Blood sugar lessons from a Type I diabetic

23. July 2008 William Davis (15)

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

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

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

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

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

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

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

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

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

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

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

Lessons about omega-3s from Japan

23. July 2008 William Davis (7)

Image courtesy of apc33.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

19. July 2008 William Davis (14)

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

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

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

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

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

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

The diets

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

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

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

Weight loss, lipids, inflammation

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

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

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

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

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

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

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

However, several unanswered questions remain:

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

I would further propose that:

Low-fat diets are dead

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

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

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

Do I sell heart scans?

18. July 2008 William Davis (12)

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

Huh?

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

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

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

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

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

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

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

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

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

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

Yeah, right.

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

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

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

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

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

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

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

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

That's it, pure and simple.

Plaque is the new cholesterol

17. July 2008 William Davis (3)

Which is more important: cholesterol or coronary plaque?

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

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

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

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

Why should heart scan be held to such a standard?

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

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

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

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

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

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

Track Your Plaque success story blows it

17. July 2008 William Davis (3)

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

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

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

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

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

Why?

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

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

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

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

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

Dr. Cannell comments on vitamin D lab tests

14. July 2008 William Davis (9)

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

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

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

Does it matter what reference lab my doctor uses?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

John Cannell, MD
The Vitamin D Council

Send your tax-deductible contributions to:

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

Privileged information

12. July 2008 William Davis (9)

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

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

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

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

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

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

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

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

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

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

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

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

Dr. Jeffrey Dach on the Track Your Plaque program

10. July 2008 William Davis (5)

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

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

CAT Coronary Calcium Scoring, Reversing Heart Disease

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

Vitamin D and programmed aging?

9. July 2008 William Davis (8)

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

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

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

From Holick, M. 2006

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

Courtesy Ipanemic

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

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

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

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

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

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

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

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

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

I don't have an answer, but it's a really intriguing idea.

All posts by william-davis

Butter: Just because it's low-carb doesn't mean it's good

21. October 2010 William Davis (59)

The diet I advocate in the Track Your Plaque program to gain control over the factors that lead us to coronary plaque and heart attack is a low-carbohydrate diet. We begin with elimination of wheat, cornstarch, oats, and sugars in the context of an overall carbohydrate-reduced diet. We refine the program by monitoring postprandial (after-meal) glucoses.

But not everything low-carb is good for you. Fried sausages, for instance, are exceptionally unhealthy, despite having little to no carbohydrates.

An emerging but potentially very powerful issue is that of Advanced Glycation End-products, or AGEs. There are two general varieties of AGEs: endogenous (formed within the body) and exogenous (formed in food that is consumed).

Endogenous AGEs form in the body as a result of high blood glucose, i.e., glycation. When exposed to any blood glucose level of 100 mg/dl or greater, some measure of glycation will develop due to a reaction between glucose and various proteins, e.g., proteins in the lens of the eye, forming cataracts over time.

Exogenous AGEs form in food, generally as a result of heating to high-temperature. (AGEs is really a catch-all term; there are actually a number of reactions that occur in foods, not all of them involving sugars. However, the "AGE" label is used to signify all the various related compounds. The values quoted here are from Dr. Helen Vlassara's Mt. Sinai Hospital laboratory; reference below.)

Beef cooked to high-temperature yields plentiful AGEs. One gram of roast beef, for instance, contains 306,238 units. This means that an 8-oz serving yields 13.8 million units AGEs. Compare this to a boiled egg with 573 units per gram, raw tomato with 234 units per gram.

Butter contains an impressive 264,873 units AGEs per gram, the highest content per gram in the entire list of 250 foods tested in the Mt. Sinai study. A couple pats of butter (10 g) therefore contains 2.64 million units. A stick of butter that you might add to cake batter to make a cake therefore yields 30 million units of AGEs.

So there's nothing wrong with the fat of butter. It's AGEs that appear to be responsible for the endothelial dysfunction/artery-constricting, insulin-blocking, oxidation and inflammation reactions that are triggered. Among all of our food choices, butter is among the worst from this viewpoint.

Throw in the peculiar "insulinotrophic" effect of butter, and you have potent distortion of metabolic pathways, courtesy of the butter on your lobster.

(AGE data from Goldberg 2004. In this analysis, carboxymethyllysine was the marker used for AGE content.)

Incidentally, the new Track Your Plaque diet will soon be released as chapter 9 of the new Track Your Plaque book on the website.

Einkorn now in Whole Foods

16. October 2010 William Davis (19)

I just saw this at Whole Foods: einkorn pasta.

In my einkorn bread experience (In search of wheat: We bake einkorn bread), I was spared the high blood glucose and neurologic and gastrointestinal effects of conventional whole wheat grain (dwarf Triticum aestivum). I shared the einkorn bread with four other people with histories of acute wheat sensitivities, only one of whom experienced a mild diffuse joint reaction, the other three not experiencing any symptoms.

Anyone wishing to try einkorn can now obtain commercial pasta from Jovial, an Italy-based manufacturer. It comes in spaghetti, linguine, rigatoni, fusilli, and penne rigate shapes.

Eli Rogosa, founder of The Heritage Wheat Conservancy, tells me that, in her experience, celiac suffers seem to not experience immunologic phenomena triggered by conventional wheat.

However, we've got to be careful here. The so-called ("diploid") "A" genome of einkorn shares many of the same genes as the ("hexaploid") "ABD" genomes of modern wheat, including overlap in the sequences coding for the 50-or so different glutens and glutenins. Most of the genes that code for the glutens that cause celiac and related illnesses reside in the "D" genome that are absent in the einkorn "A" genome. However, the "A" genome still codes for glutens. So there is potential for activating celiac disease in some people. Insufficient research has been devoted to this question. It is a question of extreme importance to people with celiac and other immune-mediated conditions, since re-exposure to the wrong form of gluten can increase risk of intestinal lymphoma 77-fold, as well as risk of other gastrointestinal cancers.

So einkorn should not be viewed as a cure-all for all things wheat, but as something to consider for a carbohydrate indulgence. Yes, indeed: It is a carbohydrate, with 61 grams ("net") carbs per 4 oz (uncooked) serving.

Should anyone give it a try, please be sure to report back your experience, especially if you have a history of wheat intolerance. If you have a glucose meter, pre- and 1-hour post values are the ones to measure to gauge the blood sugar effects of consumption. Because pasta tends to cause long sustained blood sugar rises, another value at 2-4 hours might be interesting.

Noodles without the headaches

14. October 2010 William Davis (26)

If you are looking for a wheat-free noodle or pasta, shirataki noodles are worth a try.

Shirataki noodles are low-carbohydrate (less than 3 g per 8 oz package) and, of course, do not trigger all the unhealthy effects of wheat--no blood sugar/insulin provocation, no addictive brain effects (exorphins), no gluten-mediated inflammatory effects.

(I advise avoiding gluten-free pasta alternatives made with rice flour and other common gluten alternatives, since they trigger blood sugar, small LDL, and growth of visceral fat just like wheat.)

