Blood sugar lessons from a Type I diabetic

A friend of mine is a Type I, or childhood onset, diabetic. He's had it for nearly 50 years, since age 6. He's also in the health industry and is a good observer of detail.

He made the following interesting comments to me recently when talking about the effects of various foods on blood sugar:

"When I eat normally, like some vegetables or salad and meat, I dose up to 10 units of insulin to control my blood sugar.

"If I eat a turkey sandwich on two slices of whole wheat, I usually dose 15 units. The bread makes my blood sugar go to 300 if I don't.

"If I eat a Cousins's Sub [a local submarine sandwich chain], I dose 15 units. The bread really makes my blood sugar go up.

"I can only eat a Quarter Pound from McDonald's once a year, because it make my blood sugar go nuts. I dose 15-20 units before having it, and I feel like crap for two days afterwards.

"If I eat Mexican food, I have to dose 15-20 units. For some reason, it's gotten worse over the years, and I need to dose higher and higher.

"Chinese food is the absolute worst. I dose 20-25 units before eating Chinese. I'll often have to dose more afterwards, because my blood sugar goes so berserk."


Nothing beats the real-world observations on the impact of various foods on blood sugar than the observations of people with Type I diabetes. All the insulin they get is in a syringe. Dosing needs to match intake.

Personally, though I love the taste of Americanized Chinese food, I've always been suspicious of what exactly goes into these dishes. But I was unaware of the blood sugar implications.

The impact of Mexican I believe can be attributed to the cornstarch used in the tacos and tortillas, though I also wonder if there are other starches being snuck in, as well.

Lessons about omega-3s from Japan















Image courtesy of apc33.

Japan provides a useful "laboratory" for studying the effect of a culture that relies heavily on eating fish.

The JELIS Trial, the topic of a previous Heart Scan Blog post, showed that supplementation with the single omega-3 fatty acid, EPA, 1800 mg per day (the equivalent of 10 capsules of 'standard' fish oil that contains 180 mg per day of EPA, 120 mg of DHA) significantly reduced heart attack in a Japanese population. Interestingly, this benefit was additive to the already substantial intake of omega-3 fatty acids among the general Japanese population, a population with a fraction of the heart attacks found in western populations like the U.S. (approximately 3% over 5 years in Japanese compared to several-fold higher in a comparable American group).

While there may be genetic and other cultural and lifestyle reasons behind the dramatically reduced cardiovascular risk in Japanese, it is undeniably at least partially due to the increased intake of omega-3 fatty acids from fish. Incidentally, the purported benefits of omega-3 fatty acids provide a vigorous counter-argument to the idea that all humans should be vegetarians.

Anyway, if we were to take some lessons from the Japanese and their greater habitual intake of omega-3 fatty acids from fish, they might include:

--Rural and coastal Japanese are the sub-populations with the highest reliance on fish, about a quarter-pound a day. (Gives new meaning to the idea of a "Quarter Pounder," doesn't it?) This is at least five-times greater than the intake of an average American.

--Likewise, the blood level of omega-3s in the blood of Japanese is 5-fold higher than in Americans.

--The average intake of omega-3s (EPA + DHA) among a broadly-selected population of Japanese is 850 mg per day (320 mg EPA; 520 mg DHA). Intake ranges from 300 mg per day all the way up to 3100 mg per day.

--Greater omega-3 intake (EPA + DHA) is associated with lesser carotid intimal-medial thickness, an index of body-wide atherosclerosis.

--Japanese have far less heart attack and stroke despite greater prevalence of smoking (nearly half of Japanese) and drinking.

--Total fat intake (percent of calories) is nearly identical between Americans and Japanese. It's the proportion of fat calories from omega-3 that is greater, the proportion of omega-6 that is less in Japanese.


The Japanese eat their fish in ways that we do not: As sashimi (raw, as with sushi in its various forms like Nigiri and Chirashi); fried in tempura; shaved, dried fish sprinkled on about anything you can imagine (it's not as bad as it sounds); as a snack, as in dried cuttlefish (which you can purchase in packages as a portable, sweetened fish that you eat on-the-run--I know it sounds awful, but don't poke fun at it until you've tried it); in "soups" with soba noodles. Fish is commonly consumed with rice and soy sauce, as well as other soy-based foods, such as tofu, miso (soy bean paste), or natto. 


I believe that there are some lessons to take from the Japanese and their fish-consuming habits:

1) An omega-3 fatty acid intake of at least 1000 mg per day yields measurable cardiovascular benefits. 

2) Despite the fears over mercury and pesticide residues in fish, this seems to not have played out to be a real-life effect in the Japanese, who consume five-fold greater quantities of fish. 

3) My mother was right after all when she encouraged us to eat more fish. 


DIRECT Study result: Low-carb, Mediterranean diets win weight-loss battle

Drs. Iris Shai and colleagues released results of a new Israeli study, the Dietary Intervention Randomized Controlled Trial (DIRECT) Trial, that compared three different diet strategies. Of those tested, a low-carbohydrate diet was most successful at achieving weight loss.

You can find the full-text of the study on the New England Journal of Medicine website.

322 participants followed one of three diets over two year period. Compared head-to-head, the (mean) weight loss in each group was:

• 2.9 kg (6.4 lbs) for the low-fat group
• 4.4 kg (9.7 lbs) for the Mediterranean-diet group
• 4.7 kg (10.3 lbs) for the low-carbohydrate group

(Average age 52 years at start; average body-mass index, or BMI, 31.)

The conclusion was that the low-carb diet performed the best, with 60% greater weight loss, with the Mediterranean diet a close second.


The diets

The low-fat diet was based on the American Heart Association diet, with 30% of calories from fat (10% from saturated fat) and food choices weighted towards low-fat grains, vegetables, fruits, and legumes and limited additional fats, sweets, and high-fat snacks; calorie intake of 1500 kcal per day for women and 1800 kcal per day for men was encouraged.

The Mediterranean diet was a moderate-fat diet rich in vegetables, with reduced red meat, and poultry and fish replacing beef and lamb. Total calories from fat of 35% per day or less was the goal, with most fat calories from olive oil and a handful of nuts. Like the low-fat program, calories were limited to 1500 kcal per day for women, 1800 kcal per day for men.

