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.

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.

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.

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.

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.

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.

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

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 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.

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.

The Fanatic Cook has posted a stinging criticism of the American Heart Association (AHA):

American Heart Association My Fat Translator

Beyond the nonsensical nutritional recommendations (e.g., substitute small French fries for large French fries), she lists the major financial contributors to the AHA, a Who's Who in the pharmaceutical and processed food industry.

"For an organization that brought in close to a billion dollars last year, you'd think they could come up with something a little more pronounced. If I was more cynical I'd say the AHA had an interest in keeping Americans fat . . . or at least dependent on a highly-processed, fast food diet, requiring drugs to tweak lab values."

To be sure, the AHA does a great deal of good in funding research and educating the public about the prevalence of heart and vascular disease. But their fund raising interests have clearly subverted the honesty of their nutritional advice. Sadly, it is the AHA dietary advice that hospital dietitians use in counseling people with heart disease after their heart attack, stent, or bypass surgery. After my patients are discharged from the hospital for any reason, I tell them to please forget everything the nice hospital dietitian told them. It is not okay to eat the factory farm-raised hamburger on the sugar-equivalent enriched flour bun. Low-fat ice cream is not a healthy substitute for full-fat ice cream.

The AHA is no different than the USDA and the American Diabetes Association, "official" organizations that have, in effect, sold out to industry.

Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):

Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.

There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.

In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.

Copyright 2008 Wiliam Davis, MD

Tne Philadelphia NBC affiliate's website carried this commentary from a colleague of mine:

Mark from the Lehigh Valley is curious about scans that can detect heart disease.

He asked, "I am in my early 50s. My father had a heart attack in his 40s. I am healthy with no symptoms of heart disease, should I consider a heart scan?"

"Well, Mark, occasionally family history needs to be considered more closely. If your father had coronary disease at a relatively young age at the absence of any known risk factor for heart disease for example diabetes, smoking, obesity, high blood pressure, than your level of risk should be considered more closely," Dr. Kevin Shinal, a cardiologist, said.

"There are a number of studies available to access [sic] your level of risk. One such study is a calcium score. A calcium score is a form of a CAT scan that access [sic] the calcium burden or presence of calcium in your coronary arteries. It assigns you a score and score is translated into a level of cardiovascular risk," Shinal said.

But the doctor warned because Mark doesn't have active symptoms, the scan probably wouldn't be covered by insurance.

Was there an understandable answer in there? I certainly couldn't find it.

Why pick on some yokel responding inarticulately to the local media's quest for content? Because this is, all too often, what the public hears: Ill-informed blather from someone who has little or no understanding of the issues. Maybe this doctor wanted his practice group to get some free publicity. "Doctor, could you just answer a few questions from viewers?"

Unfortunately, it's not just local media who are guilty of consulting with know-nothings with only passing knowledge of an issue. National media are guilty of it, too. The need to fill airtime with content is better filled with talking heads who present a compelling story, whether or not it is accurate or insightful, rather than an expert with deep insight into a topic who might not present as pretty a story. I've seen this countless times. A good portion of my day, in fact, is occupied responding to patient questions based on the misinformation presented in some media report.

My message of this brief rant: Be very careful of the messages delivered by the media, even if provided by some supposed "expert." In fact, I regard "experts" in health about as believable as politicians. Sure, sometimes they provide accurate information. But they often do not, or provide information with limited understanding. Or, worse, information intended to serve some hidden agenda.

Were the media to ask me to respond to the question, however, I would say:

"Yes, you should absolutely have a heart scan--yesterday! With your family history, there is no other way to accurately, easily, and inexpensively quantify the amount of coronary atherosclerosis in your heart's arteries. A stress test only uncovers advanced disease. A heart catheterization is overkill and absolutely not indicated in an asymptomatic man. Judging the presence of heart disease from cholesterol values is folly.

"What's left? A CT heart scan. So, yes, you need a CT heart scan ASAP with no doubt whatsoever."

But they didn't ask.

Although Dr. John Cannell's most recent Vitamin D Newsletter concerns the connection between autism and vitamin D, and has nothing to do with coronary plaque reversal, this fascinating discussion between a mother of an autistic boy and Dr. Cannell is so enlightening that I thought that it was still worth passing on.

I also feel very deeply for parents with autistic children, who I see struggle with the developmental difficulties their children encounter. (I even have several patients who are parents of 2 or 3 autistic children.)

As always, Dr. Cannell is at the cutting-edge of converting hard scientific information into practical use. You will note several points or questions raised:

1) Dr. Cannell advocates a powdered capsule form of vitamin D. In my experience, most powdered or tablet forms do not work. But some do. He apparently has success with the brand he specifies.

