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.
Cureality | Real People Seeking Real Cures

You've come a long way, baby

3. June 2011 William Davis (16)
In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

1. June 2011 William Davis (34)
I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

28. May 2011 William Davis (11)
An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

26. May 2011 William Davis (28)
People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

24. May 2011 William Davis (17)
Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

14. May 2011 William Davis (3)
So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 

Tell me your wheat elimination story and receive a copy of my new book, Wheat Belly

6. May 2011 William Davis (68)
I'm looking for interesting wheat-free experiences.

For the past year, I have been writing my new book, Wheat Belly . After many, many late nights and soccer games missed, it's now finished. The book will be out in fall, 2011, to be published by Rodale, the Prevention Magazine people.

Wheat Belly will provide, in excruciating detail, the discussion of how wheat was transformed from innocent wild grass to incredible genetically-altered Frankengrain and why it has become such a health nuisance.

I am looking for interesting stories of wheat elimination for the online and special editions of the book. If you have an interesting tale of wheat-elimination successes, woes, or drama, I'd like to hear about it. Even better, if you would agree to be interviewed by phone (not for live use, just for comments and detail), the editors at Rodale will help tell your story.

If we use your story, I will have a free copy of the new Wheat Belly sent to you when it becomes available.

Please post your story in the comments here. I will then need to obtain your contact info, which we will do privately.

 

Real men don't eat carbs

27. April 2011 William Davis (0)
Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen levels; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone and high estrogen, a cause for depression, emotionality, weight gain, and low libido.

--Sugar-provoking carbohydrates like wheat cause visceral fat to accumulate which, in turn, triggers prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and persistent lipoproteins, like chylomicron remnants and VLDL particles, that impair endothelial function literally within minutes to hours of ingestion. Impaired endothelial function underlies erectile dysfunction. This is why Internet spammers so enthusiastically send you offers for discounted Viagra.

--Carbohydrates increase blood sugar which provokes the process of glycation, glucose modification of proteins, that also contributes to endothelial dysfunction followed by erectile dysfunction.

Real men therefore avoid carbs.

Real men don't eat carbs

27. April 2011 William Davis (57)
Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone, high estrogen, a cause for depressions, emotionality, and weight gain.

--Consume carbohydrates like wheat and visceral fat causes prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and prolonged lipoproteins like chylomicron remnants and VLDL particles that impair endothelial function. Impaired endothelial function underlies erectile dysfunction. Eat a bagel, become impotent.
All posts by william-davis

Why does wheat cause arthritis?

13. November 2010 William Davis (48)
Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Why do morphine-blocking drugs make you lose weight?

10. November 2010 William Davis (24)
Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Heart scan tomfoolery 2

9. November 2010 William Davis (2)
In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.


Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart scan tomfoolery

4. November 2010 William Davis (12)
Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve

Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.

Can I see your linea alba?

2. November 2010 William Davis (19)
As more and more people are eliminating wheat from their diet and losing their "wheat bellies," i.e., the muffin top around their waists along with the visceral fat beneath, I am frequently seeing something I haven't seen in years: the linea alba.

Linea alba, or "white line," refers to the band of connective tissue running vertically from sternum to pubic area. It underlies the depression that separates the horizontal abdominal rectus muscles of the "six pack" abdomen.

It's like digging in your closet and finding something you thought you'd lost years earlier. Surprise! It's been there all along. Buried deep beneath the abdominal fat from dozens of deep-crust pizzas, whole wheat pasta, and whole grain sandwiches is this pleasing anatomical feature long lost from most peoples' anteriors.


Can you see your linea alba?

Dwarf mutant wheat

31. October 2010 William Davis (13)
Here's my 12-year old standing next to dwarf wheat grown near my house. The wheat is full-grown, harvested about 2 weeks after I took this photo.

Wheat is no longer the 4-foot tall "amber waves of grain" of the 20th century. Over 99% of all wheat grown worldwide is now the 18- to 24-inch tall dwarf. New size, new biochemistry, new effects on humans. I call it dwarf "mutant" wheat despite its lack of extra limbs or eyes because of the dramatic transformation required to breed this unique synthetic plant. 

Short-stature means less stalk, faster growing. The stockier stalk also means that the heavy seed head won't cause the plant to "buckle," as 4-foot tall wheat used to. 





The thousand-plus proteins of wheat that have been transformed to generate this dwarf mutant also changed wheat's relationship to consuming humans.