The low-carbohydrate diet was patterned after the popular Atkins’ program, with 8% participants achieving the ketosis that Dr. Atkins’ advocated as evidence that a fat-burning metabolism was activated, rather than sugar-burning as fuel. For the 2-month “induction phase,” 20 grams of carbohydrates per day was set as the goal, followed by 120 grams per day once the weight goal was achieved. Unlike the other two diets, calories, protein and fat were unlimited.


Weight loss, lipids, inflammation

You can see from the weight loss graph that the low-carb approach exerted the most dramatic initial weight loss. Interestingly, much of the weight-loss benefit was lost as the carbohydrate intake increased, by study design, back to 120 mg per day. However, the other two diet approaches showed similar phenomena of “giving back” some of the initial weight loss.

The low-carbohydrate diet exerted the greatest change in cholesterol, or lipid, panels: increased HDL 8.4 mg/dl vs. 6.3 mg/dl on low-fat; the triglyceride response was the most dramatic, with a reduction of 23.7 mg/dl vs. 3.7 mg/dl on low-fat. Interestingly, the LDL cholesterol-reducing effect of all three diets was modest, with the most reduction achieved by the Mediteranean diet.

The inflammatory measure, C-reactive protein (CRP), was reduced most effectively by the low-carb and Mediterranean diets, least by the low-fat diet. HbA1c, a measure of long-term blood sugar, dropped significantly more on the low-carb diet.

When the final dietary composition was examined, interestingly, there really were only modest differences among the three diets, with 8% less calories from carbs, 8% greater calories from fat, comparing low-carb to low-fat, with Mediterranean intermediate.



Taken at face value, this useful exercise quite clearly shows that, from the perspective of weight loss and correction of metabolic parameters like triglycerides, HDL,CRP, and blood sugar, low-carbohydrate wins hands down, with Mediterranean diet a close second.

It also suggests that a return to a carbohydrate intake of 120 mg/day allows a partial return of initial weight lost, as well as deterioration of metabolic parameters after the initial positive changes.

Although the study has already received some criticism for such potential flaws as the modest number of Atkins’ followers achieving ketosis (8%), suggesting lax adherence, and the reintroduction of the 120 mg/day carbohydrate advice, I can suspect that these may have been compromises drawn to satisfy some Institutional Review Board. (Whenever a study is going to be conducted involving human subjects, a study needs to pass through the review of an Institutional Review Board, or IRB. IRB’s, while charged to protect human subjects from experimental abuses, also tend to be painfully conservative and will block a study or demand changes even if they are not dangerous, but just veer too far off the mainstream.)


However, several unanswered questions remain:

1) How would the diets have compared if the carbohydrate restriction were continued for a longer period, or even indefinitely? (The divergences would likely have been dramatic.)
2) Will low-carb exert the same cardiovascular event reduction that the Mediterranean approach has shown in the Lyon study and others?
3) Are there effects on health outside of the measures followed that differ among the three diets, such as cancer? (I doubt it, especially given the modest real differences over time. But this will be the objection raised by various "official" organizations.)


I would further propose that:

Low-fat diets are dead

The AHA will cling to their version of low-fat diet, based on difficulty in changing course for any large, consensus-driven organization, not to mention the substantial ($100’s of millions) revenues derived from endorsing low-fat manufactured products. The AHA will also point to the lack of difference in LDL cholesterol among the three, since they cannot get beyond the fact that there’s more to coronary risk—a lot more—than LDL.


Off-the-shelf diets achieve off-the-shelf results

If you just need a T-shirt, a medium might fit fine. But if you’d like a nicely fitting suit or dress, then tailoring to your individual proportions is needed. When aiming towards maximizing benefits on lipoproteins and coronary risk, none of these diets achieve the kinds of changes we often need for coronary plaque reversal, as in the Track Your Plaque program. That requires making dietary changes that exert maximal effects on lipoprotein patterns.

Do I sell heart scans?

I came across a criticism of the Track Your Plaque program recently that suggested that it was nothing more than a program to sell CT heart scans.

Huh?

I suppose if you say that the Track Your Plaque program is nothing more than a way to sell heart disease prevention, omega-3 fatty acids from fish oil, vitamin D, better nutrition, and better identification of causes of heart disease . . . well, I believe that would be true.

But is the program a "front" to sell heart scans?

No, it is not, nor has it ever been.

I've heard about these peculiar suspicions about the program before. Though I've never taken them seriously, let me clear up any lingering uncertainty:


--I have no relationship with any heart scan center, scanning facility, or hospital other than to interpret heart scans.

I do not own a scanner, I have no financial interest in a scanner or scanning center, nor have I ever had any interest. I also have no plans to do so in the future. Let business people in the imaging business do that. I want no part of it. I have seen what these people go through and, frankly, I want no part of it, nor do I want the appearance that I am advocating scans to make money. I'm accused of trying to make money from scans even when I do not have any financial interest!


--I do not sell heart scans or imaging packages, nor have I ever done so.

You can't buy a scan through Track Your Plaque, The Heart Scan Blog, or through me. To me, heart scans are simply a measuring tool to identify the extent of coronary plaque, as well as a tracking tool to follow its course. Without it, there would be no Track Your Plaque. But there is also no alternative. The closest alternative would be carotid intimal-medial thickness, a technique, while useful, is a distant second choice to indirectly gauge coronary plaque by examining the thickness of the carotid lining (not carotid plaque). Perhaps in 10 years, a better measure to gauge and track coronary plaque will emerge that has superior aspects over CT heart scanning. If reasonable, safe, accessible, and quantitative, then Track Your Plaque may adopt that technology as its measuring tool.

Track Your Plaque is not about heart scanning; Track Your Plaque is about measuring and tracking plaque that, in 2008, is still best accomplished with CT heart scans.


--I make loads of money from heart scans and Track Your Plaque.

Yeah, right.

Track Your Plaque is a volunteer venture for my team; none of us get paid a penny for doing all we do, including me. We charge a membership fee on the website (somewhere around $6-7 a month) to pay our expenses, such as code writing for our proprietary software (much of it remains under development), printing costs, modest legal costs, the costs of doing business (e.g., accountant). Despite the fact that Track Your Plaque and the Heart Scan Blog occupies a substantial part of the day of the Track Your Plaque team, none of us are reimbursed for our time. I do believe, however, that this concept is so enormously powerful that it will, someday, pay us all enough to allow us to devote more time and effort to it.