2) Are there vitamin D-receptor (VDR) genotypes that respond differently? Should there be different 25 (OH) vitamin D blood level targets for different VDR genotypes? Nobody knows yet, but it will be an important question to explore in the future.

3) Is heavy metal toxicity, at least in its milder forms, a surrogate for vitamin D deficiency? (Are chelationists unwittingly treating vitamin D deficiency?)

4) If this is a genuine association, and vitamin D replenishment exerts profound neurologic effects in autistic children, does a similar, though less marked effect, hold in non-autistic children? Will children perform better, learn more effectively, etc. with vitamin D supplementation to normal levels?

5) Vitamin A--Is vitamin A with vitamin D good or bad? This one I do not have an answer to. Reading the literature Dr. Cannell cites didn't help much. (Dr. BG--Any comments? Dr. BG is a vitamin A advocate.)

Perhaps, should the association between autism and vitamin D hold, it raises more questions than it settles. But, true to my experience with vitamin D, every day I stumble on some unique, fascinating effect, all beneficial. We continue to learn new lessons about vitamin D and Dr. Cannell's insights as a practicing psychiatrist deeply concerned with vitamin D issues have helped enormously.

(Sorry, but I did not copy the links to the literature Dr. Cannell cites. To obtain the links, go to the original Vitamin D Newsletter.)

The Vitamin D Newsletter
June 2008

This month we feature a remarkable series of letters from a mother of an autistic son who treated her child with vitamin D. It is the first case report in the medical literature suggesting vitamin D has a treatment effect in autism.

First, a brief case report and then a more detailed exchange of emails between the mother and me.

Case Report:

John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter. A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me. I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D, John's language began to return and he was no longer as fearful of being alone. At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbacteriosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day.

Before you read the series of emails between the mother and me, I'd like to caution that this is only a case report of sorts and does not prove a treatment effect. Spontaneous remissions, while rare in autism, have been reported, thus the supplemental vitamin D may have had nothing to do with his improvement. If the response is due to vitamin D, there is no assurance it will prove lasting. I think it unlikely that older autistic children or individuals with severe autism will show these sorts of apparent improvements. Furthermore, autism is a multifactorial disease with strong genetic roots and it is highly unlikely that treatment of vitamin D deficiency in all autistic children will result in similar improvements. Finally, I did not examine this child, and I am relying on the child's mother to report both his condition and his apparent response to vitamin D treatment. However, the mother agreed to speak with the press about her son and allow for independent confirmation of the apparent treatment response.

Below are the emails, edited for brevity, clarity, and confidentiality.

Dear Dr. Cannell:

I am writing because I believe my son John is strongly affected by vitamin D and I need some advice. John is seven and autistic and weighs 50 pounds. We live in the northeastern part of the United States . He starts spending lots of time outside in May and continues until September. Every year, like clockwork, he has the same patterns of behavior and ability. After about six weeks of sun exposure, every July, he begins feeling much better, seems to be comfortable in his skin, does not have as much self-stimulatory behavior, can eat a variety of foods and has language. This past summer, he was using 14-word sentences. By the end of November, he can't even ask you for a cup of juice. He becomes more exclusive, has emotional highs and lows, has tantrums and is easily frustrated.

His 25(OH)D level on April 15th was 25 ng/ml but he had already been going out in the sun so his level must have been lower in the winter. I have had his genetics tested (Nutrigenomic) and he has mutations in his vitamin D receptors:

VDR Bsm/Taq ++
VDR Fok --
VDR Taq ++

My first question, does it sound like the changes in his behaviors and abilities could be caused by lack of vitamin D? Could you elaborate on the time it would take to get adequate amounts of vitamin D to start seeing positive results? For example, even if he starts going out in the sun in May, it's usually not until July that I see positive changes. Then would it take a month or two to go back to being deficient, thus explaining his 'regression' by the time November comes around. Secondly, I am looking at different forms of vitamin D therapy: a vitamin D lamp, vitamin D3 cream, or oral vitamin D. Can you tell me what might be the best form during the winter months?

Thank you very much for your time and attention.

Jane, Boston MA

Dear Jane:

Yes, it is possible your son's autism is related to vitamin D. Such seasonality has been reported before in autism, both in an individual and in autistic children at a summer camp. Although suggestive, such seasonality does not prove a vitamin D connection. Sun exposure, unless it is full body, takes several months to get vitamin D levels up. If sunblock or clothes are worn sun exposure will not get 25(OH)D levels much above 30 ng/ml. As far as the "mutations" you list, they are actually vitamin D receptor (VDR) polymorphisms and not referred to as mutations although all such changes occurred through mutations at some time in the past. VDR polymorphisms are simply the different structures of the vitamin D receptor that different people have and they are widely distributed. A pilot study of actual VDR receptor mutations did not detect VDR mutations in 24 autistic individuals but they did not assess for VDR polymorphisms. However, a highly significant association exists between one VDR polymorphism and larger head size. Mean head circumference is larger in autism.