I made a stir-fry using the shirataki-tofu noodles, shown below. (Tofu is added to make the noodles more noodly in consistency, as opposed to the chewier non-tofu variety.) The noodles were a lot like the ramen I used to eat as a kid. They were filling and tasted great in the sesame oil, soy sauce, tofu, and vegetables I used.

The noodles are easy to use. Just drain liquid out of package. (The noodles come in water.) Rinse in collander 30 seconds, then boil for 3 minutes. Add to your stir-fry or other dish. Some manufacturers, such as House Foods, also have angel hair and fettucine style noodles.

You're fried

13. October 2010 William Davis (26)

If I could invent a food that illustrates nearly all of the shortcomings of the American diet, it would be French fries, the familiar fixture of fast food.

What we have come to view as French fries contain just about every one of the unhealthy ingredients that lead us down the path of obesity, diabetes, heart disease, high blood pressure, etc.

Let's take them one by one:

Potato starch--Potato starch exerts an effect on blood sugar similar to that of table sugar, only worse. (Glycemic index french fries 75; glycemic index sucrose 65.)

Advanced Glycation End-products (AGEs)--AGEs form when proteins and fats are subjected to high temperature cooking; the longer the high temperature, the more the food reaction creating AGEs proceeds. AGEs are the likely culprit in roasted and fried foods that made it appear that saturated fats were bad, when it was really AGEs all along. AGEs have been shown to block insulin's effects, increase blood sugar, cause endothelial dysfunction and high blood pressure.

Acrylamides--Acrylamides, like AGEs, are created through high-temperature heating. French fries are unusually rich in AGEs. Brewed coffee also contains a small quantity, while French fries contain 82-fold greater quantities, among the highest of all known sources of acrylamides.

Oxidized oils--The amount of oxidized oils will depend on what sort of oil was used for frying. As more restaurants are trying to get away from hydrogenated oils, many are turning back to polyunsaturates. Others are turning to commercial-grade oils that contain both hydrogenated and polyunsaturates. If oils are permitted to oxidize, then they will trigger oxidative phenomena in your body upon consumptions, e.g., LDL oxidation (Staprans 1994).

In other words, the innocent appearing French fry unavoidably triggers oxidation, all the phenomena triggered by high blood glucose (high insulin, glycation, visceral fat accumulation), along with the cascade of effects arising from AGEs and acrylamides.

Top your French fries with some ketchup made with high-fructose corn syrup that exagerrates AGE formation, visceral fat, and distorts postprandial (after-eating) effects.

Is it any wonder that we've lost control over diet?

Bosom buddies

9. October 2010 William Davis (22)

Male breast reduction surgery is a booming business. While most industries are in a downward tailspin, breast reduction surgery in men is growing at double-digit rates.

Other efforts, some legitimate, some not, are also cropping up, all intended to help men deal with this embarassing problem:

Exercise programs to reduce male breast size.

Liposuction--Not just for the belly!

Plastic surgery

Gynexin--a supplement that purportedly reduces male breast size.

Conventional medical treatment also includes estrogen blocking drugs, the same ones used to treat breast cancer, drugs like tamoxifen. There's even clothing intended to make breasts less obvious.

While male breast enlargement--"gynecomastia"--can occasionally occur due to rare endocrinologic problems, such as high prolactin hormone levels (hyperprolactinemia) or somewhat more commonly as failed testosterone production (hypogonadism), the vast majority of men who suffer with this problem simply have high estrogen levels.

Makes sense: Women develop larger breasts during development mostly due to increased levels of estrogen. A parallel situation in men likewise stimulates breast tissue.

So where does the excess estrogen come from?

Visceral fat converts testosterone to estrogen. Men with excess visceral fat therefore develop low levels of testosterone and high levels of estrogen. Estrogen levels can, in fact, be substantially higher compared to slender males.

So what foods cause the accumulation of visceral fat and, thereby, increased estrogen and decreased testosterone?

Foods that increase blood glucose and insulin to the greatest degree are the foods that begin this cascade. The common foods that increase blood sugar the most? Here's a list, starting with most blood glucose-insulin provoke at the top, least at the bottom:

Gluten-free foods (dried, pulverized cornstarch, rice starch, potato starch, tapioca starch)
Whole wheat bread
Sucrose
Milky Way bars
Snickers bars

So the whole wheat sandwiches you've been eating increase blood sugar and insulin, leading to visceral fat. (And, yes, whole wheat bread increases blood sugar higher than Milky Way bars and Snickers bars.) The more visceral fat grows, the more resistant to the effects of insulin you become, further escalating blood sugar. Estrogen increases, testosterone drops, mammary gland tissue grows, normal male breasts grow to B- or C-cup size.

Yet again, an entire industry is growing from the unintended consequence of conventional advice. In this instance, the advice to "eat more healthy whole grains" leads to this booming industry of male breast reduction efforts from surgery to medications to clothing. The REAL solution: Eliminate the foods that start the process in the first place.

Don't be a dipstick

3. October 2010 William Davis (32)

If I want to know how much oil is in my car's engine, I check the dipstick.

The dipstick provides a gauge of the amount of oil in my engine. If the dipstick registers "full" because there an oil mark at one inch, I understand that there's more than one inch of oil in my engine. The dipstick provides an indirect gauge of the amount of oil in my engine.

That's what cholesterol was meant to provide: A gauge, a "dipstick," for the kind of lipoproteins (lipid-carrying proteins) in the bloodstream.

Lipoproteins are a collection of particles that are larger than a single cholesterol molecule but much smaller than a red blood cell. Lipoproteins consist of many components: various proteins, phospholipids, lots of triglycerides, as well as cholesterol. In the 1960s, methods to characterize lipoproteins were not widely available, so the cholesterol in lipoproteins were used as a "dipstick" to assess low-density lipoproteins ("LDL cholesterol") and high-density lipoproteins ("HDL cholesterol"). (Actually, even "LDL cholesterol" was not measured, but was derived from "total cholesterol," the quantity of cholesterol in all lipoprotein fractions.)

Some other component of lipoproteins could have been measured instead of cholesterol, such as apoprotein B, apoprotein C, or others, all meant to act as the "dipstick" for various lipoproteins.

Relying on cholesterol to characterize lipoproteins provides a misleading picture. Imagine watching cars go by at high speed while standing on the side of the highway. You want to count how many people--not cars, but people--go by in a given amount of time. Because you cannot make out the detail of each and every car whizzing by, you count the number of cars and assume that each car carries two people. Whether it's rush hour, Sunday morning, late evening, rainy, sunny, or snowing, you make the same assumption: two people per car.

That's what cholesterol does: It is assuming that each and every lipoprotein particle (car) carries the same amount of cholesterol (people).

But that may, obviously, not be true. A bus goes by carrying 25 people. Plenty of cars may carry just the driver. People carpooling may be in cars carrying 3 or 4 people. Assuming just 2 people per car can send your estimates way off course.

