Dr. Cannell on vitamin D and cancer

Here is Dr. John Cannell's Vitamin D Council Newsletter reprinted in its entirety. It answers some of the questions that came up on The Heart Scan Blog about the recent release of a study of vitamin D and cancer



The Vitamin D Newsletter

December, 2007

Does vitamin D prevent cancer? If it does, will doctors who ignore the research end up with blood on their hands? The press makes it easy for doctors to believe what they want to believe. Below are six stories about the same scientific study; read the six different headlines. According to your a priori beliefs, you can choose the story you want to believe and read that one. Don't feel bad, we all do it. As Walter Lippman once said, "We do not see and then believe, we believe and then we see."


Vitamin D cuts colon cancer death risk



Study Finds No Connection Between Vitamin D And Overall Cancer Deaths



Vitamin D protects against colorectal cancer



Vitamin D May Not Cut Cancer Deaths



Vitamin D protects against colorectal cancer



Scientists advise a vitamin D downgrade as there is no real proof ...




Another option is to read the study yourself.


Freedman DM, et al. Prospective Study of Serum Vitamin D and Cancer Mortality in the United States. J Natl Cancer Inst. 2007 Oct 30; [Epub ahead of print]




What Dr. Freedman actually discovered is that when you take a very large group of people (16,818), some as young as seventeen, measure their vitamin D levels, and then wait about ten years to see who dies from cancer, you find 536 die and that a vitamin D level from ten years earlier is not a good predictor of who will die from cancer. However, even a level drawn ten years earlier predicted that those with the lowest level were four times more likely to die from colon cancer, suggesting, as Ed Giovannucci has, that colon cancer may be exquisitely sensitive to vitamin D. Furthermore, 28 women got breast cancer, 20 in the group with the lowest vitamin D level but only 8 in the highest. The breast cancer findings were not statistically significant - even during a very long breast cancer awareness month - but can you imagine what critics at the American Cancer Society would be telling women if the numbers were reversed, if the 20 women who got breast cancer were in the high vitamin D group?



Another large epidemiological study appeared about breast cancer the very next day. This time, the press passed on the story and the American Cancer Society was mum, no editorials by Dr. Lichtenfeld, their spokesman, in spite of breast cancer awareness month.



Abbas S, et al. Serum 25-hydroxyvitamin D and risk of postmenopausal breast cancer - results of a large case-control study. Carcinogenesis. 2007 Oct 31; [Epub ahead of print]



In the above study, 1,394 women with breast cancer were case-controlled with a similar number of women without breast cancer. The women with breast cancer were three times more likely to have low vitamin D levels. That is a lot of women who may be dying during next year's breast cancer awareness month.



Both of the above studies were epidemiological, not randomized controlled trials. Of course a randomized controlled trial has already shown a 60% reduction in internal cancers in women taking even a modest 1,100 IU per day of vitamin D.



Lappe JM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.



What is interesting is the difference in the response of the Canadian Cancer Society and the American Cancer Society. The Canadian Cancer Society has advised all Canadians to take 1,000 IU per day - not enough but a good first step - and for immediate additional large scale clinical trials. The Canadians simply performed a risk/benefit analysis. What is the risk of treating vitamin D deficiency versus what are the potential benefits? They quote the American Food and Nutrition Board, which says 2,000 IU/day is safe for anyone over the age on one to take, on their own, without being under the care of a physician. If there is little or no risk, then the next question is what are the potential benefits of treating vitamin D deficiency? This is not quantum mechanics.



Cancer society calls for major vitamin D trial



The Canadians acted because the Canadian government knows it could save billions of dollars by treating vitamin D deficiency.



Vitamin D Deficiency Drains $9 billion From Canadian Health Care ...



If wide spread treatment of vitamin D deficiency became the rule, ask yourself, "Who would be helped and who would be hurt." First ask yourself that question about Canada and then about the USA. Remember, in Canada, the government directly pays for its citizen's health insurance; in the USA, private insurance is the norm. In Canada, the government is realizing they could save billions if vitamin D deficiencies were treated. In the USA, a large segment of the medical industry would be hurt, some anti-cancer drug manufacturers would have to close their doors, thousands of patents would become worthless, lucrative consulting contracts between industry and cancer researchers would dry up.