Yan J, et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett 2005;380(1-2):37-41.

Handoko HY, et al. Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures. Am J Hum Biol 2006;18(3):415-7.

Lainhart JE, et al. Head circumference and height in autism: a study by the Collaborative Program of Excellence in Autism. Am J Med Genet A 2006;140(21):2257-74.

Lainhart JE, et al. Macrocephaly in children and adults with autism. J Am Acad Child Adolesc Psychiatry 1997;36(2):282-90.

I emailed the world's foremost expert on VDR polymorphisms asking him about your son's polymorphisms and his reply, quite technical, is below.

Dear John:

I apologize for the delay in getting back to you regarding VDR polymorphisms. Initial studies by Eisman and coworkers many years ago suggested that several of the polymorphs identified above in the VDR gene (Bsm/Tag) correlated strongly with osteoporosis. Despite the hoopla, subsequent analyses by many different investigators did not really confirm these results, i.e. only a very modest (3%) correlation. This spawned multiple studies searching for correlations between VDR polymorph's and cancer, autoimmune disease and so forth. It is fair to say from all of these studies that the correlation is at best weak, and in most cases non-existent. Part of this may be due to the fact that the Bsm and Taq polymorphs are located in VDR gene introns and as a first approximation cannot affect the VDR protein's function. This is not an absolute statement, however, as our work is now showing that regulatory regions that control the VDR's expression are located within introns as well as upstream. Therefore the possibility exists that these polymorphs could affect expression, although we have not found these regions to contain enhancers yet. This is clearly where gene and disease studies are going. The only polymorph that could affect function is the Fok1 site, which we identified many years ago following our initial cloning and structural analysis of the human VDR gene. The presence of this site leads to the expression of a shorter VDR protein (424 aa) that is purported to have a slight increase in transcriptional activity (10%?) vs the large protein (427 aa). The above analysis suggests that this polymorph is absent, leading to production of the larger perhaps less active protein. On a single patient basis, it is really difficult to conclude anything regarding this finding. Indeed, despite large numbers of patients, the VDR polymorph have not really revealed any significant insight. Given the summer correlations, it is probably more likely that the individual is low in vitamin D3 in winter.

Sincerely,

Professor John Doe

Thus, one of your son's polymorphisms may have less functionality but that should be easily overcome by higher vitamin D levels. The first thing to do is stop all vitamin A, multivitamins containing vitamin A, or cod liver oil and start vitamin D. As you will see below, vitamin A antagonizes the action of vitamin D and he should have plenty of vitamin A if he eats colorful vegetables, colorful fruit, eggs and fortified oatmeal. As far as vitamin D, I think the easiest way to give vitamin D is powdered capsules, not a cream. You can open the capsule and put the powder in about anything, such as juice. To buy the capsules, go toBio Tech Pharmacal and buy both a bottle of the 5,000 and the 1,000 IU capsules. He should take one 5,000 IU capsule a day for two weeks then take 2,000 IU per day. After a month, go to the doctor and have another 25-hydroxy-vitamin D blood test. Do not let your doctor order a 1,25-dihydroxy-vitamin D as it will give you and your doctor false information about your son's vitamin D status. The other option is buying a Sperti vitamin D light. Daily use of the light on both sides of his trunk will raise levels fairly quickly but he should still have a 25(OH)D blood test every month to assure his levels rise to the mid level of normal ranges, about 70 ng/ml. Vitamin D is very safe. Your son would have to take more than 10,000 IU a day for more than a year to have any risk of toxicity. If he improves and his level is 50 ng/ml, the next question is would he improve even more if his level was 70 ng/ml? Some lifeguards have levels of 80-100 ng/ml; normal ranges in the labs in the USA are 30 -100 ng/ml (ideal ranges are 50 -100 ng/ml.) If you have any more questions, let me know. I certainly want to know how he is doing.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been one week on 5,000 IUs of vitamin D3 daily and already we're getting some language back! We haven't had original language since probably around the end of November. The only language we have had in the past five months has been verbal scripting. Today John has already told me "turn off the TV" and "clean up the water". This is all very exciting. Will it last? I will continue to keep you updated on progress and change in behavior. One more thing, all winter long he was afraid to be by himself anywhere. Now he is starting to be able to be in another room or outside by himself.

Thanks so much,

Jane

Dear Jane:

I can't tell you how happy I am for you. I suspect John will continue to improve. Do you have any parent rating scales or does his treating pediatrician have any objective rating scales? If you have before and after rating scales or his treating doctor does then it becomes important to track his progress on an objective measure. Jane, if you are a member of any autism discussion groups, you should post about this, including doses used. If your son's case is typical, then hundreds of thousands of autistic children may be helped with vitamin D.