Personally, I can't wait to devote more time and effort to this concept that is simple, logical, and effective. More research is needed, more development is needed, more discussion is needed. Right now, it is all accomplished outside of our busy schedules, including my full-time cardiology practice. I continue to have 7 am procedures, middle-of-the-night calls, weekend hospital rounds and emergencies (though virtually none of these are the patients involved in prevention, but the "other" people: atrial fibrillation, elderly heart failure patients, rhythm disorders, cardiomyopathies, pulmonary hypertension, peripheral vascular disease, the non-compliant).


--The book, Track Your Plaque, is a gimmick to sell you a heart scan.

No, it's a program that relies on this technology. But there's no special deal, no discounts, no steering to heart scan centers that I have a special arrangement with. No such thing exists, nor has there ever been such an arrangement.


I've heard it all. Early on, when I was helping my friend, Steve Burlingame and his wife, Nancy, set up Milwaukee Heart Scan, I helped by providing medical oversite, education of physicians and public, and interpreting heart scans. After all, in the "early days," nobody knew anything about heart scans. It was a long, hard climb against ignorance, habit, entrenched thinking, stubbornness, and stupidity. I've been paid next to nothing for all this. I told Steve long ago that, given the extraordinary expenses of maintaining an independent scanning center, that he should first pay his expenses, pay his technologists, receptionists, and nurse, pay himself, then pay me for reading scans if he had any money left over. Most of the time, Steve had nothing left over and I was paid nothing.

So, while some of my colleagues were assuming that I was rolling in money from "promoting" heart scans, the reality was that I was doing nearly everything for free. (It certainly wasn't the high life I was living; I don't drive a Mercedes, take fancy vacations, none of that. In fact, I work about 51 weeks a year.)

Why do I do this if it doesn't yield a big flow of money? Because I believe in it as a superior path to the conventional. If I were simply interested in making more money--I wouldn't do it. I would simply do what all my cardiology colleagues are doing: more heart catheterizations, more angioplasties and stents, learning how to do carotid stents, iliac stents, peripheral angioplasty, renal stents, acquiring the skills to put in defibrillators, new device insertion like umbrellas in the interatrial septum, etc. There's plenty more money in that. It's also not that hard. I know, because that is my background: high-risk cardiac interventions. That's what I was trained to do, that's what I did from a number years, until I started to see that this was nothing more than "putting out fires" in people who became increasingly ill and reliant on bail-out procedures. It makes lots of money, but it is also fundamentally wrong.

So, no, I do not sell heart scans, nor is the Track Your Plaque program or The Heart Scan Blog meant to promote heart scans except as a tool for tracking this disease.

That's it, pure and simple.

Plaque is the new cholesterol

Which is more important: cholesterol or coronary plaque?

Ask what Dr. Michael Eades' calls "statinators," and you will likely receive a befuddled look. Or, you might receive comments like "Measuring plaque has never been shown to reduce mortality."

While risk factors for heart disease are important, no doubt (my office practice is about half lipid consultation and complex hyperlipidemia management), for many they have become an end in themselves. In other words, LDL cholesterol in particular dominates thinking so much that it has caused many to exclude the fact that plaque---coronary atherosclerotic plaque---is the disease itself.

Dozens of studies, from the St. Francis Heart Study to the 25,000-participant UCLA registry, to the recently-released MESA database (ethic differences, women, as well as superiority to carotid measures) have repeatedly shown that heart scan scores (coronary artery calcium scores) are superior to conventional risk factors (usually via the Framingham risk score) for predicting future heart attack and other events. And the differences are not minor incremental differences. The predictive power of plaque measurement via heart scanning is multiples better: 4 times, 10 times, 20 times or more in various subgroups.

Much of what we do in medicine is not based on long-term studies of outcome, pitting some diagnostic measure or treatment against placebo. It is already standard practice to measure plaque via heart catheterization, crudely via stress testing, and increasingly popular CT coronary angiography. None of these methods have been subjected to studies comparing testing vs. not testing in a large population, followed by some program of prevention to assess differences in mortality, heart attack, and other events.

Why should heart scan be held to such a standard?

Dr. Scott Grundy, lipid guru and one of the experts who sat on the Adult Treatment Panel-II for lipid management guidelines, recently stated [emphasis added]:

"Imaging has at least 3 virtues. It individualizes risk assessment beyond use of age, which is a less reliable surrogate for atherosclerosis burden; it provides an integrated assessment of the lifetime exposure to risk factors; and it identifies individuals who are susceptible to developing atherosclerosis beyond established risk factors. Also of importance, in the absence of detectable atherosclerosis, short-term risk appears to be very low."

Well said, and from a vocal statinator, to boot.

Sadly, Dr. Grundy goes on to say how plaque imaging can serve to better determine who will benefit from statin drug use.

Of course, you and I know that there is far more to reduction of cardiovascular risk applied to a framework of serial plaque quantification ("tracking plaque"!) than statin drugs. I doubt that a man as intelligent as Dr. Grundy truly believes this. I suspect that he is simply stating what he knows what will be published without resistance in the standard medical literature, trying to achieve a modest incremental success just by raising consciousness about heart scanning and plaque imaging: first things first.

Maybe next will be a plaque-tracking, or even a plaque-reducing, mainstream conversation, just like the one we've been conducting for the past four years.

Track Your Plaque success story blows it

Joe was a Track Your Plaque Success Story. With a starting heart scan score of 278, he dropped it 12 months later to 264, a 5% reduction. Though not a huge reduction, Joe's risk for a heart attack or other coronary event was virtually zero. I was very proud of Joe.

Among the culprit lipoprotein patterns that caused Joe's plaque was lipoprotein(a), or Lp(a). Niacin was therefore crucial to his program. It was among the principal reasons he dropped his heart scan score and reduced his risk for heart attack so dramatically.

Since he retired, Joe has been freewheeling around the country, traveling and having a great time. He consequently stopped thinking about his heart disease and Lp(a). He also tired of the occasional hot flushes he'd experienced with niacin. Though the flushes were promptly aborted by drinking two glasses of water, he simply didn't want to be bothered.

So when Joe saw this interesting and tantalizing "flush-free niacin" on the store shelf, he grabbed it.

Joe came back to the office. His blood pressure was 190/94, so high that he was having occasional chest pains from it (which can happen when something called "left ventricular diastolic dysfunction" develops from hypertension). His lipoprotein patterns were terrible, including a big upward jump in Lp(a) and drop in HDL. So I asked him to have another heart scan right away: Score 371, a 40% increase. In other words, his program went down the toilet.

Why?