Both Canadians and Americans are shocked to think their doctors care about money, are in the illness business. In some ways people think of their doctors like they do their local public schools. They know medicine is a business and know doctors do things for money but they don't think their own doctors do. Likewise they think public schools are in bad shape but think their local schools are above average. They think their doctor is above average, like their "Lake Woebegone" kids.

Lake Woebegone Effect

The fact is that doctors, hospitals, regional cancer centers, and the cancer drug manufacturers are all in business to make money and all of these businesses make money off the sick, not off the well. Just a fact, but, as Aldous Huxley once observed, "Facts do not cease to exist because they are ignored."



Vitamin D will save the Canadian government enormous amounts of money but will cause widespread economic disruption in the USA. Do the physicians leading the American Cancer Society have strong economic ties to the cancer industry in the form of patents, stock options, and consulting fees? If so, what do you expect them to do? What would you do? It's simple. You would believe what you have to believe, what you need to believe, that is, anything with the word "vitamin" in it is simply the latest Laetrile. Look to Canada, not the USA, to lead the way.



Vitamin D may fight cancer


What about American physicians? They are apparently waiting for the American trial lawyers to smell a tort. After all, the case is quite simple. Doctor, did you advise Mrs. Jones to avoid the sun? Doctor, did you tell her the sun is the source of 90% of circulating stores of vitamin D? Doctor, did you prescribe vitamin D to make up for what the sun would not be making? Doctor, did you measure her vitamin D levels? So you had no way of knowing if your sun-avoidance advice resulted in vitamin D deficiency? Doctor, do you know our expert tested her vitamin D level and it was less than 20? Doctor, did you tell her about any of the studies indicating vitamin D deficiency causes cancer? Doctor, did you know Mrs. Jones has terminal breast cancer and will be leaving behind a loving husband and two young children?

And what about the American Cancer Society? Dr. Lichtenfeld, their spokesman, quickly gave his opinion; from what I can tell the first time he ever commented on a vitamin D study. That is, he has ignored the hundreds of positive epidemiological studies, ignored the incredible randomized controlled trial, but he jumped on this one:

Maybe Vitamin D Isn't The Answer After All

Dr. Lichtenfeld, implied the Canadian Cancer Society has acted precipitously in recommending that all Canadians take 1,000 IU of vitamin D daily. He implied that Americans should placidly wait until more randomized controlled trials, such as Lappe JM, et al (above), accumulate before they address their vitamin D deficiency. That is, nothing should be done until more randomized controlled trials prove vitamin D prevents cancer, one randomized controlled trial is not enough; epidemiological studies are not enough, animal studies are not enough, multiple anti-cancer mechanisms of action are not enough? If that is his position, I challenge him to point to one human randomized controlled trial that proves smoking is dangerous?

If he cannot, then he must admit that the American Cancer Society's position on smoking is entirely derived from epidemiological studies, animal studies, and a demonstrable mechanism of action, not on human randomized controlled trials? Vitamin D not only has hundreds of epidemiological studies, thousand of animal studies, and at least four anti-cancer mechanisms of action, vitamin D deficiency has something smoking does not have, it has a high quality randomized controlled trial. If future randomized controlled trials fail to show vitamin D prevents cancer - and Dr. Lichtenfeld better hope they do - he can have the satisfaction of saying "I told you so." If future randomized controlled trials confirm vitamin D prevents cancer, then he needs to look at his hands, the red he sees is the blood of needless cancer deaths.

John Cannell, MD

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422



This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know.

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"Yes, Johnnie, there really is an Easter bunny"

A Heart Scan Blog reader recently posted this comment:

You wouldn't believe the trouble I'm having trying to get someone to give me a CT Heart Scan without trying to talk me into a Coronary CTA [CT angiogram]. Every facility I've talked to keeps harping on the issue that calcium scoring only shows "hard" plaque...and not soft.