John Cannell

Dear Dr. Cannell:

It has been two weeks on 5,000 IU per day and I want to inform you that we are having continued success with language. Continued in the sense that it is consistent, it wasn't just a one day fluke. In addition, he is taking himself to the bathroom; this is another thing that goes away in winter months. I usually have to catch him holding it in and then suggest he go, but now he is going completely by himself. In therapy last week, he started drawing again. He drew a bee and then ran around the room buzzing. His toileting is consistent with his therapists, not just mommy. Last night, I asked him to count to 10 for me and he did - quite enthusiastically. Then I said what does J-O-H-N spell? It took him a bit but then he said "John."

Unfortunately, the last scale taken was when he was 3 when he had his first developmental evaluation. But we do track behavior and language on a weekly basis. The forms we fill out give a good indication as to how he is doing.

I belong to a parent forum. It was created by a doctor named Amy Yasko. She's a PhD, a researcher, not a medical doctor. It was through her that I got John's genetics tested. She advocates vitamin D as being very crucial. I will post something on her forum for the parents there. However, if the parents on the forum are following her recommendations, they should be taking it already - 2000 IUs in winter and 1000 IUs in summer is her recommendation. I will post something on the forum to really emphasize how important vitamin D is.

Jane

Dear Jane:

I'm glad the improvements are continuing. I see Dr. Yasko recommends 10,000 IU of vitamin A/day as well as cod liver oil. I strongly disagree. Make sure your son is taking neither vitamin A nor cod liver oil. Rather, make sure he eats colored fruits and vegetables as well as fortified oatmeal. Vitamin A interferes with vitamin D's function, especially at the doses Dr. Yasko recommends.

Vitamin A antagonizes the action of vitamin D. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. Furthermore, the consumption of preformed retinols, even in amounts consumed by many Americans in both multivitamins and cod liver oil appears to be causing low-grade, but widespread, bone toxicity, perhaps through its antagonism of vitamin D. In a recent dietary intake study, Kyungwon et al found high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma and they found a clear relationship between vitamin D and vitamin A intakes as the women in the highest quintile of vitamin D intake also ingested almost 10,000 IU of retinols/day. As early as 1933, Hess et al warned about vitamin A consumption, concluding, “as to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.”

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hess’s prophecy of a passing fad proved premature and many Americans continue to consume “absurd” and dangerous quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinols (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinols (5,000 to 15,000 IU or in some cases 30,000 IU).

John Cannell

Dear Dr. Cannell:

It has been three weeks and he went from 5,000 IU of vitamin D per day to 2,000 IU per day a week ago. His language is increasing. He's now back to saying the things he wants with some prompting. He also has gut dysbiosis and I'm sure the D is helping with microbes in his gut. He has a lot of problems with his immune system and bacteria and viruses. Also, doesn't vitamin D aid in the production of glutathione? I feel that could be a big part of his increased language.

Jane

Dear Jane:

Yes, abnormal immune responses are associated with both autism and vitamin D deficiency. For example, autistic individuals have immune abnormalities that show a striking similarity to the immune functions affected by vitamin D. Animal evidence indicates some vitamin D deficiency induced brain damage may be malleable, that is, vitamin D may partially reverse the brain damage, if given early enough. These studies offer hope that sunlight or oral vitamin D, especially in young autistic children, may have a treatment effect.

Ashwood P, et al. The immune response in autism: a new frontier for autism research. J Leukoc Biol 2006;80(1):1-15.

Cantorna MT, et al. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system. Am J Clin Nutr 2004;80(6 Suppl):1717S-20S.

Burne TH, et al. Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiol Behav 2004;81(4):651-5.

Both the brain and the blood of autistic individuals show evidence of ongoing chronic inflammation and oxidative stress. That is, the disease process is probably increasingly destructive. Further hope for a treatment effect rests in activated vitamin D's powerful anti-inflammatory properties. Its administration reduces production of inflammatory cytokines in the brain, which have consistently been associated with cognitive impairment. Furthermore, activated vitamin D is remarkably neuroprotective by stimulating neurotropin release, reducing toxic cellular calcium levels in the brain, inhibiting the production of nitrous oxide, and by its immunomodulating properties, especially in reducing inflammatory cytokines and by increasing brain glutathione.

Moore ME, Piazza A, McCartney Y, Lynch MA. Evidence that vitamin D3 reverses age-related inflammatory changes in the rat hippocampus. Biochem Soc Trans 2005;33(Pt 4):573-7.