Simple: Flush-free niacin. I've said it before (No flush = No effect and No flush niacin kills) and I'll say it again:

Flush-free or No-flush niacin is a complete, unadulterated, completely ineffective SCAM.

Flush-free or no-flush niacin is not a substitute for niacin. Joe is yet another example of how dangerous this scam can be. It turned one of our great success stories into a failure.

Please, please, please do not fall for this misleading and potentially dangerous scam product. While the product itself is not intrinsically dangerous, it denies you the benefits of the real thing: niacin.

Thankfully, the mistake in Joe's program was caught before a heart attack or other catastrophe. He did manage to pass a stress test, though with a flagrantly out-of-control blood pressure response. We'll get him back on track--but with niacin, the real thing.

Dr. Cannell comments on vitamin D lab tests

As always, Dr. John Cannell of The Vitamin D Council continues to teach us new lessons about vitamin D.

Apparently, Dr. Cannell is swamped with the attention that vitamin D is drawing, largely due to his efforts to publicize the enormous deficiency of Americans and his great talent for articulating the science. The most current newsletter, while a bit haphazard, makes some excellent new points that I reprint here.

(I did not reprint his conversation about "any form of vitamin D" being acceptable. My experience differs: In nearly 1000 patients who have taken vitamin D supplements, my experience is that most tablet forms are inconsistently absorbed, sometimes not absorbed at all. I therefore advocate only use of gelcaps or liquids. I'm told by members of Track Your Plaque, however, that they are witnessing reliable increases in blood levels of vitamin D by taking the powdered form of Bio Tech Pharmacal's product.)


Does it matter what reference lab my doctor uses?

Yes, it might make a huge difference. A number of methods exist to measure 25(OH)D in commercial labs. The two most common are mass spectrometry and a chemiluminescence method, LIAISON. The first, mass spectrometry, is highly accurate in the hands of experienced technicians given enough time to do the test properly. However, in the hands of a normally trained technician at a commercial reference lab overwhelmed with 25(OH)D tests, it may give falsely elevated readings, that is, it tells you are OK when in fact you are vitamin D deficient. The second method, chemiluminescence, LIAISON, was recently developed and is the most accurate of the screening, high throughput, methods; LabCorp uses it. Quest Diagnostics reference lab uses mass spec. Again, both Quest and LabCorp are overwhelmed by 25(OH)D requests. The problem is that the faster the technicians do the mass spec test, the more inaccurate it is likely to be. If your 25(OH)D blood test says "Quest Diagnostics" on the top, do not believe you have an adequate level (> 50 ng/ml). You may or may not; the test may be falsely elevated. Let me give you an example. A doctor at my hospital had Quest Diagnostics do a 25(OH)D. It came back as 99 ng/ml of ergocalciferol. He is not taking ergocalciferol (D2), he has never taken ergocalciferol, only cholecalciferol, and he is not taking enough to get a level of 99 ng/ml, 50 ng/ml at the most. His email to Dr. Brett Holmquist at Quest about why Quest identified a substance he was not taking went unanswered other than to say "any friend of Dr. Cannell's is a friend of ours."

Long story short: if your lab report says "LabCorp" on the top, it is probably accurate; if it says Quest Diagnostic, it may be falsely elevated. While LabCorp has also been overwhelmed with 25(OH)D requests, the LIAISON method they use is relatively easy to do and does not rely on technician skill as much as the mass spec methods do. I'm not saying this because I'm a consultant for DiaSorin, who makes LIAISON, I'm saying it because it is true. If you don't believe me, get Quest to make me an offer to be their consultant at 10 times what DiaSorin is supposed to be paying me ($10,000 per year) and see how fast I turn Quest down. If Quest fixes their test, I'd love to consult. The ironic thing: I've made both Quest and LabCorp lots of money via this newsletter, the website, and by repeatedly telling the press that people need to know their 25(OH)D level, which has contributed to the skyrocketing sales of 25(OH)D blood tests.

Demand for vitamin D tests soars as nutrient's potential benefits touted.

Here you can help. Find out which labs in your town use Quest Diagnostics and which use LabCorp. Have a 25(OH)D test at both labs the same day (you will have to pay for them yourself). Then send both results to the Vitamin D Council address below. If Quest Diagnostics does not fix their 25(OH)D test, the Vitamin D Council will fix it for them.



My doctor prescribed Drisdol, 50,000 IU per week. What is it?

Drisdol is a prescription of 50,000 IU tablets of ergocalciferol or D2. Ergocalciferol is not vitamin D but it is similar. It is made by irradiating ergosterol, which is found in many living things, such as yeast. D2 is not normally found in humans and most studies show it does not raise 25(OH)D levels as well as human vitamin D (cholecalciferol or D3) does. However, Drisdol is a lot better than nothing. The best thing to do, if you are vitamin D deficient, and a human, is to take human vitamin D, cholecalciferol, A.K.A. vitamin D3.



What is the ideal level of 25(OH)D?

We don't know. However, thanks to Bruce Hollis, Robert Heaney, Neil Binkley, and others, we now know the minimal acceptable level. It is 50 ng/ml. In a recent study, Heaney et al enlarged on Bruce Hollis's seminal work by analyzing five studies in which both the parent compound, cholecalciferol, and 25(OH)D levels were measured. It turn out that the body does not reliably begin storing the parent compound (cholecalciferol) in fat and muscle tissue until 25(OH)D levels get above 50 ng/ml. The average person starts to store cholecalciferol at 40 ng/ml, but at 50 ng/ml, virtually everyone begins to store it for future use. That is, at levels below 50 ng/ml, the body is usually using up the vitamin D as fast as you make it or take it, indicating chronic substrate starvation, not a good thing.

Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4.

Heaney RP, Armas LA, Shary JR, Bell NH, Binkley N, Hollis BW. 25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions. Am J Clin Nutr. 2008 Jun;87(6):1738-42.



I have advanced renal failure and I'm on dialysis, how much vitamin D should I take?

The same as everyone else. Since I have told you about commercial labs ripping you off, let's add some drug companies. Patients with advanced renal failure need activated vitamin D or one of it's analogs, available by prescription. This is very important as their kidneys cannot make enough 1,25-dihydroxy-vitamin D (calcitriol) to maintain serum calcium. However, the rest of their tissues activate vitamin D just fine and when those tissues get enough, and when the kidneys get more vitamin D, the calcitriol spills out into the blood, lowering their need for prescription calcitriol or one of its analogs. The companies that make the analogs don't like that, it means reduced sales. So these companies do nothing, the scientists behind these companies say nothing, and renal failure patients die prematurely from one of the vitamin D deficiency diseases.

