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.
Cureality | Real People Seeking Real Cures

Kitchen sink approach for Lp(a)


Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Making Dr. Friedewald an honest man

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

Some basic vitamin D issues

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.


Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.


Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.


Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.


Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.


Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

“How much vitamin D should I take?”

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

You probably don't take enough fish oil

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:


Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents



Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Vitamin D and HDL

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies


At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)

Weight loss and blood pressure

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise.

Blood pressure also shows a curious pattern that is largely dependent on age.

Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most.

How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop.

Why the age-dependent difference?

It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop.

But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.

"I lost 30 lbs and my triglycerides went . . . up?"

Brad needed to lose weight.

At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly.

He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise).

Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats.

Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years.

His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"

Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.

So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's.

Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.

In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.

I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it.

I call these changes "transitional" changes in lipids.

Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.

Divorce court for the doctor-patient relationship?

The doctor-patient relationship has gone sour.

This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:

Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.

Exploitation of trust, my observation that the enormous gap in heart disease prevention between the woefully ignorant (by necessity) level of sophistication of the primary care physician and the procedure-obsessed cardiologist leads to an exploitation of humans-for-heart-procedures because of the failure to institute genuine preventive efforts.

Bait and switch , a description of how a minor test or symptom can reap a bonanza of medical testing; a $20 "screening" test yields $10's of thousands in hospital procedures. If it were entirely due to the imprecision of medical testing and detection of disease, that might be forgivable. But it often is not: It has become utterly distorted by the profit model.



Lest you think that I am a kook ranting off in some backwoods corner (Milwaukee), here are the comments of New York Times' Health Editor Tara Parker-Pope in a series called Doctor and Patient, Now at Odds:

Lately I've been hearing a lot from patients who are frustrated, angry, and distrustful of doctors. Their feelings speak to a growing disconnect between doctors and patients and worries that drug companies, insurance rules, and hospital cost-cutting are influencing the care and advice that doctors provide.

Research shows that even among patients who like their personal physicians, there is a simmering distrust of the medical system and the doctors who work inside it.


(There's also a series of candid video interviews with people who echo these sentiments.)

There are a number of reasons for this increasing "disconnect," some of them articulated by Ms. Parker-Pope, others detailed in my blog posts.

The solutions, however, will not be found by advancing technology: the newest robotic surgery, a better defibrillator, a new statin drug, the next best chemotherapeutic agent. It will not be found by adding a new wing to the hospital. It will not be found by the reorganization of healthcare delivery achieved by converting primary care and specialty practice into an arm of hospital care. It will not be improved by employing "hospitalists." It will not emerge from legislation controlling insurance company practices. It certainly will not come from increasing marketing dollars spent by drug companies (who make $4 for every $1 spent on direct-to-consumer marketing).

The solutions will come from shifting the idea of care from a paternalistic, "I'm the doctor and I'll tell you what to do" approach, to the doctor-as-advocate-and-supporter of the patient. The physician should act as someone with a particular sort of expertise that can advise a patient.

But a caveat: The patient MUST be informed.

Proper information will not originate with the doctor. It will originate with internet-based information portals and tools that help you understand the issues, often with far greater depth than your doctor could ever provide. The physician needs to accept this role, one of advocate, adviser, but not of being in charge, not of viewing the patient as profit-center, not as an opponent in a power struggle.

Sadly, the last few years in online information portals has been dominated by the drug company-dominated websites like WebMD, nothing more than a deliverer of the conventional wisdom with nothing whatsoever aimed towards empowering patients in a self-directed healthcare model.

Some people call the emerging new empowered and information-armed patient Medicine 2.0. Unfortunately, Medicine 2.0 will first benefit the intellectual upper crust of Americans, the web-savvy and motivated to engage in health issues. But, give it 10 years, and we will witness the effects on an unprecedented broad scale. Part of the Information Age is acceleration of information dissemination. Imagine your children, facile with a computer mouse, posting comments on FaceBook, doing homework with Google and Wikipedia, now turning their attentions to health.

It will be a startling change.

In the meantime, be wary. Be empowered. Think increasingly about self-direction in your health.


In a comment to the Bait and switch post, Jennytoo offered an insightful response:

You are getting to the essence of the problem, and it's not just cardiology that is rife with what is, at bottom, malpractice.

There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor. The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.") are useless sops to the concept of prevention.

It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.

It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less. They are:

(1) education on and promotion of a true low-carbohydrate, whole foods, diet,
(2) measurement and supplementation of Vitamin D3,
(3) supplementation with DHA/EPA (found in Fish Oils), and
(4) measurement and supplementation of intracellular magnesium.

I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items. The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being. (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)

If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for. But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.

Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors. In the meantime, we can be self-reliant in our own prevention practices.


Wow. A woman after my own heart.

How much fish oil is enough?


This post just furthers this line of thinking out loud: How much fish oil is "enough"?

Observations over the last 30 years followed this path: If a little bit of omega-3 fatty acids from fish are beneficial in reducing cardiovascular events, and a moderate intake is even better, is even more better? When have we reached a plateau? When do adverse effects outweigh the benefits?

Some insight can be gained through studies that examined blood levels of omega-3s. Let's take a look at some data from 2002, a comparison of men dying from heart disease vs. controls in the Physicians' Health Study, Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death.

This is a table that shows the blood levels of various fatty acids Group with sudden death vs Control Group:




Several observations jump out:

--The total omega-3 blood content differed significantly, 4.82 vs 5.24% ("Total long-chain n-3 polyunsaturated")
--Total omega-6 content did not differ
--Arachidonic acid (AA) content did not differ
--Linolenic acid content did not differ (i.e., plant sourced omega-3)

The fact that neither omega-6 nor arachidonic acid content differed counters the argument that Simopoulos has made that the omega-6 to omega-3 ratio (intake, not blood levels) is what counts. It also argues against the EPA to AA ratio (and similar manipulations) that some have argued is important. In this study, only the omega-3 level itself made a difference; no ratio was necessary to distinguish sudden death victims vs controls.

Further, quartiles of omega-3 blood levels showed graded reductions of risk:




An omega-3 blood level of 6.87% conferred greatest risk reduction. Depending on the model of statistical analysis, risk reductions of up to 81-90% were observed. Wow.

Taken at face value, this study would argue that:

--An omega-3 fatty acid blood level of 6.87% (or greater?) is ideal
--The omega-3 fatty acid blood level stands alone as a predictor without resorting to any further manipulation of numbers, such as relating EPA and/or DHA to AA levels.

Of course, this is just one study, though an important one. It is also not a study based on any intervention, just an observational effort. But it does add to our understanding.


We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.