Cohen-Lahav M, Shany S, Tobvin D, Chaimovitz C, Douvdevani A. Vitamin D decreases NFkappaB activity by increasing IkappaBalpha levels. Nephrol Dial Transplant 2006;21(4):889-97

Kalueff AV, Eremin KO, Tuohimaa P. Mechanisms of neuroprotective action of vitamin d(3). Biochemistry (Mosc) 2004;69(7):738-41.

This last function of vitamin D, increasing cellular levels of glutathione, may explain the purported link between heavy metals, oxidative stress, and autism. For example, activated vitamin D reduces iron-induced and zinc-induced oxidative injuries in rat brain. The primary route for the neurotoxicity of most heavy metals is through depletion of glutathione and subsequent generation of reactive oxygen and nitrogen species. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals. Several studies indicate autistic individuals have difficulty excreting heavy metals, especially mercury. If vitamin D deficient brains are unable to utilize glutathione properly, and thus unable to remove heavy metals, they may be oxidatively damaged by heavy metal loads normal children easily excrete. The amount of activated vitamin D in the brain directly depends on how much vitamin D is made in the skin or put in the mouth.

Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab 2002;13(3):100-5.

Chen KB, Lin AM, Chiu TH. Systemic vitamin D3 attenuated oxidative injuries in the locus coeruleus of rat brain. Ann N Y Acad Sci 2003;993:313-24.

Lin AM, Chen KB, Chao PL. Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS. Ann N Y Acad Sci 2005;1053:319-29.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12(10):1161-208

Kern JK, Jones AM. Evidence of toxicity, oxidative stress, and neuronal insult in autism. J Toxicol Environ Health B Crit Rev 2006;9(6):485-99.

Sincerely,

John Cannell

Dear Dr. Cannell:

It has been a month now and John's Improvements are continuing. In the last week, he has been using his muscles more, he goes on the swing outside and lifts his legs and bends in ways that take core muscle strength. This is yet another skill or interest that left and is returning. I will report more next week.
Jane

Conclusion:

It is too early to say vitamin D has a treatment effect in autism. However, a simple risk/benefit analysis suggests that autistic children should be diagnosed and aggressively treated for vitamin D deficiency. If readers want to learn more about vitamin D and autism, they can obtain the entire paper on the link below. Unfortunately, Elsevier charges $31.50 to download it. You can read a similar document for free on the website, where we first published the theory a year ago.

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9.

http://vitamindcouncil.org/newsletter/2007-may.shtml

In summation, autistic children should be given enough vitamin D to get their 25(OH)D levels up to the mid to high range of normals, that is, 70 ng/ml (175 nmol/L in countries that use the metric system). In the absence of sun exposure, this usually requires long-term administration of about 1,000 IU/day per 20 pounds of body weight with a loading dose of 2,000 IU of vitamin D/day for every 20 pounds of body weight for the first two weeks. As individual variation in response is very high, they should have 25(OH)D blood tests every month until their level has stabilized around 70 ng/ml. They should stop all products containing preformed retinols (vitamin A), especially cod liver oil.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. As we are a 501(3)(c) non-profit corporation, dedicated to ending vitamin D deficiency and not making money, the Vitamin D Council does not copyright this newsletter. Please reproduce it and post it on Internet sites. If this newsletter proves useful to a child you know with autism, the Vitamin D Council asks for a donation as we have not been able to secure a grant and our bank account balance is again below $5,000. Send your tax-deductible contributions to:

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

Rather than the headline New Study Could Change Heart Disease Diagnosis And Treatment being run in Utah TV and newspapers, instead it should read:

Make big money fast with CT scans!

Is your bottom line shrinking? Have you fallen on hard economic times? Is competition from other hospitals and providers threatening your financial health?

Then we have a solution: Do a CT coronary angiogram on everybody! Look for disease in people with no symptoms, scare the heck out of them, and voila! Instant need for bypass surgery!

Ka-ching!! That'll be $100,000, please.

Do it again, and again, and again, and your hospital will be quickly in the black in no time!

And, for the savvy marketer, tell the newspapers that you're going to conduct a study to see if this approach works--even before the study gets started! Even if the study pans, you'll come out a winner because you did it in the name of "research"!

Apparently a group of cardiologists at the Intermountain Medical Center and LDS Hospital in Salt Lake City, with the financial assistance of Siemens, a manufacturer of CT scanners, is funding a 1000-patient study of diabetics, all without symptoms of heart disease, half of whom will undergo "screening" CT coronary angiograms (not heart scans) followed by bypass surgery, if "needed". The other half will receive conventional, "aggressive" medical therapy. "Aggressive" means cholesterol treatment, blood pressure control, and blood sugar control (no kidding).

The outcomes of the two groups will be compared after two years.