That is precisely what happens when your doctor tries to use conventional cholesterol values (total cholesterol, LDL cholesterol) to gauge the lipoproteins in your bloodstream. Measuring cholesterol can also provide the false impression that cholesterol is the cause of heart disease, even though it was originally meant to simply serve as a "dipstick."

What we need to do is to characterize lipoproteins themselves. We can distinguish them by size, number, density, charge, and the type and form of proteins contained within. It provides greater insight into the composition of lipoproteins in the blood. It provides greater insight into the causes underlying coronary atherosclerotic plaque. It can also tell us what dietary changes trigger different particle patterns and how to correct them.

Until you have a full lipoprotein analysis, you can never know for certain 1) if you will have heart disease in your future, or 2) how your heart disease was caused.

Unfortunately, the vast majority of doctors are perfectly content to just count cars going by and assume two people per car, i.e., confine assessment of your heart disease risk using cholesterol . . . just as drug industry marketing has instructed them.

It's not your job to educate your doctor. If he or she refuses to provide access to lipoprotein testing to better determine your heart disease risk, then consider going out on your own. Many of our Track Your Plaque program followers have obtained lipoprotein testing on their own through Direct Labs.

The ultimate insurance company cost savings

29. September 2010 William Davis (48)

I had a very disturbing conversation with a physician who is employed by an insurance company last week.

I admitted a patient in the hospital for very clear-cut reasons. She is one of my few non-compliant patients, doing none of the strategies I advocate--no fish oil, no vitamin D, no correction of her substantial lipoprotein abnormalities, not even medication. Much of this was because of difficult finances, some of it is because she is from the generation (she is in her late 70s) that tends to ignore preventive health, some of it is because she is a kind of happy-go-lucky personality. So her disease has been progressive and, now, life-threatening, including an abdominal aneurysm near-bursting in size (well above the 5.5 cm cutoff). The patient is also a sweet, cuddly grandmother. I have a hard time bullying nice little old ladies.

While she was in the hospital, the social worker told me that her case was being reviewed by her insurer and would likely be denied. Their medical officer wanted to speak to me.

So the medical officer called me and started asking pointed questions. "Why did you do that test? You know that she's not been compliant. Are you sure you want to do that? I don't think that's a good idea." In other words, this was not just a review of the case. This was an opportunity for the insurance company to intervene in the actual care of the patient.

Then the kicker: "Have you considered not doing anything and . . . just letting nature take its course?"

At first, I was stunned. "You mean let the patient die?"

Expressed in such blatant terms, while he was trying to be diplomatic, made him back down. "Well, uh, no, but she is a high-risk patient."

Anyway, this was the first instance I've encountered in which the insurance company is not just in the business of reviewing a case, but actually trying to intervene during the hospital stay, to the point of making the ultimate healthcare cost savings: Letting the patient die.

Unfortunately, never having had an experience like this before, I did not think to record the conversation or take notes. I am wondering if this is an issue to be taken up by the Insurance Board . . . or is this a taste of things to come as the health insurers fall under increasing pressure with the legislative changes underway?

Salvation from halogenation

24. September 2010 William Davis (26)

Iodine is a halogen.

On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior.

Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.

Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.

What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland.

While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products, has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)

We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides.

Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.

I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.

Lipitor-ologist

22. September 2010 William Davis (30)

One of the things I do in practice is consult in complex hyperlipidemias, the collection of lipoprotein disorders that usually, but not always, lead to atherosclerosis.

First order of business: Make the diagnosis--familial combined hyperlipidemia, hypoalphalipoproteinemia, lipoprotein(a), familial heterozygous hypercholesterolemia, familial hypertriglyceridemia, hyperapoprotein B with metabolic syndrome, etc. These are the disorders that start with a genetic variant, e.g., a missing or dysfunctional enzyme or signal protein, such as lipoprotein lipase or apo C3.

I then ask: What can be done that is easy and safe and preferably related to diet and lifestyle?

By following an effective diet, many of these abnormalities can be dramatically corrected, sometimes completely. Familial hypertriglyceridemia, for instance, an inherited disorder of lipoprotein lipase in which triglyceride levels can exceed 1000 mg/dl, high enough to cause pancreatic damage, responds incredibly well to carbohydrate restriction and over-the-counter fish oil. I have a number of these people who enjoy triglyceride levels below 100 mg/dl--unheard of in conventionally treated people with this disorder.

Then why is it that, time after time, I see these people in consult, often as second or third opinions from lipidologists (presumed lipid specialists) or cardiologists, when the only solutions offered are 1) Lipitor or other statin drug, and 2) a low-fat diet? Occasionally, an aggressive lipidologist might offer niacin, a fibrate drug (Tricor or fenofibrate), or Lovaza (prescription fish oil).

Sadly, the world of lipid disorders has been reduced to prescribing a statin drug and little else, 9 times out of 10.

I don't mean to rant, but I continue to be shocked at the incredible influence the drug industry has over not just prescribing patterns, but thinking patterns. Perhaps I should say non-thinking patterns. The drugs make it too easy to feel like the doctor is doing something when, in truth, they are doing the minimum (at best) and missing an opportunity to provide true health-empowering advice that is far more likely to yield maximum control over these patterns with little to no medication.

All in all, I am grateful that there is a growing discipline of "lipidology," a specialty devoted to diagnosing and treating hyperlipidemias. Unfortunately, much of the education of the lipidologist is too heavily influenced by the pharmaceutical industry. Not surprisingly, the drug people favor "education" that highlights their high-revenue products.

Seeing a lipidologist is still better than seeing most primary care physicians or cardiologists. Just beware that you might be walking into the hands of someone who is simply the unwitting puppet of the pharmaceutical industry.

Robb Wolf's new Paleo Solution

20. September 2010 William Davis (16)

The Paleo Solution: The Original Human Diet

I have to say: I'm impressed. If you would like insight into why a "Paleo" nutritional approach works on a biochemical level--why you lose weight, burn fat, and gain overall better health--then Robb's book is worth devoting a few hours to, of not a reread or two.

Robb has a particular knack for organizing and presenting information in a way that makes it immediately accessible. You will gain an appreciation for how far American nutritional habits have veered off course.

Because Robb brings expertise from his academic biochemistry background, as well as personal trainer and educator running a successful gym in northern California, NorCal Strength and Conditioning, he delivers a book packed with information that is extremely easy to convert to immediate action in health and exercise. He seems to anticipate all the little problems and objections that people come up with along the way, dealing with them in his characteristic lighthearted way, providing practical, rational solutions.

Robb's book nicely complements what Dr. Loren Cordain has written in his The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat and The Paleo Diet for Athletes: A Nutritional Formula for Peak Athletic Performance. (My wife is now reading The Paleo Diet for Athletes and loves it. I'm going to add Robb's book to her reading list for her to read next.)

If nutrition has you stumped, if the USDA food pyramid still sounds like a reasonable path, or if you just would like to understand nutrition a little bitter, especially its biochemical ins and outs, Robb's book is a wonderful place to start.

