantime.
All posts by william-davis

Fish oil: What's the difference?

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour. 

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.






To B or not to B

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.
All posts by william-davis

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
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