To understand the absurdity of this study, note that they are proposing what amounts to "prophylactic" bypass surgery, since the participants are without symptoms. Since there are no stress tests, a measurement of flow or functional capacity (exercise tolerance) cannot be factored in. Decisions will be made on the basis of severity of "blockages" in asymptomatic people, a hazardous notion that has never been shown to provide benefit. No doubt: Some diabetics with extensive disease may obtain benefit from screening, but many more will undergo what amounts to unnecessary bypass that provides no benefit. We already know from studies dating back over 20 years to the days of the original CASS (Coronary Artery Surgery Study) that putting asymptomatic people through bypass surgery willy-nilly does not reduce mortality.

Of course, the "aggressive" preventive treatment they propose is more like the least common denominator level of treatment. In fact, I would characterize the "aggressive" preventive treatment as ridiculous. Doing less would be malpractice. Much more could be done, but doing a lot more would pose a real challenge to the bypass arm of the trial.

But the smell of money drives such efforts: More CT angiograms, more hospitalization for bypass surgery. The payoff to the hospitals from this effort is likely to exceed $5 to $10 million, all money that they might not have otherwise seen. The ill-informed people in the local media gush with enthusiasm, the hospital acts like they are at the cutting edge of medical technology, the doctors pose as saviors.

All this time, real preventive efforts go unmentioned. No fish oil (28% reduction in heart attack, 45% reduction in sudden death from heart attack), no genuine diet efforts (i.e., not the diabetes-promoting American Diabetes Association diet), no effort to identify sources of coronary risk beyond LDL cholesterol (low HDL,small LDL,and postprandial or after-eating abnormalities, for instance, are prominent sources of risk in diabetics), no vitamin D. In my view, the preventive arm of the study amounts to doing virtually nothing beyond prescribing statin drugs.

Don't fall for it.

The Fountain of Youth, Louis Cranach the Younger (1546)

In the Track Your Plaque program, we sometimes use the adrenal hormone, DHEA. It is a fascinating and--surprisingly--an over-the-counter hormone that can be useful and safe when used properly.

DHEA can be useful for:

--Reduction of Lp(a)--Though more effective in females, it can also be useful in males. In the women, DHEA often reduces Lp(a) 15-18%, somewhat less in males. The lower the starting DHEA, the greater the Lp(a) reduction.

--Improved libido--in both men and women. The effect is modest. It's magnified when used with other strategies. Although this is not specifically a goal in the program, it sure helps to get side-benefits like this, rather than unwanted side-effects.

--Increased energy and mood--The boost in mood is, for many, the most perceptible effect: More ambition, more stamina, greater staying power in work and exercise.

--Reduction in abdominal (visceral) fat--A modest effect, but one that, over a long period of use (>6 months) can yield improved insulin responses.

Most commonly, I will suggest DHEA supplementation when blood levels allow. Some people, however, Google "DHEA" and come back horrified that I would suggest such a dangerous supplement.

"I read that it makes women grow mustaches and makes their voices deeper!"

And it does--if you take a lot.

10-15 years ago, when the benefits of DHEA became apparent, some people wanted to believe that DHEA was the fountain of youth. People interested in the anti-aging potential for DHEA figured that, if 50 mg per day made you feel energized and vigorous, what would be the effect of 1000 mg, 2000 mg, or 3000 mg per day? A number of clinical trials were conducted using these doses and, interestingly, depression can lift, men and women increase muscle mass, there is a slight increase in bone density, even pain symptoms from rheumatoid arthritis and lupus may improve. But . . . women grow mustaches, become sexually aggressive, and develop deep voices. Men can become hyperaggressive or overly emotional.

No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose.

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

The only side-effects I see at these doses are 1) excessive assertiveness or crabbiness, and 2) insomnia if taken at bedtime.

In my experience, DHEA is a benign hormone, provided it is taken in limited doses and not abused. An occasional female younger than 55 years old will be able to tolerate only 10-20 mg per day before developing the edgy side-effects, but I've never witnessed masculinizing side-effects at these low doses, nor have I ever seen excessive increases in testosterone in men or women. (Women can raise testosterone levels slightly, but almost never enough to exert much effect beyond modestly increased libido.)

Copyright 2008 William Davis, MD

Here is detailed comment from a reader who figured out the wheat (and dairy) issue on her own with impressive results.

Though it seems an unpardonable over-simplification of diet, this concept of eliminating wheat-based products (along with obvious unhealthy foods like candy and soda) yields unexpectedly large results, as our reader relates.

Hi Dr. Davis,

Several years ago, chronic untreated asthma infections hospitalized me. I thought it was recurring bronchitis as I'd never had asthma in my life. Killed much of the alveoli... took awhile to de-crap the lungs and regrow the alveoli. Got assigned a cardiologist sort-of by accident while in the hospital for that (couple days of constant heated steroid, stress, a pain + situation combined, elevated my heart rate to 298 for a brief time). When I went to see him, he wrote me a prescription for the Eades' PPLP [Protein Power LifePlan] book.