All posts by william-davis

Why healthy can make us fat

13. سبتمبر 2007 William Davis (0)

Brian Wansink, author of Mindless Eating: Why we eat more than we think (see yesterday's Heart Scan Blog post), also has a Blog. Despite the bland advice offered on much of the Prevention Magazine and website, Wansink's Food Think Blog is a winner.

In a recent post, Wansink quotes a report from Science Daily that described a study he recently published in the Journal of Consumer Research. Wansink's study describes how just applying the label "healthy" to fast food choices increased consumers' calorie intake:

"When we see a fast-food restaurant like Subway advertising its low-calorie sandwiches, we think, 'It's OK: I can eat a sandwich there and then have a high-calorie dessert,' when, in fact, some Subway sandwiches contain more calories than a Big Mac."

In one study, Chandon and Wansink had consumers guess how many calories are in sandwiches from two restaurants. They estimated that sandwiches contain 35% fewer calories when they come from restaurants claiming to be healthy than when they are from restaurants not making this claim.

The result of this calorie underestimation? Consumers then chose beverages, side dishes, and desserts containing up to 131% more calories when the main course was positioned as "healthy" compared to when it was not--even though, in the study, the "healthy" main course already contained 50% more calories than the "unhealthy" one.

"These studies help explain why the success of fast-food restaurants serving lower-calorie foods has not led to the expected reduction in total calorie intake and in obesity rates," the authors write.

Interesting. In fact, I've had many patients say that they eat at Subway or similar chains and choose the "healthy" options. "That's got to be better than a cheeseburger and fries!" Perhaps not. (Of course, you can't leave Subway or other fast food operation feasting on wheat products.)

Wansink can be counted on for some truly fascinating observations into many behaviors that are subconscious but explain at least part of the reason why we're so fat. Though his Blog has a relatively short history of posts, there's lots of great commentary.

Pierre Chandon and Brian Wansink. "The Biasing Health Halos of Fast Food Restaurant Health Claims: Lower Calorie Estimates and Higher Side-Dish Consumption Intentions" Journal of Consumer Research, October 2007.

Outsmarting the enemy

12. سبتمبر 2007 William Davis (2)

"Everyone--every single one of us--eats how much we eat largely because of what's around us. We overeat not because of hunger but because of family and friends, packages and plates, names and numbers, labels and lights, colors and candles, shapes and smells, distractions and distances, cupboards and containers. This list is almost as endless as it's invisible.

Invisible?

Most of us are blissfully unaware of what influences how much we eat . . . We all think we're too smart to be tricked by packages, lighting, or plates. We might acknowledge that others could be tricked, but not us. That is what makes mindless eating so dangerous. We are almost never aware that it is happening to us."

So opens Brian Wansink's book, Mindless Eating: Why we eat more than we think.

Wansink studies consumer behavior at Cornell University. He's the guy who scrutinizes in excruciating detail why we eat what we do, what factors determine what we eat like food color and smell, the company we keep, product packaging. He works without food industry funding, though there are plenty of researchers who do this sort of research funded by the likes of Kraft, Nabisco, and Kellogg's.

His book is packed full of the conclusions he and his team have come to over the years studying our buying and eating habits. While this information could (and is) be easily used by the food industry to coerce us to eat more and more, understanding many of the concepts Wansink talks about can also open your eyes to their clever tactics.

He especially details how our internal satiety signals fail us when external cues are present that easily trip us up. He talks about one experiment he ran in which soup bowls were rigged with concealed rubber tubes in the bottom that continually replenished the soup as the person consumed it. Thus, with the bowl continually refilled, the eater had no idea how much he or she had consumed. When the quantity of soup eaten from the endless bowl was compared to people eating from standard bowls, there was as much as a three-fold increase in the quantity and calories eaten.

Just be aware that, while Wansink is an expert in consumer eating behavior, he is not necessarily an expert in nutrition. Just as a card shark can show you lots of clever tricks to hoodwink your opponent, he might not be the best person to teach you how to play bridge.

For a great hint at some of the interesting and all-too-human observations Wansink makes, the online Prevention Magazine posted a brief video:

http://link.brightcove.com/services/link/bcpid1155399889/bclid1171884988/bctid1113465050

We might not be able to stop Big Food from selling garbage foods, but we can at least be armed with insight into how we are subconsciously coerced into eating more.

Test Of Scanner Saves A Doctor's Life

11. سبتمبر 2007 William Davis (5)

Read the story online at http://www.courant.com/news/health/hc-luckydoc.artsep10,0,7572510.story?coll=hc_features_promo

I personally hate these stories, the ones that turn heart scans into drama by describing how someone had a heart scan, then turned out to have so much coronary plaque that they had to have bypass surgery.

But I point this one out because the story is related in an interesting way. It highlights the utter ignorance that operates in heart disease detection.

The story highlights how a 50-year-old, 5 ft 8, 150 lb slender, exercising neurologist underwent a CT coronary angiogram in a newly installed device in a Hartford, Connecticut hospital (not a heart scan) that detected entirely unsuspected severe and diffuse coronary disease. You know the rest: abnormal stress test, heart catheterization, bypass surgery of the hapless doctor-now-patient, followed by grateful patient saying things like "This machine saved my life."

It probably is true. You've seen these stories before. I've witnessed these sorts of headline-makers for the past decade. I remain surprised that it still happens.

The doctor is not some ignorant, uninformed man who can't even fill out his income tax forms. Yet how does a man like this walk around with life-threatening disease and not know it? Why does it still make headlines?

Anyway, despite all my jawing about heart scans and early heart disease detection, many physicians and the public remain in the stone age of heart disease. Even though this neurologist's story made headlines, the many other people who 1) identified their heart disease earlier with a simple heart scan, then 2) took action to put a stop to it, do not make headlines. But that's the way to go.

Why isn't the rest of the story being told? Why was this man's heart disease uncovered only in its late phases? Hartford, Connecticut is not some backwater. I've been there. It's a major city with large hospitals and a University Medical Center. But a professional with presumed knowledge of health and his doctor(s) allowed this to happen?

In other words, this is not a story of success, but of failure--failure to identify coronary disease years earlier when preventive action would have prevented bypass. But that's not such a compelling headline, is it?

As an aside, I'll bet you that this man has lipoprotein(a), a severe small LDL pattern, and severe deficiency of vitamin D. Correct these and it's unlikely he'll need bypass again. But that's kind of boring, isn't it?

The great food industry deception

8. سبتمبر 2007 William Davis (1)

I'd forgotten what a powerful report Peter Jennings and ABC News produced about the enormous deception perpetrated by the food industry and its effects on health until Dr. Joe Mercola posted the YouTube clips from the report on Mercola.com.

(This is not meant to be an endorsement of everything Dr. Mercola has to say. He says lots of things; I agree with only a fraction of it. But this is a gem.)

Although made in 2004, the report remains every bit as relevant today as it was then. It concerns me deeply that, despite reports like this being broadcast to Americans, the obesity epidemic continues unabated. In fact, it's worse just in the short three years since then.