Vieth R. Vitamin D toxicity, policy, and science. J Bone Miner Res. 2007 Dec;22 Suppl 2:V64-8.



When I asked my doctor for a 25(OH)D blood test, he just laughed and said it was all idiotic. What can I do?

Help me unleash the dogs of war, the plaintiff attorneys. If you read about past nutritional epidemics caused by society, such as beriberi or pellagra, you will realize that education alone will take decades. Physicians successfully fought against the idea that thiamine deficiency caused beriberi for decades. However, things are different now. The agents of change in modern America, as obnoxious as they are, are plaintiff attorneys. Once the first malpractice lawsuits claiming undiagnosed and untreated vitamin D deficiency led to breast cancer, autism, heart disease, etc., get past summary judgment, and they will, and end up in front of a jury, and they will, things will change rapidly. One of the main reason physicians do what they do is fear of lawsuits. In a matter of months, arrogance and ignorance will give way to 25(OH)D tests and vitamin D supplementation.

Goodwin JS, Tangum MR. Battling quackery: attitudes about micronutrient supplements in American academic medicine. Arch Intern Med. 1998 Nov 9;158(20):2187-91.


And, to help support Dr. Cannell's efforts (I sent him a check for $250 a few months back; time for more), here is his contact info:

John Cannell, MD
The Vitamin D Council

Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

Privileged information

In 1910, taking a person's blood pressure was considered revolutionary, a high-tech practice that was of uncertain benefit.

Dr. Harvey Cushing of Johns Hopkins Hospital in Baltimore had observed a blood pressure device while traveling in Europe, developed by Dr. Sciopione Riva-Rocci. Cushing brought this new technology back with him to the U.S. and promptly promoted its use, convinced that this insight into gauging the forcefulness of blood pressure would yield useful clinical insights.

But, in 1910, practicing physicians rejected this new technology, preferring to use their well-established and widely practiced technique of pulse palpation (feeling the pulse), skeptical that the new tool added value. Medical practice of the day was rich with descriptions of the strength and character of the pulse: pulsus parvus et tardus (the slow rising pulse of aortic valve stenosis), the dicrotic notch of aortic valve closure transmitted to the pulse, the "water-hammer" pulse of aortic valve insufficiency.

Over the next 20 years, however, the medical community finally gave way to the new technique, although only physicians were allowed to use blood pressure devices, as nurses were regarded as incapable of mastering the skills required to perform the procedure properly.

Stethoscopes were also gaining in popularity in the early 20th century, but were also the exclusive province of physicians trained in their use. Nurses were not allowed to use stethoscopes until the 1960s. Even then, nurses were not allowed to call them "stethoscopes," but "nurse-o-scopes" or "assistoscopes," and the nurses' version of the device was manufactured to look different to avoid confusion with the "real" doctor's tool.

And just half a century ago, if you wanted to look at a medical textbook, you would have to go to the library and ask for special permission. The librarian would lower her glasses and look you up and down to determine whether or not you were some kind of pervert. Only then might you be granted permission to peer into the pictures of organs and naked bodies.

Such has been the spirit of medicine for centuries: Medicine and its practices are meant to be secret, the insider knowledge of a privileged few.

Fast forward to 2008: The Information Age has overturned the rules of privileged information. Now you have access to the same information as I do, the same information available to practicing physicians. The playing field has been levelled.

Curiously, while information access has advanced at an instantaneous digital pace, attitudes in medicine continue to evolve at the traditional analog crawl. Many of my colleagues continue to be dismayed at the new public access to health information, belittle patients for excessive curiosity about their health, lament the erosion of their healthcare-directing authority. And while new concepts race ahead as we race towards a wiki-like collective growth in healthcare knowledge, physicians are still mired by their reluctance to abdicate their once-lofty positions as chief holders of secrets.

I believe that this is part of the reason why family doctors and cardiologists have been slow to adopt technologies like heart scans and self-empowering programs like Track Your Plaque: processes that take heart disease prevention away from the hands of physicians and place more control into the hands of the people.

Imagine the horror felt by physicians in 1935 of a young upstart nurse boldly trying to use a stethoscope to take a patient's blood pressure. You can imagine the internal horror now being felt as you and I dare to take control over heart disease and deny them the chance to put in four stents, three bypass grafts, then direct our future health habits.

But technology has a way of marching on. It will encounter resistance, bumps, and blind-alleys, but it will go on.

Dr. Jeffrey Dach on the Track Your Plaque program

Dr. Jeffrey Dach posted a great piece on his blog, Bioidentical Hormone Blog , about his perspective on the Track Your Plaque program.

It's worth reading even for those familiar with the program, just to see a slightly different perspective. He also included many great graphics to illustrate his points.

CAT Coronary Calcium Scoring, Reversing Heart Disease












Also, see Dr. Dach's Heart Disease: Part 2, for some novel thoughts.

Vitamin D and programmed aging?

As we age, we lose the capacity to activate vitamin D in the skin.

Studies suggest that, between ages 20 and 70, there is a 75% reduction in the ability to activate vitamin D. The capacity of conversion from 25 (OH) vitamin D to 1,25 di(OH) vitamin D also diminishes.

Holick M. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease.



From Holick, M. 2006

This would explain why 70-year olds come to the office, just back from the Caribbean sporting dark brown tans, are still deficient, often severely, in blood levels of vitamin D (25(OH) vitamin D). A tan does not equal vitamin D.














Courtesy Ipanemic


A practical way of looking at it is that anyone 40 years old or older has lost the majority of ability for vitamin D activation.

This often makes me wonder if the loss of vitamin D activating potential is nature's way to get rid of us. After all, after 40, we've pretty much had our opportunity to recreate and make our contribution to the species (at least in a primitive world in which humans evolved): we've exhausted our reproductive usefulness to the species.

Is the programmed decline of vitamin D skin activation a way to ensure that we develop diseases of senescence (aging)? The list of potential consequences of vitamin D deficiency includes: osteoporosis, poor balance and coordination, falls and fractures; cancer of the breast, bladder, colon, prostate, and blood; reductions in HDL, increases in triglycerides; increased inflammation (C-reactive protein, CRP); declining memory and mentation; coronary heart disease.

Isn't that also pretty much a list that describes aging?