Medical education in the days of Big Pharma

30. October 2010 William Davis (43)
I received this detailed email from an unexpected source: a 3rd-year medical student.

In her email, Theresa describes her frustrations in what she is witnessing for the first time, proceeding through her training and getting exposed to the realities of medical life.

Medical training, particularly clinical training from the 3rd and 4th years of medical school, onwards through internship, residency, and fellowship training, consists largely of bullying, "pimping" (meaning rapid-fire grilling of questions at trainees), and sleep deprivation. It is an extended hazing period meant to demoralize and inculcate the trainee into following the lead of superiors. Buck the system and you're . . . out. Imagine you've just sunk $190,000 and 8 years of college into getting to your internship. You are not going to chance being thrown out on principle. So you just swallow your pride, go along with the game, and echo all the answers they want you to repeat.

While Theresa laments the sad state of modern American pharmaceutical- and procedure-obsessed medicine, she provides me with hope that some young people training to practice medicine today will carve out their own paths, not the one laid for them by the pharmaceutical industry, nor fall for the temptation of higher-paying procedural specialties like orthopedics and cardiology. I am impressed with her ability to see this so early in her career.


Dr. Davis,

I am a 3rd year medical student at ________ University. I came across
your blog today, and I'm very glad I did. I appreciate the value of your time,
so I want to be as succinct as possible while still getting across what I'm
really thinking and feeling:

From what I gathered exploring your blog for a while this afternoon, the
wellness strategies you incorporate into your practice are some of the exact
things I want to do with my future patients. Personally, I strongly believe in
staying healthy by eating right, staying active, etc. For instance, I don't eat
grains or much in the way of starches and sugars. So I love the fact that you
are helping your patients make these powerful and foundational changes in their
lives.

As I'm sure was your experience, a full appreciation of nutrition and lifestyle
as a first-line health strategy is not something that was taught to me in
medical school. I came to school with this deep conviction already in my heart
and mind, and now, on my 3rd year rotations, I am still conflicted and at a loss
as to how I'm going to be able to practice medicine the way I want to, which is
to incorporate these all-important principles into the care of my patients.

What I've come to understand about the medical field today is that the
information that exists is primarily subsidized by the pharmaceutical industry,
and dictated to medical professionals as "evidence-based" treatment guidelines
and recommendations by organizations with sincere and official sounding names
like American Heart Association and American Cancer Society. Add to that the
pressure of potential malpractice litigation and the complexities of the
insurance reimbursement game, and it seems to me like what you get is a bunch of
diagnostic and medication management algorithms that any half-trained monkey
could follow. In his sleep. Which I guess would be alright if at least they
weren't algorithms based on misguided, self-serving, profit-seeking Big Pharma,
Food Inc, insurance conglomerates, and agri-politics (I think I just made that
word up.)

A lot of well-intentioned physicians are just parroting the party
line, as their patients dutifully and gratefully chomp down their statins and
diabetes drugs and blood pressure pills. And I'm sorry, but "diabetes
education" programs with curriculum put together by drug companies? How is that
even legal? Massive corporations raking in massive profits that are dependent
on uncontrolled blood sugars telling people how to best control their blood
sugars?!

Anyway, forgive my rant. What I'm getting at is this: How can I practice
medicine, with the freedom to educate/coach/treat my patients with diet and
lifestyle changes to mitigate/reverse their chronic health conditions? Without
feeling like I automatically have to first and foremost prescribe the litany of
drugs dictated by "evidence-based" guidelines? Without excessive fear of
litigation or loss of credibility among my peers? Without having to lie through
my teeth to my patients, and tell them that eating low-fat and heart-healthy
whole grains is the best way (implication also being the only scientifically
proven way) to control their diabetes, lower their cholesterol, etc, etc, etc?

I want my patients to have the full benefit of honest nutrition and lifestyle
information, and medications and surgery as necessary. I'm afraid that there
isn't room for this kind of holistic emphasis in the medical profession today.
Are there residencies that include this kind of training or at least respect
these "unconventional" philosophies? Are there clinics or practice groups that
would allow me to practice with this emphasis, or is there a bias against docs
who do not necessarily conform to the party position? Will I have no other
option but to go it alone under the auspices of my own shingle? How do you
handle these kinds of issues in your professional life?

Sincerely,
Theresa M.