It's taken awhile, since it's required radical gradual changes in most aspects of my overly Type-A life, but I'm now about 140 lbs lighter, and hopefully much more in the future.

Miraculously, after 10 days on a hard meat-eggs-cheese-veggie-berry approach (which I sadly confess was mostly pepperoni & mozz nuked... I was busy! ;-)), all my medical symptoms disappeared too. Acid reflux, acne, brain-fog, rashes, 'severe asthma', allergies, etc. etc. By trial and error I realized I wrongly attributed that to lowcarbing when it was getting off gluten that actually did it for me. Which since I'm lowcarb also means all the crap my celiac boyfriend can eat, I can't. Lowcarb does many great things for me (just dropping all the bloating and increasing the energy level are awesome), but getting off wheat was critical.

I've since found that a single tablespoon of "milk" in the morning, or something with wheat (say a tortilla), will make me ravenous *specifically for milk and wheat* all day. Conversely, I can be eating lowcarb and then eat total junk--but something without gluten--and not have it bother me much at all. But one pumpernickel slice at Outback and I am DOOMED. It doesn't always happen that instant; will-power has some sway; but the odds of my making a 'poor decision that leads to cascade failure and totally abandoning my eating plan' in the next 48 hours is astronomically higher if milk or wheat were involved. Oddly, cheese does not seem to affect me this way.

When I was younger (I'm 42 now) I had to stop drinking milk. If I drank some I wanted more. If I drank more I needed more. If I drank more, that was it: I'd be stumbling to the kitchen in the dark at 3am, drinking out of the carton, falling gasping against the refrigerator after several long gulps, like a heroin addict who just got a fix. I finally realized that since I'd lived on a ton of milk my whole life, maybe this was a milk problem; so I usually stayed away from it. So then it turned out wheat/gluten were an issue too. Which made me realize how much of my life was filled with not-eating most of the time (very busy, workaholic, but very sedentary), but when I did eat, ingesting amazing amounts of wheat products. I'm astounded that my whole life I mostly ate things I am apparently intolerant to "or something." Sometimes I wonder how much different even my brain would be if it'd been different.

This might contribute to my ending up weighing 500# at one point. The only amazing thing is that I didn't get a disease. (Well I did--obesity--but I mean any others.) I'm from a family of people who are mostly fat, mostly alcoholic, and mostly dead of cancer. I'm just fat, worse than the others but otherwise seemingly ok. Now I'm starting to think that maybe my whole family may have some 'issue' with the primary foods of our culture.

I tell friends that my horrible chronic acid reflux was solved merely by getting off gluten. They nearly all say, "I could never give up bread!" (Isn't it funny, you never hear people say, "Oh man, I could never give up broccoli!") I tried to convince one young friend to try it; her doctor told her eating more protein and fat was unhealthy, and gave her a prescription (this is lifetime--it doesn't cure it, merely treats the symptom) to a drug to help with acid reflux. I said you're kidding me, you think taking a drug the rest of your life is healthier than trading your pasta for a steak?? Go figure.

I still haven't figured out the milk connection (or why I seem ok with cheese for some reason; maybe there is a dosage-difference, or the sugar combined with it has some effect), but I think it's pretty clear that dropping milk and wheat has very radically changed my life for the better. I may actually live, which being a single mom to an awesome 11 year old girl, is a good thing.

Best,
P.

Given the confusion over what constitutes the "ideal" diet, a discussion that has been hotly debated for decades, some people become very angry that we still don't agree on what is truly healthy.

"Why should I even try if the experts don't agree? They say something is bad one day, then say it's okay the next!"

But that's a short-sighted half-truth born of frustration. We have certainly zigzagged in our understanding of diet over the years. The grand national experiment in low-fat eating, for instance, clearly failed to improve our health. In fact, the opposite occurred: The largest epidemic of obesity and diabetes in world history. You could get angry from this failed experiment . . . or you could learn from it, take what lessons we can and improve on it.

Step back for a moment and consider: In what other age could we even have this discussion?

If we lived in a world where you were hungry, your children were hungry, and you didn't know where the day's food was to be found, we would have no need whatsoever for this conversation: You would take whatever you could find, kill, or steal.

Say you woke up this morning and your cabinets and refrigerator were empty. The stores were far away or non-existent. You and your family would have to improvise, to forage or hunt your day's food. It would require hours. You wouldn't fuss about glycemic index, or saturated fat, or whether or not sugar or wheat was present. You would just eat whatever you could get your hands on. When caloric deprivation threatens, we take what is available.