A fascinating argument in support of this idea came from study from St Thomas’ Hospital and the London School of Medicine:

Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women

Telomeres are the "tails" of DNA that were formerly thought to be mistakes, just coding for nonsense. But more recent thinking has proposed that telomeres may provide a counting mechanism that shortens with aging and accelerates with stress and illness. This study suggests that both vitamin D and inflammation (CRP) impact telomere length: the lower the vitamin D, the shorter the telomere length, particularly when inflammation is greater.
















Data supporting vitamin D's effects on preventing or treating cancer, osteoporosis, lipid abnormalities, inflammation, cardiovascular disease, etc., is developing rapidly.

Now the big question: If declining vitamin D is nature's way of ensuring our decline and death, does maintaining higher vitamin D also maintain youthfulness?

I don't have an answer, but it's a really intriguing idea.
All posts by william-davis

The Track Your Plaque “Rule of 60”

The Track Your Plaque recommended targets for conventional lipids (i.e., LDL, HDL, triglycerides) are LDL 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl: 60-60-60.

Not only is this set of values easy to remember—60-60-60—but is grounded in science and the results of clinical trials.

LDL 60 mg/dl
The LDL target is based on experiences such as that of the Reversal Trial, the PROVE-IT Trial, and the Asteroid Trial, all of which showed that LDL cholesterol values in the range of 60 mg/dl dramatically enhance the likelihood of stopping plaque growth or achieving regression, reducing risk of heart attack more than more lenient LDL targets.


HDL 60 mg/dl
Achieving HDL cholesterol of 60 mg/dl is not as well grounded as LDL targets, mostly because increasing HDL is more difficult. There’s also no tremendously profitable way to raise HDL, as there is for reducing LDL (statin drugs). But epidemiologic observations strongly suggest that HDL of 60 mg/dl provides maximum control over both coronary plaque growth, as well as slashing rates of heart attack. Numerous smaller trials have borne this phenomenon out.


Triglycerides 60 mg/dl
Triglycerides of 60 mg/dl is based principally on studies that have shown a virtual elimination of abnormal lipoproteins, especially small LDL, when this value is achieved. Reduction of triglycerides is an effective means to reduce hidden lipoproteins like small LDL and VLDL. Triglycerides in the conventionally acceptable range of 100-150 mg/dl can be associated with dramatic abnormalities of lipoproteins.


Thus, the Track Your Plaque “Rule of 60”. In our day to day experience of trying to stamp out plaque growth from its terrifyingly rapid 30% per year, or reversing it—-dropping your heart scan score—-the Rule of 60 has held up time and again. Getting your lipids to 60 mg/dl does not guarantee that plaque growth stops, but it appears to be a necessary requirement that tips the scales heavily in your favor.

Those of you who’ve discussed lipid targets with your doctor will quickly recognize that the Track Your Plaque targets appear laughably ambitious, perhaps unnecessary. Recall that your doctor likely has no idea of what coronary plaque regression means. He/she likely conforms to the lax targets set by the National Cholesterol Education Panel (NCEP). (These targets depend on a number of factors such as whether you’re diabetic, sex, risk factors, etc.) Based on trial experiences like the few mentioned above, as well as my experience with purposeful coronary plaque reversal, the lipid guidelines as advocated by NCEP guarantee heart disease. Let me emphasize that again: Follow the guidelines set by the NCEP for your doctor to follow, and progression of heart disease is a virtual certainty. At best, it may slow growth of plaque and delay your heart attack or bypass surgery, but it will not stop it.

Now, that point made, let me make another: Just knowing about the targets and even becoming a member of the Track Your Plaque program does not mean that your lipids with automatically go to 60-60-60. We’ve actually had an occasional person tell us that they were disappointed that, by becoming Members, why hadn’t their lipids gone to 60-60-60?

Knowing that the 60-60-60 targets provide real advantage is not the same as actually achieving them.

A little bit of fish oil


The British National Health Service (NHS) has announced that, in light of the substantial data documenting that omega-3 fatty acid intake from fish reduces likelihood of cardiovascular events by around 40%, that Brits discharged from hospital following a heart attack should be "prescribed" 1000 mg of prescription fish oil per day.

Hardly a revolutionary concept. Part of the timidity of the British NHS seems to relate to the potential cost to the government, since apparently much of the cost will be borne by the government-subsidized health system.

But prescription fish oil? Why prescription fish oil? Prescription Omacor, one capsule per day, costs around $70 (U.S.) per month. If I go to Sam's Club the same quantity of omega-3 fatty acids (in three capsules) will cost around $2.50. That's less than 5% of the cost of the prescription form.

Omacor is clearly more concentrated. But is the prescription form better--more effective, more purified, less contaminated, etc.? I have seen no independent verification of this. Of course, manufacturers make all sorts of claims. The only independent, unbiased testing I'm aware of comes from organizations like Consumer Reports and www.consumerlabs.com. Omacor has not been compared to non-prescription fish oil in any of their analyses. Head-to-head comparison of Omacor to nutritional supplement fish oil is unlikely to come from Solvay, the manufacturer of Omacor. Drug companies powerfully resist head-to-head comparisons, fearing it will not play out in their favor. Let the public remain ignorant and hope marketing conquers all.

Why would the NHS only recommend eating fish and prescription fish oil? I don't know, but it smells awfully fishy to me. As soon as an opportunity for profit is built into a treatment, all of a sudden it gains endorsement. Perhaps lobbying by those parties with potential for profit drove the process.

Nonetheless, despite the filthy politics and under-the-table dealings, some good comes out of the NHS's action: broader recognition of the power of fish oil. Perhaps when a British patient or an American patient gets discharged with a prescription for Omacor, the patient will take the initiative and go to the health food store instead and save him (or his insurer) $67.50 per month.

For your coronary plaque control program and control and/or reversal of your heart scan score, we start at 4000 mg per day of standard fish oil, providing 1200 mg per day of omega-3 oils. This amount as a nutritional supplement costs only a few dollars a month. And you have the satisfaction of not only taking a powerful step for your health, but also not enriching the overflowing pockets of drug companies.

AHA: Doctors don't have time for prevention

Doctors "don't have enough time to educate their patients and to stop and think about what measures the patient really needs," says Dr. Raymond Gibbons, new head of the American Heart Association.

Dr. Gibbons highlighted how the system reimburses generously for performing procedures, but reimburses relatively little (often just a few dollars) for providing preventive counseling. He claims to have several ideas for solutions.