A ray of hope! Perhaps Theresa is just the first among many more medical students who refuse to submit to the brainwashing practices of the pharmaceutical industry, the same mind manipulation that has hopelessly turned most of my colleagues into their unwitting puppets.

I'll be interested in watching how Theresa's experience unfolds. I've asked her to keep us informed every so often.

The Great Low-Carb Connector

28. October 2010 William Davis (15)
The effusive Jimmy Moore of Livin' La Vida Low-Carb asked me to help get the word out about his new podcast subscription service, The Livin' La Vida Low-Carb Show Fan Club.

Jimmy has been The Great Connector for the low-carb discussion, from his ubiquitous online and social media presence, to his annual low-carb cruise. He has also broadcast first class interviews of nutritional notables like Gary Taubes, Dr. Robert Lustig, and blogger Stephan Guyenet. His Fan Club expands listener involvement in the podcast process and, potentially, greater access to his guests:

My faithful listeners have long been asking me about how they can become even more engaged in the behind-the-scenes workings of the show to get the inside scoop about what’s coming next. I’ve heard people ask specifically for access to transcripts of the most popular podcasts, a listing of the interviews I’m currently working on with the ability to ask questions of those guests, to have sneak peek of audio from not-yet-released interviews and more. My amazing podcast producer, Kevin Kennedy-Spaein, and I have been discussing how to best do this for a while in an effort to meet the demands of our biggest fans and we think we’ve got just the answer for you. Introducing The Livin’ La Vida Low-Carb Show Fan Club!

This is for all intents and purposes the quintessential destination for people who can’t get enough of this podcast that goes much deeper than discussion about the low-carb lifestyle. Yes, I speak with a lot of people who are supporters of carbohydrate-restricted diets, but I also talk with fitness gurus, people who support alternative eating plans, those who have interesting theories and beliefs regarding health and much more. Wouldn’t you love to have a chance to know who’s coming up in my schedule to be able to ask them questions BEFORE I interview them? Keep in mind that my interviews are pre-recorded and air sometimes as much as 5-6 months afterwards. Members of the “fan club” would know all about who’s coming and likely will have their question asked on the air just for signing up to be a part of this exciting new addition to “The Livin’ La Vida Low-Carb Show.”

Jimmy is the guy who is bringing this disparate and widely-spread community together. He's the guy we all know, he knows "everybody." I'm looking forward to seeing how this new project makes a more involved, personal delivery of interaction possible.

New Track Your Plaque record!

27. October 2010 William Davis (19)
The record for the largest drop in heart scan score (by percentage of starting score) has been held for around three years, with 63% reduction in score.

Well, the longstanding record was broken this week: 75% reduction in score.

At the start, Freddie has disastrous lipid values:

LDL cholesterol 263 mg/dl
HDL 26 mg/dl
Triglycerides 323 mg/dl
Total cholesterol 354 mg/dl

Lipoproteins (NMR) were worse:

LDL particle number 3360 nmol/L
Small LDL 2677 nmol/L

Heart scan score: 732

Interestingly, Freddie had virtually no vitamin D in his body, with a 25-hydroxy vitamin D level that was unmeasurable.

Freddie was miserably intolerant to statin drugs, with even the smallest dose resulting in intolerable muscle aches. That's when his doctor sent him to me.

Because I felt that the dominant abnormality in Freddie's lipids and lipoproteins was small LDL particles, representing 80% of total LDL particle number, we focused his program on correcting this parameter. Freddie's program was therefore focused elimination of wheat, cornstarch, oats, and sugars, along with an eventual vitamin D dose of 20,000 units to finally achieve a 25-hydroxy vitamin D level of 66 ng/ml. No statin drug in sight.

43 lbs of weight loss and 18 months later, a second heart scan score: 183--a 75% reduction.

While the rest of the world continues to insist that coronary calcium (heart scan) scores cannot be reduced, I am seeing records being broken. I add Freddie's experience to the rapidly growing list of people who have not just stopped coronary plaque from growing, but are seizing control and reducing it, sometimes to dramatic degrees.

The Anti-AGEing Diet

22. October 2010 William Davis (36)
Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.

There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic "mis-reading" that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.

One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer's dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works--debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)

There are two general ways to develop AGEs:

1) Endogenous--High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the "normal," expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.

A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.

2) Exogenous--AGEs (here especially is where the "AGE" label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.

The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.

Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.

If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.

The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.