But we live in a world of plenty--of enormous excess--that allows us choices. It is a world that encourages eating more than is required for existence, a world tailored more to indulgence than to simple satiety or sustenance. That's when distinctions among food types and quality make a difference. But it is a dilemma born of riches.

Starvation and caloric deprivation would settle the argument for us very quickly. It doesn't mean that we shouldn't continue to debate the finer points of diet. But don't do it with anger or frustration. Do it GRATEFULLY, recognizing that we are lucky to be able to have such a conversation in the first place.

Image courtesy Food and Agriculture Organization of the United Nations.

I frequently peruse conventional health websites to keep track of their message. One painfully conventional (read "drug company-supported") website that echoes the standard advice on heart disease and heart health is Everyday Health .

Since I subscribe to the newsletters for many conventional sites, I received an e-mail that took me to this Q & A about HDL cholesterol:

Q: I'm 36 years old and my good cholesterol is too low. What can I do?
– Nilsa, Florida

Dr. Lori Mosca of New York-Presbyterian Hospital responds:

A: A woman's HDL goal should be greater than 50 mg/dL (greater than 40 mg/dL in men). You can raise your HDL levels by eating a diet low in saturated fat and trans fat but high in monounsaturated fats. Lose weight if you need to and get at least 30 minutes of moderate-intensity exercise on a minimum of four days per week. If you smoke, quit. Despite positive lifestyle changes, though, some individuals may still be candidates for HDL-raising drug therapy because they are at increased risk for cardiovascular disease. Discuss your options with your health care provider.

Are you satisified with that answer? I certainly am not.

First of all, is this something you've never heard before? "Eat right, exercise, cut your unhealthy fats." Then why do people who follow this sort of conventional advice often still fail? Is the next step always medication?

Here's the part that Dr. Mosca and other conventional, drug-minded "authorities" have left out:

To raise HDL powerfully--not to 40 mg/dl for males or 50 mg/dl for females, but to 60, 70 or 80 mg/dl--think about the following strategies:

--Eliminate wheat and cornstarch products. I have droned on endlessly about this concept, but it is enormously effective. While the weight loss that inevitably follows elimination of these foods adds to the HDL-raising effect, there is also an independent effect, as well.

--Fish oil--The omega-3 fatty acids in fish oil reduce triglycerides. Triglycerides accelerate the destruction of HDL. Remove triglycerides, HDL goes up. (Though krill oil may share, even surpass this effect, we need more data than the single manufacturer-sponsored study.) Of course, this requires real doses, not the namby-pamby doses you often read about.

--Vitamin D--Achieving normal levels of 25(OH) vitamin D raises HDL with power I have never witnessed from any other strategy before, barring weight loss of 30+ lbs. Readers of the Heart Scan Blog know that just taking vitamin D is not enough. Verification with blood levels is an absolute necessity, particularly if raising HDL maximally is among your goals.

--Adding back saturated fat. I say "adding back" since most of us (including myself) went too far down the "saturated fat is bad" path over the past few years. While I do not advocate a carte blanche approach to saturated fat, I believe that adding back eggs (preferably free-range and/or omega-3 rich), lean meats, and hard cheeses is a good idea. The saturated fat in these foods raise HDL 5 or more mg/dl.

--Dark chocolate--Or other cocoa prepartions. What a cool way to raise HDL! Reach for the lowest-sugar, highest cocoa preparations.

--Alcoholic beverages--I am partial to the red wine/flavonoid-rich concept, being a wine drinker. Although all alcoholic beverages raise HDL due to the ethanol content, for benefits beyond alcohol (as well as to avoid wheat-based drinks like beer), I do believe that the bulk of data argue for flavonoid-rich red wines from southern France, Italy, and California.

--Achieve ideal weight--The toughest of all. But eliminating wheat and cornstarch makes it far easier.

Follow the conventional advice of those like Dr. Lori Mosca, and the majority of people will fail. ("It just so happens that I have a prescription drug just for that purpose!")

Buck the conventional advice, adopt strategies that won't be found in the drug ads, nor be provided by the conventionally-thinking, and you can succeed to heights you never thought possible.

Copyright 2008 William Davis, MD

Blood sugar lessons from a Type I diabetic

Lessons about omega-3s from Japan

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

Do I sell heart scans?

Plaque is the new cholesterol

Track Your Plaque success story blows it

Dr. Cannell comments on vitamin D lab tests

Privileged information

Dr. Jeffrey Dach on the Track Your Plaque program

Vitamin D and programmed aging?

Fanatic Cook on the American Heart Association

Sleep for heart health

Is normal TSH too high?

Talking heads

Vitamin D Newsletter-Autism and Vitamin D

"Make big money fast with CT scans"

Is DHEA dangerous?

Wheat addiction: 140 lbs lost

Diet: Don't be angry, be GRATEFUL

HDL for Dummies