Good for Dr. Gibbons. There's no doubt that the lack of truly effective preventive information and counseling is a systemic, built-in flaw in the current medical environment. It is especially true in heart disease.

Another problem: "If a doctor didn't say it, it must not be true." That's the attitude of many of my colleagues. Despite their broad and systematic failure to provide preventive counseling, most physicians (my colleagues the cardiologists especially) pooh-pooh information that comes from other sources. Yet, it's my prediction that much of healthcare will go the way of optometry--direct access to care, often delivered in non-healthcare settings like a store or mall. People are hungry for truly self-empowering health information. Too many physicians can't or won't provide it. You've got to turn elsewhere for it.

That's one of the main reasons I set up the Track Your Plaque program. It's direct access to self-empowering information. A flaw: You still require the assistance of a physician to obtain lab values, lipoproteins, and to monitor certain treatments (e.g., niacin at higher doses). If I knew of a way around this, I'd tell you. But right now I don't. We remain constrained by legal and moral obligations.

Nonetheless, phenomena like CT heart scanning and the Track Your Plaque program are just a taste of things to come.

Confusion about Lp(a)

Since the recent reader question about Lp(a), I've had several other instances of confusion over Lp(a).

To help you navigate through some of the often confusing issues behind this complex genetic abnormality, here are some common sense rules to follow. When you ask your doctor to draw a Lp(a), try to be certain that:

--the same laboratory is always used. Just going from lab to lab can account for huge variation in Lp(a). As standardization proceeds internationally, this will be become less important. But in 2006, it's still an issue.

--you and your doctor resist the temptation to check Lp(a) frequently. I saw a patient recently who was having Lp(a) levels nearly every month. This is pointless. Lp(a) changes very slowly. Checking it frequently will not allow any treatment to be fully reflected. All you'll observe is random variation that can be frustrating. We wait at least 6 months before re-checking after a new treatment is introduced.

If you have a choice, I would recommend you opt for the measure provided by Liposcience (NMR). The technique they use is a particle count measure, rather than a weight-based measure. This may be more accurate, particularly when Lp(a) is small.

Lp(a) remains among the more difficult patterns to understand and correct. Don't be surprised if you encounter a lot of confusion from your doctor, as well. You may end up providing much of his/her education.

Calculus of the cardiologist

I call this the "calculus of the cardiologist":

Heart procedures = big money

More procedures = more big money

You do the math. If you do more procedures, you get more money.
What if your patients don't need more procedures? That's easy. You lower the bar on reasons to do procedures. You scare the pants off people and lead them to think that all heart disease or questions about heart disease are potentially life-threatening. You could even appear to be doing the patient a big favor. "My Lord! This is potentially dangerous. We need to perform a procedure without delay!"

There are incentives beyond direct cash payment. A patient of mine today showed me a memo to employees in his company that showed why certain hospitals are targeted for care. The criteria for choosing centers was based on number of procedures performed. In other words, the more procedures performed at a hospital, the more procedures will be directed there. Of course, this makes sense at some level. More procedures can also mean greater skill.

But have we lost sight of the fact that the mission is not more procedures and more money, but to get rid of a disease? If the intensity of effort devoted to heart procedures were re-directed to early detection, prevention, and reversal of disease, we'd have half the hospitals we now have. We'd also chop a huge chunk out of the national healthcare budget.

Lipoprotein(a) treatment alternatives

A question from a reader:


Two years ago, my doctor recommended a comprehensive lipid screening because both of my parents had heart disease. My only blood component way out of line was LP (a) [lipoprotein(a)]. It was 130. According to the lab that conducted the screening, Berkeley Heart Lab, a level above 30 should be cause for concern. I was stunned that mine was more than quadruple the danger level.

I began taking two grams [2000 mg] of niacin a day in addition to the Lipitor I was already taking. The next reading, a few months later, was 87. Over a period of about 18 months, I had a total of four readings from Berkley Heart Lab. My LP (a) fluctuated in the 80-130 range – still way above normal. My doctor said there was little else I could do to control it.

That doctor has since retired. I now see another doctor who uses a different lab. My first LP (a) reading with him a few months ago was 17, which is normal. I am still taking the same amount of niacin and Lipitor and I can’t think of anything that would account for the huge discrepancy. I’m going to have another test again soon.

Is one of the labs giving erroneous readings? If so, how can I tell which? If Berkeley Heart Lab is correct, is there anything I can do about my increased coronary risk due to high LP (a)?

Tom D.

Tom's frustration on the variation of Lp(a) is due to the fact that laboratories run the Lp(a) test by several different techniques and will generate tremendous variation in values. The key is to stick to the same measure over and over from the same lab, else you'll be terribly confused and frustrated. Tom essentially should ignore the value obtained that was unexpectedly low.

Another issue: Lp(a) is a turtle. It responds very slowly. In fact, we rarely check it more than once or twice a year. Check it too soon after a treatment change and it won't fully reflect the effect. You've got to wait at least several months before re-checking.

How about treatment alternatives? They are:

--More niacin. Not my favorite choice, since niacin >2000 mg per day begins to generate more side-effects, but it is a choice. You can go to 4000-5000 per day, but only with your doctor's supervision due to liver effects.

--Testosterone for males. We use topical testosterone from Women's International Pharmacy in Madison, Wisconson. Prescription patches like Testim are also effective.

--Estrogen for females. This is less "clean" than testosterone, introducing questions about endometrial and breast cancer risk, but it is a choice.

--DHEA--A small effect but every little bit can help. We use 25-50 mg per day, depending on blood levels and only if you're 45 years old or older.

--l-carnitine--In my experience, a small effect. It requires 2000 mg per day, which is expensive. Sometimes, an expected large effect develops, so it's worth a try if it fits in your budget.

--Fibrates--These are the drugs Tricor and Lopid. I don't like these agents very much because I think they're weak, including the effect on Lp(a) reduction. But they are choices for you and your doctor.

Lastly, you can simply be guided by your heart scan score. For example, if Tom's initial heart scan score is 200, and he continues his current program and one year later his score is 300, then alternative treatments are worth considering. But what if Tom's score is 189--he's regressed his coronary plaque. Then, who cares what his Lp(a) is?

Another issue to keep in mind is that, in the presence of Lp(a), keeping LDL to very low numbers (e.g., 60 mg/dl) may added value in preventing coronary plaque growth.

Trapped in a low-fat world

If you would like to...