Be aware of what the food industry is up to. They intensively market high profit margin foods to us--and especially our children--to increase sales. As Jennings points out, the U.S. government (USDA) is, for a variety of reasons both good and bad, complicit with this massive deception. While many media reports continue to focus on lack of exercise as the root cause for the obesity epidemic, it is really the active and purposeful selling of processed junk foods to Americans that is principally to blame.

By the way, how many of these foods proudly boast the American Heart Association Check Mark of approval?

Part 1

Part 2

Part 3

Part 4

Part 5

Dr. Joseph Prendergast and l-arginine

7. سبتمبر 2007 William Davis (21)

In response to a discussion started by Track Your Plaque Member, Rich, on the Member Forum, I tracked down Dr. Joseph Prendergast, who had posted a video on his unique experiences, both personal and professional, with l-arginine.

Dr. Prendergast describes some of this in a brief webcast. Here, I quote Rich:

“This 90-second video by a Palo Alto physician (internal/endocrine, diabetes specialist) will totally blow your mind.

http://enews.endocrinemetabolic.com/2007/08/16-12-years.html

You will see in the link below that he reversed his personal atherosclerotic disease, diagnosed in abdominal aorta at age 37—completely reversed. He's now much older."

http://www.endocrinemetabolic.com/about/press/larginine.pdf

I contacted Dr. Prendergast to find out more.

Dr. Joseph Predergast is founder of the Endocrine Metabolic Medical Center in Palo Alto, California, focused on providing care for people with diabetes. In addition to the website, he provides Blogs and newsletters, though most of his conversation is about diabetes issues. Dr. Predergast’s website is located at http://www.endocrinemetabolic.com.

I asked Dr. Prendergast several questions about his l-arginine experience. His brief answers are below.

1) What dose of l-arginine have you employed in your patients and why this dose?

The dose is 3 - 6 grams as suggested by the Stanford Cardiovascular Research Department Chairman John Cooke. http://med.stanford.edu/profiles/John_Cooke/

2) I gather that you have preference for specific preparations of l-arginine. Can you say why some preparations seem superior to others in your experience?

I started with pharmaceutical l-arginine from the pharmacy. I gradually began to add components that would augment the power of the l-arginine and have gone through 12–15 different products. I have completely reversed my own very severe atherosclerosis discovered at age 37 and there has been less than 0.05% cardiovascular disease in my endocrine practice in almost 17 years. Both my exams were evaluated with CT technology. I am now using ProArgi9 Plus that includes several anti-aging components and will likely never switch. http://www.synergyworldwide.com/synergycorp/home.aspx

3) Are you employing any other unique practices in your patients to reduce cardiovascular events?

Withdrawing as many prescription drugs as possible.

Interesting. Of course, I also advocate l-arginine as a facilitator of atherosclerotic plaque regression, though I am not as ebullient about its use as Dr. Prendergast.

Instead, I see l-arginine as a method that yields forced normalization of “endothelial dysfunction,” the abnormal constriction and other effects that develop when abnormal lipoproteins and unhealthy food by-products are present in the circulation. Endothelial dysfunction is an inevitable accompaniment of plaque.

However, unlike Dr. Predergast’s experience, despite our use of doses higher than he uses, I have never seen plaque regression just using l-arginine alone. Nonetheless, it’s good to hear that others are seeing at least some positive effects.

By the way, we have also had some positive posts on our Forum about the ProArgi9 product he uses.

Dr. Dwight Lundell on omega-3s and CLA

7. سبتمبر 2007 William Davis (15)

An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."

Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.

You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.

Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.

In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety?this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness?also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.

I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.

Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!

More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.

Note: We are planning a full Special Report on CLA for the Track Your Plaque website in future.

High-tech heart attack proofing

5. سبتمبر 2007 William Davis (7)

I was reminiscing the other day about what I was taught about heart disease in medical school some 20 years ago.

In the 1980s, the world was still (and remains) fascinated with this (then) novel "solution" to heart disease called coronary bypass surgery. As medical students, we all fought for a chance to watch a bypass operation being performed. And there was lots of opportunity. I was a medical student at St. Louis University School of Medicine, a center that boasted of a busy thoracic surgery service, performing up to 10 bypass operations every day.

Back then, coronary angioplasty was just a twinkle in Andreas Gruentzig's eye, still contemplating whether it was possible to put an inflatable device in the blockages of coronary arteries to re-establish blood flow. Risk detection for heart disease consisted of EKGs, screening for symptoms, detection of heart failure, and tests that are long forgotten in the dust bin of medical curiosities, tests like systolic-time intervals, phonocardiography (using amplified sound to detect abnormal heart sounds), and detailed physical examination. Treatment for heart attack involved nitroglycerin and extended bedrest. Bypass surgery would come after you recovered.

In other words, NONE of the tools we now use in the Track Your Plaque program for heart disease control and reversal were available just twenty years ago. There was no lipoprotein testing, no CT heart scans. Nobody recognized the power of omega-3 fatty acids (although epidemiologic observations were just beginning to suggest that eating fish might be the source of reduced risk for heart attack and cardiovascular death). Vitamin D? Why, that's in your milk so your babies don't get rickets.

So much of what we do today was not available then, nor were they even in the crystal ball of forward-looking people. I certainly had no idea whatsoever that I'd be talking and obsessing today about reversal of heart disease based on what I saw and learned back then.

Things have certainly come a long way and all for the better. The problem is that much of the world is stuck in 1985 and haven't yet heard that coronary disease is a manageable and reversible process. They've been sidetracked by the fiction propagated by the likes of Dr. Dean Ornish, the nonsense of low-fat diets aided and abetted by the food manufacturing industry and the USDA, the extravagant claims of some practitioners and the supplement industry. They haven't yet stumbled on the real-life experiences that are chronicled here in this Blog and the accompanying Track Your Plaque website.

Our program has been criticized for being too "high-tech," involving too many sophisticated measures like small LDL, lipoprotein(a) treatment, vitamin D blood levels. But when you see a woman reduce her heart scan score 63%, or a school principal's score plummet 51%, then that's reward in itself.

It's all about plaque

5. سبتمبر 2007 William Davis

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

Taken at face value, this study would argue that:

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

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

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

Omega-6 / omega-3 ratio

7. August 2008 William Davis (11)

Most of us already know that the intake of omega-6 fatty acids in the American diet has gone overboard, much at the expense of the omega-3 fraction. This occurred as a result of the misguided advice of the 1970s and 1980s to eat polyunsaturated oils like corn, sunflower, and safflower, because of their presumed cholesterol-reducing properties compared to saturated fats. However, more recent examinations of this advice have suggested that the omega-6 fraction of oils present in polyunsaturated oils may amplify arachidonic acid and other inflammatory patterns despite the reduction in cholesterol (total and LDL).

Dr. Artemis Simopoulos of the Center for Genetics, Nutrition and Health in Washington, D.C. has written extensively on the role of omega-6 and omega-3 fatty acids in diet.