I also had a nurse today tell me that 30% of the people that end up needing a coronary catheterization had calcium scores of ZERO. That doesn't sound right to me. What determines whether or not someone needs a coronary catheterization anyway?



There was a time not long ago when I saw heart scan centers as the emerging champions of heart disease detection and prevention. Heart scans, after all, provided the only rational means to directly uncover hidden coronary plaque. They also offered a method of tracking progression--or regression--of coronary plaque. No other tool can do that. Carotid ultrasound (IMT)? Indirectly and imperfectly, since it measures thickening of the carotid artery lining, partially removed from the influences that create coronary atherosclerotic plaque. Cholesterol? A miserable failure for a whole host of reasons.

Then something happened. General Electric bought the developer and manufacturer of the electron-beam tomography CT scanner, Imatron. (Initial press releases were glowing: The Future of Electron Beam Tomography Looks Better than Ever.The new eSpeed C300 electron beam tomographic scanner features the industry’s fastest temporal resolution, and is now backed by the strength of GE Medical Systems. Imatron and GE have joined forces to provide comprehensive solutions for entrepreneurs and innovative medical practitioners.)

Within short order, GE scrapped the entire company and program, despite the development of an extraordinary device, the C-300, introduced in 2001, and the eSpeed, introduced in 2003, both yanked by GE. The C-300 and eSpeed were technological marvels, providing heart scans at incredible speed with minimal radiation.

Why would GE do such a thing, buy Imatron and its patent rights, along with the fabulous new eSpeed device, then dissolve the company that developed the technology and scrap the entire package?

Well, first of all they can afford to, whether or not the device represented a technological advancement. Second (and this is my reading-between-the-lines interpretation of the events), it was in their best financial interest. Not in the interest of the public's health, nor the technology of heart scanning, but they believed that focusing on the multi-detector technology to be more financially rewarding to GE.

GE, along with Toshiba, Siemens, and Philips, saw the dollar signs of big money with the innovations in multi-detector technology (MDCT). They began to envision a broader acceptance of these devices into mainstream practice with the technological improvements in CT angiography, a device (or several) in every hospital and major clinic.

Anyway, this represents a long and winding return to the original issue: How I once believed that heart scan centers would be champions of heart disease detection and reversal. This has, unfortunately, not proven to be true.

Yes, there are heart scan centers where you can obtain a heart scan and also connect with people and physicians who believe in prevention of this disease. I believe that Milwaukee Heart Scan is that way, as is Dr. Bill Blanchet's Front Range Preventive Imaging, Dr. Roger White's Holistica Hawaii, and Dr. John Rumberger's Princeton Longevity Center.

But the truth is that most heart scan centers have evolved into places that offer heart scans, but more as grudging lip service to the concept of early detection earned with sweat and tears by the early efforts of the heart scan centers. But the more financially rewarding offering of CT coronary angiograms, while a useful service when used properly, has corrupted the prevention and reversal equation. "Entry level" CT heart scans have been subverted in the quest for profit.

CT angiograms pay better: $1800-4000, compared to $100-500 for a heart scan (usually about $250). More importantly, who can resist the detection of a "suspicious" 50% blockage that might benefit from the "real" test, a heart catheterization? Can anyone honestly allow a 50% blockage to be without a stent?

CT angiograms not only yield more revenue, they also serve as an effective prelude to "downstream" revenue. By this equation, a CT angiogram easily becomes a $40,000 hospital procedure with a stent or two, or three, or occasionally a $100,000 bypass. Keep in mind that the majority of people who are persuaded that a simple heart scans are not good enough and would be better off with the "superior" test of CT angiography are asymptomatic--without symptoms of chest pain, breathelessness, etc. Thus, the argument is that people without symptoms, usually with normal stress tests, benefit from prophylactic revascularization procedures like stents and bypass.

