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.

Pre-diabetes: An explanation for explosive coronary plaque growth

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."


Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.


Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.

Vitamin D--A coronary risk factor

Look up "coronary risk factors" in any text and you'll find high cholesterol, smoking, diabetes, and high blood pressure listed. You won't find deficiency of vitamin D listed.

Ask 99% of physicians if a deficiency of vitamin D is a coronary risk factor and you'll get rolling eyes and a sigh.

Yet, in the Track Your Plaque experience, vitamin D is emerging as a very important factor in coronary plaque development. We have observed that there are a substantial number of people whose lipids and lipoproteins are not abnormal enough to fully explain their heart scan score. In other words, there seems to be something else necessary to satisfactorily explain the magnitude of coronary plaque.

I believe that severe vitamin D deficiency is at least one of the most important factors. We've seen many people with blood levels of vitamin in the range of severe deficiency (<20 ng/ml of 25-OH-Vitamin D3) yet bland lipids and lipoproteins.

Correcting vitamin D blood levels to 50 ng/ml also seems to be among the required factors in stopping coronary plaque growth, or stopping your heart scan score from increasing.

Keep your eye on this extremely important and exciting issue. Sadly, it won't be propelled into the media like the conversation about cholesterol or high-tech procedures, since no company stands to profit from it. But you and I don't have to play that game.

Cholesterol is dead!

I saw a patient in the office yesterday. He came to me for an opinion regarding his high heart scan score of 525, putting him in the 90th percentile (5% annual risk of heart attack).

His doctor had been puzzled because his LDL cholesterols had ranged from 110 to 131 mg--actually below average. (The average LDL for the U.S. is 132 mg.) Likewise, HDL was a favorable 63 mg.

Lipoprotein analysis told the story loud and clear. His LDL particle number, a far more precise measure of LDL, was 2448 nmol/l. This means that his true LDL was more like 240-250 mg! (You can get a sense for what the true LDL is from LDL particle number by dropping the last digit: 2448 becomes 244.) Conventional LDL was therefore inaccurate by over 100 mg.

He also had a severe small LDL particle pattern. The cause of his coronary plaque was a large excess of small LDL particles. LDL cholesterol (and total cholesterol, likewise) didn't even hint at this pattern. Nor did his favorable HDL.

Think of LDL particle number as an actual count of LDL particles per volume, e.g., number of particles per cc of blood. This makes it easier to conceptualize. LDL particle number is the measure you get when you have an NMR lipoprotein profile, our preferred method of lipoprotein testing. If this is unavailable to you, apoprotein B is a reasonable second choice, though not as accurate in my view. More info on NMR is available at their website, www.lipoprofile.com.

How to make a $1 million in cardiology

Want to make a $1,000,000 as a cardiologist in the next year? It's easy. All you have to do is:

1) Perform heart catheterizations or other procedures on anybody you can, even if it's not necessary. Perform them even if the patient has no symptoms and the stress test is normal.

2) Perform heart catheterizations if the patient is too timid or ill-informed to object.

3) Insert coronary stents in blockages, even when they're minor and it's not necessary.

4) Turn every heart procedure into a revenue-producing stream by looking for other profit opportunties, such as minor kidney artery blockages.

5) Heart disease is frightening. Scare the heck out of patients by exagerrating the dangers so they'll go through testing and procedures gratefully.


Sound absurd? Well, it would be if these weren't all true.

These are real examples, as awful as it sounds. I've witnessed all these behaviors. Not just occasionally, but with regularity.

Just today, I encountered a colleague who performs heart catheterizations routinely (up to several per day) when any symptom is present and the stress test is entirely normal. This is grossly inappropriate.

Your protection is being better-informed and avoid being sucked into the vast and frightening cardiovascular machine of revenue-yielding procedures. Part of your protection is to get a CT heart scan, then engage in a program of heart disease prevention.

Doctor, do I have lipoprotein (a)?

I met Joyce today for a 2nd opinion. She told me about this conversation she'd had with her cardiologist:

"Doctor, do you think I could have lipoprotein (a)? I read about how it can cause heart attacks even when cholesterol is controlled."

"What does it matter? Even if you have it, there's nothing we can do about it. There's no treatment for it."

Joyce was understandably groping for some means to prevent her coronary disease from causing more danger. At 56, she'd already survived a heart attack that resulted in two stents to her left anterior descending. Around 9 months later, she received a 3rd stent to another artery.

Her doctor had put her on Pravachol and said that was enough. "We know that cholesterol causes heart disease and the Pravachol reduces it. Why do we need to know anything more?"

So Joyce came to me for another view. I explained to her that there are, in fact, several ways to deal with lipoprotein(a). It is, without a doubt, among the more difficult patterns to manage--but not impossible. In fact, we have a growing list of participants in the Track Your Plaque program who have stopped or reduced their heart scan scores.

I continue to be horrified at the level of ignorance that prevails among my colleagues, the cardiologists, and the primary care community. If your doctor gives you advice like this, get a new doctor.
All posts by william-davis

Are you hungry?

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

The Paleo approach to meal frequency

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:


We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.



In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.


The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Even mummies do it


Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Life Extension article on iodine

Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

The healthiest people are the most iodine deficient

Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

It's the score, stupid

Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Heart Scan Blog Redux: Cheers to flavonoids

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.