In a review entitled The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cadiovacular Disease and Other Chronic Disease , Dr. Simopoulos collects the following comparison of omega-6 to omega-3 ratios from various populations:

Paleolithic humans 0.79
Greece (prior to 1960) 1.00-2.00
Current Japan 4.00
Current India, rural 5-6.1
Current United Kindom and northern Europe 15.00
Current United States 16.74
Current India, urban 38-50

(The numbers refer to the ratio of omega-6 to omega-3 intake.)

If we believe the observations of Dr. Loren Cordain and others, while paleolithic man died of trauma and infectious diseases, they did not die of heart disease. Paleolithic human intake of omega-3 exceeded that of omega-6.

Likewise, the traditionally low cardiac event regions of the world like Japan and Greece have less omega-3 intake than Paleolithic man, but still many times more than the U.S. and U.K.

Worst of all with an enormous preponderance of omega-6 over omega-3 are urban Indians, who experience among the highest rates of heart disease in the world.

Just for perspective, let's assume you eat an 1800 calorie per day diet, of which 30% of calories come from fat. This would amount to 540 calories per day from fat. With 9 calories per gram of fat, this means that there are 60 grams, or 60,000 mg, of fat in your diet per day.

Paleolithic man has been found to have existed on a diet consisting of 21% of calories from fats. Again assuming an 1800 calorie per day diet, that comes to 42 grams of fat per day (42,000 mg).

If we were to try to recreate the Paleolithic fat composition of diet, we would ingest 21,000 mg of omega-3 fatty acids (EPA, DHA, linolenic acid) per day. Even recreating a Japanese experience with a 4:1 ratio, it would mean 8400 mg of omega-3 per day. (Curiously, this does not agree with all estimates of Japanese intake of omega-3s.)

No matter how you look at it, cultures with lower rates of cardiovascular disease take in greater--much greater--quantities of omega-3 fatty acids.

So don't complain about your six fish oil capsules (usually containing 6000 mg of total oil, 1800 mg omega-3s)!

Dr. Bernadine Healy on heart scans

5. August 2008 William Davis (1)

A Heart Scan Blog reader brought the following tidbit to my attention.

Cardiologist and now writer for U.S. News and World Report, Dr. Bernadine Healy, wrote this editorial, a glowing endorsement of heart scans:

The approach is beautifully simple. Calcium accumulates in advanced plaques, so calcium visible in the heart's arteries indicates atherosclerosis. An exploding number of studies in the past few years have unequivocally shown that the calcium score predicts both heart attack and sudden death. As a generalization, patients with scores between 100 and 400 face three to four times the risk of a heart attack or death compared with others at the same age with a zero score. Over 400, that elevated risk more than doubles.

Most doctors rely instead on the Framingham calculator, which estimates a symptom-free person's risk of a heart attack in the next 10 years based on smoking history, blood pressure, cholesterol levels, sex, and age. It's available free online from the National Institutes of Health. Most people taking the test will have minimal or no coronary disease, though risk estimates over 9 percent should inspire vigorous preventive efforts. For some, however, coronary heart disease is sneaky, and Framingham will underestimate what lies ahead. Roughly half of those who suffer a major heart attack or sudden coronary death are symptom free. Calcium scores are additive to Framingham; they pick up the individual surprises by using X-ray vision to look inside the heart. No wonder insurance companies are scrambling to use coronary calcium scores—life insurers, that is.

Dr. Bernadine Healy is no small-time player. In addition to her academic credentials, she is former chief of the National Institutes of Health (the first woman to hold the influential post), former head of the American Red Cross, and former deputy director of the White House Office of Science and Technology Policy under the Reagan administration. An endorsement of CT heart scans, though written under the guise of a probing editorial, will do an enormous amount of good to overcome the hurdles in gaining wider acceptance of heart scans.

Those of us applying heart scans in everyday practice have long appreciated their enormous power to detect and track coronary plaque. Framingham scoring can't even touch the certainty and quantification provided by heart scans in day-to-day life. Hundreds of studies have validated their use, but they still suffer from lying in the shadows of the procedural bullies aiming to boost the number of heart catheterizations, angioplasties, stents, bypass surgeries.

Dr. Healy, a voice with great weight, not just a political figure but also a cardiologist and scientist, has done a great service to broadcast the message of heart scanning.

Mercury and fish oil

2. August 2008 William Davis (9)

As time passes, the dose of fish oil advocated in the Track Your Plaque program is going upward.

While epidemiologic studies, like the Chicago Western Electric Study and the Nurses' Health Study suggest that decreases in mortality from heart disease begin by just eating fish a couple times per month, there are newer data that suggest greater quantities confer greater benefits.

In the last Heart Scan Blog post, I discussed the recently-released ERA JUMP Study that demonstrated a relationship between higher omega-3 fatty acid blood content and reduced quantities of carotid and coronary plaque. The JELIS Study demonstrated a 19% reduction in cardiovascular events when fish-consuming Japanese added 1800 mg of EPA (only).

However, the suggestion that increased quantities of fish oil potentially yield greater protection from heart attack and facilitate coronary plaque regression is also stirring up worries about mercury exposure. So I dug up a Heart Scan Blog post from a year ago that discussed this issue and reprint it here.

I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor [now Lovaza], or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.

I am not advocating ad libitum eating of fish. Sadly, this may be related to excessive accumulation of contaminants. I am suggesting that greater quantities of omega-3 fatty acids from relatively contaminant- and mercury-free fish oil capsules.

More on this in an upcoming webinar on the Track Your Plaque website: Fish Oil and the Track Your Plaque Program - Is More Better?

ERA JUMP: Omega-3 fatty acids and plaque

1. August 2008 William Davis (5)

The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Mediterranean diet and blood sugar

31. July 2008 William Davis (6)

Data such as that from the Lyon Heart Study have demonstrated that a so-called Mediterranean diet substantially reduces risk for heart attack.

But there are aspects of the Mediterranean diet and lifestyle that are not entirely sorted out.

For instance, what specific component(s) of the diet provide the benefit? Is it olive oil and linolenic acid? Is it red wine? Is it the reduced exposure to processed snack foods that Americans are indundated with? Is it their more slender builds and greater tendency to walk? How about exposure to the Mediterranean sun? What about the inclusion of breads, since in the Track Your Plaque program I advocate elimination of wheat products for many abnormalities?

Anyway, here's a wonderfully thoughtful set of observations from Anna about her experiences traveling Italy, trying to understand the details of the Mediterranean diet while also trying to keep blood sugar under control.

I just returned from a two week stay in Italy, doing a bit of my own "Mediterranean Diet" experiments. When practical, we sought out food sources and places to eat that were typical for the local area, and tried as much as possible/practical to stay away from establishments that mostly catered to tourist tastes. I was really curious to see how the mythical "Mediterranean Diet" we Americans are urged to follow compared to the foods really consumed in Italy.