--Reduce (good) HDL

--Raise triglycerides, sometimes by hundreds of points

--Raise blood sugar into the pre-diabetic range

--Raise blood pressure

--Accelerate coronary plaque growth

then go on a low-fat diet like the one promoted by long-time super low-fat advocate, Dr. Dean Ornish. Every day I have to educate patients that a low-fat diet as advocated by Dr. Ornish is a destructive, counter-productive process that makes coronary plaque grow and increases your heart scan score.

If you want to gain control over coronary plaque, do not follow the Ornish program or anything resembling it. The Ornish program is a dead end.

Instead, the crucial components of a healthy diet for plaque control are:

--Low saturated and hydrogenated fat, but not low all fats.

--High monounsaturated and omega-3 fats

--Low glycemic index (i.e., slow sugar release)

--High fiber

That simple. An excellent program to put these limits to practical use is the South Beach Diet. Or, follow the more detailed guidelines on the Track Your Plaque website (open content section).

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Eat fish three times a day

Patients commonly ask, "Why can't I get vitamin D from food? I drink milk and eat fish."

They're absolutely right: both vitamin D and some oily fish contain vitamin D. However, it's a matter of quantity. An 8 oz. glass of milk contains 100 units of vitamin D (at least it's supposed to; this is not always true). A serving of oily fish like salmon or herring may contain up to 400 units. Thus, if you ate fish three times a day like the Eskimos or the Inuit, you might obtain sufficient vitamin D to prevent the broad and alarming spectrum of phenomena associated with deficiency.

I suspect that most people don't want to eat fish three times a day, nor drink the 20 to 50 glasses of milk per day that would be required to obtain a truly healthy quantity of vitamin D.

The vocal and outspoken Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) has written eloquently on the potential relationship between influenza and vitamin D deficiency. He and his co-authors on a recently published paper point out that the peculiar and unexplained seasonality of influenza corresponds to vitamin D levels. Read his eloquent discussion in Medical News Today at http://www.medicalnewstoday.com/medicalnews.php?newsid=51913.

In the article, Dr. Cannell explains:

"The vitamin D steroid hormone system has always had its origins in the skin, not in the mouth. Until quite recently, when dermatologists and governments began warning us about the dangers of sunlight, humans made enormous quantities of vitamin D where humans have always made it, where naked skin meets the ultraviolet B radiation of sunlight.
We just cannot get adequate amounts of vitamin D from our diet. If we don't expose ourselves to ultraviolet light, we must get vitamin D from dietary supplements...Today, most humans only make about a thousand units of vitamin D a day from sun exposure; many people, such as the elderly or African Americans, make much less than that. How much did humans normally make? A single, twenty-minute, full body exposure to summer sun will trigger the delivery of 20,000 units of vitamin D into the circulation of most people within 48 hours. Twenty thousand units, that's the single most important fact about vitamin D. Compare that to the 100 units you get from a glass of milk, or the several hundred daily units the U.S. government recommend as “Adequate Intake.” It's what we call an “order of magnitude” difference.

"Humans evolved naked in sub-equatorial Africa, where the sun shines directly overhead much of the year and where our species must have obtained tens of thousands of units of vitamin D every day, in spite of our skin developing heavy melanin concentrations (racial pigmentation) for protecting the deeper layers of the skin. Even after humans migrated to temperate latitudes, where our skin rapidly lightened to allow for more rapid vitamin D production, humans worked outdoors. However, in the last three hundred years, we began to work indoors; in the last one hundred years, we began to travel inside cars; in the last several decades, we began to lather on sunblock and consciously avoid sunlight. All of these things lower vitamin D blood levels. The inescapable conclusion is that vitamin D levels in modern humans are not just low - they are aberrantly low."


Like Dr. Cannell, I am absolutely convinced that vitamin D deficiency plays an important role in a number of illnesses, including coronary disease. The more we mind our patients/participants vitamin D status (blood levels of 25-OH-vitamin D3), the more easily we gain control over LDL cholesterol, pre-diabetic patterns, blood pressure, blood sugar, and coronary plaque. In fact, I am becoming rapidly convinced that vitamin D deficiency is an extremely important coronary risk factor.

Because I live in Wisconsin (bbrrrrr!) where seeing the sun is a cause for celebration and sun exposure is possible three months a year, I take 6000 units per day vitamin D. This is the amount necessary to raise my blood levels into the true, physiologic range of 50-70 ng/ml. My wife takes 2000 units per day, and each of my kids takes 1000 units per day, though I believe that my 14-year old son (my size now) should take more. We'll judge by blood levels.

If there is a little-known secret to reducing heart scan scores, vitamin D is that "secret".

To read more from Dr. Cannell or to subscribe to his free and very informative newsletter, go to Vitamin D Council

What if I had a cure for coronary disease?

If I had a cure for coronary disease, what would it look like? What would constitute cure? Would you recognize it if I showed it to you?

In the strictest sense, "cure" means an absolute elimination of any sign of coronary plaque, as well as elimination of any and all dangers associated with coronary disease. It would also mean elimination of the factors that created coronary atherosclerotic plaque in the first place.

In a more practical sense, you could argue that "cure" means a reduction of the amount of material that constitute coronary disease along with a dramatic reduction of the associated risks (i.e., heart attack).

You might call this second, more lax definition "regression" or "reversal".

Is "cure" in the strictest sense possible? No, not to my knowledge in 2006. Yes, there are many (kooks) who claim this is possible, but there's no objective evidence of this occurring.

Regression, or reversal, however, is indeed possible. In fact, I've seen it countless times following the participants in the Track Your Plaque program. If your heart scan score goes from 1000 (a bad score with high risk for heart attack) to 750, you've experienced a large reduction in the amount of atherosclerotic plaque that is behind coronary disease. You've also reduced your risk of an "event" like heart attack to near zero (provided you remain on the program that achieved regression in the first place).

Unfortunately, with present technology regression or reversal does not mean that the original causes of coornary plaque are eliminated. They're just controlled. Fish oil, for example, powerfully reduces triglyceride-containing lipoproteins that trigger coronary plaque growth. But if you stop fish oil, the evil lipoproteins come right back and start injuring your coronaries, causing more plaque growth.

The Track Your Plaque program is the closest thing I know of to a "cure" for coronary disease, that is, "cure" in the sense of regression or reversal. Perhaps in future we'll have a "cure" in the strict sense. Until now, this program is the best there is.