The first week, we stayed in a rural Tuscan farmhouse apartment (agriturismo), so many, if not most of our meals were prepared by me with ingredients I bought at the local grocery store (Coop) or the outdoor market in Siena. In addition, I purchased really fantastic free-range eggs from the farm where we were staying. (Between some language issues and seasonality, eggs and wine were what we could buy from them - though I was tantalized by the not-quite-ripe figs heavy on many trees). Mostly, our meals consisted of simple and easily prepared fresh fruits and vegetables, rustic cured meats (salami, proscuitto, pancetta, etc.) hand-sliced at the deli down the road, fresh sausages, various Italian cheeses, plus plenty of espresso. It was a bit disappointing to find underripe fruit & tomatoes as well as old green beans in the grocery stores, not to mention too many low fat and highly processed foods, but all over Europe the food supply is becoming more industrialized, more centralized, and homogenous, so I'm not too surprised that it happens even in Italy. But even with the smaller grocery store size, the amount of in-season produce was abundant, yet one still was better off shipping from the perimeter of the store, venturing into the aisles only for spices, olive oil, vinegar, coffee, etc. Without the knowledge of where to go and the language to really talk in depth about food with people, I wasn't able to find truly direct and local sources for as many foods as I would have liked, but still, we ate well enough!

The first week I maintained blood sugar levels very similar to those I get at home, because except for the Italian specialties, we ate much like we always do. A few rare exceptions to my normal BG tests were after indulging in locally made gelato or a evening limoncello cordial, but even then, the BG rise was relatively modest and to me, acceptable under the circumstance. Even with the gelato indulgences, it felt like I might have even lost a few pounds by the end of the first week and my FBG didn't rise much over 100.

The second week we stayed in two cities (Florence & Rome), and I didn't prepare any of my own food because I didn't have a kitchen/fridge. I found it impossible to get eggs anywhere for breakfast, and the tickets our hotels provided for a "continental" breakfast at a nearby café/bar was always for a coffee or hot chocolate drink and some sort of bread or roll (croissant, brioche, danish, etc.). At first I just paid extra for a plate of salami and cheese if that was available - or went to a small grocery store for some plain yogurt, but then I decided to go off low-carb and conduct a short term experiment, though I didn't consume nearly as many carbs as a typical Italian or tourist would.

So I breakfasted with a brioche roll or plain croissant for breakfast with my cappuccino, but unfortunately no additional butter was available. I didn't feel "full" enough with such a breakfast and I was usually starving an hour or two later. Additionally, when I ate the "continental" breakfast, I noticed immediate water retention - my ankles, lower legs, and knees looked like someone else's at the end of a day walking and sightseeing, swollen heavy. Exercising my feet and lower legs while waiting in lines or sitting didn't seem to help.

Food is much more expensive in Europe than in the US, and the declining US$ made everything especially expensive (not to mention the higher cost of dining out rather than cooking at home), so we tried to manage food costs by eating simple lunches at local take-away places, avoiding the corporate fast food chains. I was getting tired of salami/proscuitto & cheese plates, but the typical "quick" option was usually a panini (sandwich). At first I tried to find alternatives to paninis, but the available salads were designed for side dishes, not main meals and rarely had any protein, and the fillings of the expensive sandwiches were too skimpy to just eat without the bread. So I started to eat panini, although I sometimes removed as much as half of the bread (though it was nearly always very excellent quality pan toasted flatbreads or crusty baguette rolls, not sliced America bread). So of course, my post-prandial BGs rose, as did my FBG. I also found my hunger tended to come back much too soon and I think overall I ate more than usual in terms of volume.

Then we deviated from the "Italian" lunch foods and found a better midday meal option (quick, cheaper, and easier to customize for LC) - stopping at one of the numerous kebab shops and ordering a kebab plate with salad, hold the bread (not Italian, but still Mediterranean, I guess). I felt much better fueled on kebab plates (more filling and enough protein) than paninis, though I must say I still appreciated the taste of caprese paninis (slices of fresh mozzerella and tomato, basil leaves, mustard dressing on crusty, pan-toasted flat bread). If I followed my appetite, I could have eaten two caprese paninis.

We had some great evening dinners, at places also frequented by locals. This often was a fixed price dinner of several courses ("we feed you what we want you to eat"). Multi-course meals included house wine, and invariably consisted of antipasta (usually LC, such as a cold meat and cheese plate), pasta course (much smaller servings than typical US pasta dishes), main course plus some side vegetables, and dessert/coffee. These were often the best meals we experienced, full of local flavor and tradition (sometimes with a grandmotherly type doing the cooking), and definitely of very good quality, though we noticed the saltiness overall tended to be on the high side. I ate from every course, including some of the excellent bread (dipped in plenty of olive oil) and usually about half of the pasta served (2 oz dry?), plus about half of the dessert. After these meals I always ran BGs higher than usual, varying from moderately high (120-160 - at home I would consider this very high for me) to very high (over 180). By late in the week, my FBG was into the 115 range every morning (usually I can keep it 90-100 on LC food). Nearly everything that week was delicious, well-prepared food, but the high carb items definitely were not good for my BG control in the long run.

And most days I was doing plenty of walking, sprinting for the Metro subway trains, stair climbing (4th and 5/6th floor hotel rooms!), etc. but since I didn't have my usual housework to do, it probably wasn't too different from my usual exertion level.

So it was very interesting to experience the "Mediterranean Diet" first hand. Meats and cheeses were plentiful, fruits and vegetables played a much more minor role (main courses didn't come with vegetables other than what was in the sauce, but had to be ordered as additional items), but the overall carbs were decidedly too many. As I expected, it wasn't nearly as pasta-heavy as is portrayed in the US media/health press, but it is still full of too much grain and sugar, IMO. Low fat has become the norm in many dairy products, sadly, and if the grocery stores are any indication, modern families are gravitating towards highly processed, industrial foods. Sugar seems to be in everything (I quickly learned to order my caffe freddo con panno or latte sensa zuccero - iced coffee with cream or milk without sugar) after realizing that adding lots of sugar was the norm).

And, after several days of breakfasting at the café near our Rome hotel (where carbs were the only option in the morning), I learned that our very buff, muscular, very flat-stomached, café owner doesn't eat pasta (said as he proudly patted his 6 pack abs). I probably could have stuck closer to the carb intake I know works better for my BG control, but I figured if I was going to go off my LC way of eating and experiment, this was the time and place.

And yes, there were far fewer really obese people than in the US and lots of very slender people, but I could still see there were *plenty* of overweight, probably pre-diabetic and diabetic Italians (very visible problems with lower extremities, ranging from what looked like diabetic skin issues, walking problems, acanthosis nigricans, etc.). Older people do seem to be generally more fit than in the US (fit from everyday life, not exercise regimes), but there were plenty of "wheat bellies" on men old and young, even more young women with "muffin tops", and simply too many overweight children (very worrisome trend). So it may well be more the relaxed Italian way of living life (or a combination of other factors such as less air conditioning, strong family bonds, lots of sun, etc?) that keeps Italian CVD rates lower than the American rates, more than the mythical "Mediterranean diet".

Who is your doctor?

27. July 2008 William Davis (7)

Primary care physicians are the initial entry point for healthcare for the majority of Americans.

Develop pneumonia; go to your family or internal medicine physician (internist) to be prescribed an antibiotic. Need your blood pressure or cholesterol checked? Develop a sore knee or swelling in your leg? Once again, go to your primary care physician.

Image courtesy Dedde'

Primary care physicians are a patient’s guide to a bewildering array of technology and specialists. If you require a specific diagnostic test or consultation with a specialist, your primary care physician will help you navigate through the maze, choosing the path that is best for you. He or she will order a chest x-ray for a cough and fever, provide vaccines to prevent flu or pneumococcal pneumonia, perform an annual physical. If you require hospitalization, your primary care physician will admit you. He or she will order diagnostic tests like MRI’s, ultrasounds, x-rays, and blood testing, usually performed in the hospital or a hospital-owned facility. If you require the services of a gastroenterologist, orthopedist, general surgeon, or neurologist, your primary care physician will refer you to the appropriate specialist.

That’s how it’s supposed to work, at least in principle. In fact, during the first eight decades of the 20th century, it did work that work way for the most part. Your primary care physician acted not just as a provider of healthcare, but as your advocate, someone who knew you and worked to protect your welfare. Your family doctor often knew your parents, maybe even delivered you at birth, and cared for your children. His children often went to the same schools as your children. He and his family lived in the same town and sometimes went to the same church.

That hardly happens any more. It’s more likely you got the name of your primary care physician from a doctor referral service provided by a hospital. Or you picked a name off a list provided by your health insurer. It’s also common to see one doctor, only to see another a year later. Two, three, or more different primary care physicians over a five-year period are common. Doctors come and go, since physician turnover in clinics and practices has been on the increase for years. Insurance companies frequently force policyholders to change doctors, requiring you to choose from a list.

The end result of this shuffling of primary care is increasing impersonality of the relationship. You probably don’t know your primary care physician outside of the 10-minute interaction you had six months ago. She probably never met your mother and will likely not care for your children. Two years from now, she will likely not be your doctor any more, replaced by someone else who obtains the details of your health from a chart. Your chart is more likely to be electronic, with the details of your health history listed in a checklist. There’s little room to detail the idiosyncrasies and quirks of your unique personality or health profile. Throw into this impersonal equation the fact that many doctors have become scared of patients because of potential for lawsuits, often over the most trivial of issues, or because of an error of oversight or misdiagnosis.

This flawed and impersonal system, though emotionally unsatisfying, can still work if each doctor who assumes a patient’s care maintains the ethic of putting health and welfare above all.

But what if your primary care physician is not just an advocate for your welfare, but is a representative of the hospital? What if there are hidden, unspoken financial incentives paid to your doctor to direct you to the hospital for diagnostic testing, hospitalization, and referral to specialists? If a headache becomes a $4800 MRI, or chest pain becomes a $4200 nuclear stress test, then a $14,000 heart catheterization, your primary care physician becomes the purveyor of far greater financial opportunity for the hospital. The entire interaction, founded on the proposition that your doctor actually cares about you, collapses in a heap of financially motivated testing and procedures. It appears to work, and you and your family can still obtain access to healthcare. The problem is that you’re likely to get too much of it.

This message has not been lost on the shrewd administrators at hospitals. Take a look at the ranks of primary care physicians who refer patients to some of your local hospitals. It is typical that a hospital system maintains several hundred primary care physicians on their payroll, all of whom are expected to refer patients to the hospital, cardiologists, and other proceduralists. Why so many?

Most primary care physicians today have signed contracts with a hospital. In other words, they are employees of the hospital. This practice is not unusual: the American Medical Association reported that 4 of 5 primary care physicians are now bound by such employment arrangements across the U.S. In effect, 80% of primary care physicians are legally bound by contract to direct patients to cardiologists who work at hospitals.

On top of contractual obligations, there are financial incentives for the volume of procedures that are generated as a result of referrals. The more procedures generated from an internist’s or family practitioner’s practice, the greater the end-of-year productivity bonus will be, not uncommonly totaling tens of thousands of dollars. Dr. Ted Phillips (not his real name, since he declined to allow me to use it) received a bonus check of $9,437 this year for his “productivity,” defined murkily as the return on specialist referrals. While the bonus may have helped him pay for his son’s college tuition, it clearly was a situation that made him acutely uncomfortable when asked.

Several primary care physicians are also quietly dismissed every year from the ranks of employed physicians for not maintaining a minimum flow of patients into the system.

Another hazardous point of entry: Many patients enter the hospital through the emergency room (ER). A patient in the emergency room is at his or her most vulnerable, seeking help for an urgent complaint and usually willing to accept whatever the ER physician advises. Hospitals know this. That’s why many systems insist that the ER physicians be employees of the hospital, with their practice habits subject to control. A patient goes to the ER with chest pain or breathlessness. The worst thing that can happen from a financial standpoint is for the patient to be evaluated and discharged. For this reason, a growing number of hospitals employ ER physicians, then proceed to legislate practice patterns. Consulting a cardiologist is strongly encouraged, since they generally provide access to the downstream revenue-producing procedures offered in the hospital. That way, what might have been a four hour, $2500 ER visit is converted into a $10,000 to $40,000 hospital stay, even when nothing was wrong in the first place. There are millions of people nationwide who have the hospital bills to prove it after being discharged with a diagnosis of indigestion.

Caveat emptor: Buyer beware.

Kitchen sink approach for Lp(a)

29. August 2008 William Davis (12)

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

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

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

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

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

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

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

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

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

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

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

Making Dr. Friedewald an honest man

28. August 2008 William Davis (3)

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

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

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

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

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

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

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

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

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

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

Some basic vitamin D issues

24. August 2008 William Davis (7)

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

Anne said:

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

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

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

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

Twinb asked:

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

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

Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

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

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

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

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

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

“How much vitamin D should I take?”

22. August 2008 William Davis (17)

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

“How much vitamin D should I take?”

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

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

Utter nonsense.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

You probably don't take enough fish oil

20. August 2008 William Davis (17)

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

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

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

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

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

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

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

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

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

But what dose is sufficient? What dose is ideal?

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

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

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

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

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

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

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

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

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

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

Vitamin D and HDL

19. August 2008 William Davis (23)

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

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

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies

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

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

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

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

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

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

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

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

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

Why? How?

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

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

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

Weight loss and blood pressure

15. August 2008 William Davis (6)

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

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

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

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

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

Why the age-dependent difference?

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

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

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

13. August 2008 William Davis (6)

Brad needed to lose weight.

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

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

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

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

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

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

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

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

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

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

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

I call these changes "transitional" changes in lipids.

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

Divorce court for the doctor-patient relationship?

10. August 2008 William Davis (4)

The doctor-patient relationship has gone sour.

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

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

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

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

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

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

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

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

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

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

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

But a caveat: The patient MUST be informed.

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

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

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

It will be a startling change.

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

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

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

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

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

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

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

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

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

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

Wow. A woman after my own heart.

How much fish oil is enough?

9. August 2008 William Davis (7)

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

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

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

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

Several observations jump out:

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

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

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