There are no data whatsoever to support this practice. People who have no symptoms attributable to heart disease and have normal stress tests do NOT benefit from heart procedures like heart catheterization. They do, of course, benefit from asking why they have atherosclerotic plaque in the first place, followed by a preventive program to correct the causes.

So, beware: It is the heart scan I believe in, a technique involving low radiation and low revenue potential. CT angiograms are useful tests, but often offered for the wrong reasons. If we all keep in mind that the economics of testing more often than not determine what is being told to us, then it all makes sense. If you want a simple heart scan, just say so. No--insist on it.

Take trust out of the equation. Don't trust people in health care anymore than you'd trust the used car salesman with "a great deal."

Finally, in answer to the reader's last comment about 30% of people needing heart catheterizations having zero calcium scores, this is absolute unadulterated nonsense. I'm hoping that the nurse who said this was taken out of context. Her comments are, at best, misleading. That's why I conduct this Heart Scan Blog and our website, www.cureality.com. They are your unbiased sources of information on what is true, honest, and not tainted by the smell of lots of procedural revenue.

Diabetes: controlled or . . . cured?

Russ had a beer belly, a big protuberant, hanging-over-the belt-on-top-of-skinny-legs sort of beer belly. Except he didn't get it from beer (only). Yes, he did drink beer, up to 3 or 4 per day on weekends, rarely during the week.

Russ got his "beer belly" from snack foods, processed foods, and yes, wheat products.

He came to my office for consultation for unexplained breathlessness. His primary care physician was stumped and asked for an opinion.

So, part of Russ' evaluation included laboratory work. Russ proved to have a blood sugar (glucose) of 136 mg/dl, well into the diabetic range. His insulin level was 102 microunits/ml, way above the desirable range of <10. I interpreted this to mean that Russ had early diabetes but still maintained vigorous pancreatic function, since the pancreas is the abdominal organ responsible for insulin production. In pre-diabetes and early diabetes, insulin levels can be high, reflecting the revved up output of the pancreas. However, the pancreas eventually "burns out," unable to keep up with the demand to product enormous quantities of insulin. That's when blood sugar skyrockets.

Along with the blood sugar and insulin, Russ showed all the expected markers of this syndrome (the "metabolic syndrome"): low HDL of 34 mg/dl, high triglycerides of 257 mg/dl, severe small LDL (80% of total LDL), high c-reactive protein, and high blood pressure.

A heart scan showed a surprisingly small amount of coronary plaque with a score of only 4. Thus, Russ' symptoms were unlikely to represent a coronary issue ("ischemia"). Breathlessness was far more likely to be from 1) his obesity and protuberant abdomen, large enough to encroach on his chest and lung volume, and 2) high blood pressure (which can, in turn, lead to high heart pressure and breathlessness, often called "left ventricular diastolic dysfunction").

I persuaded Russ to eliminate his previously flagrant and abundant over-reliance on wheat products and snack foods. Two months later, 15 lbs lighter, and a modestly less protuberant beer belly, Russ' laboratory evealuation showed:

--Blood sugar 90 mg/dl--normal.

--Insulin 12 microunit/ml--darn near normal.

Blood pressure was down 20 points. Russ' breathlessness was now entirely gone. He has another 30-40 lbs to go, but he's off to a great start. He is now clearly, solidly, and confidently NON-diabetic.

I see experiences like this every day, as do committed diabetes fighters like Jenny at Diabetes Update.

Why isn't this common practice? If pre-diabetes and diabetes can be cured by such a simple approach, why isn't it more widely embraced? After all, what other devastating diseases can claim to have such a simple, straightforward way to achieve cure?

And why does the American Diabetes Association (ADA) actually condone the inclusion of abundant carbohydrates in diabetics? Their modified food pyramid shows the widest part of the pyramid filled with "breads, grains, and other starches."



How about this question taken from a Q&A on the ADA website:

Can I eat foods with sugar in them?

For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


The answer is simple. Just as the American Heart Association focuses on ways to deliver the message of palliation, so does the ADA. So ADA diet advice is designed to help diabetics maintain a stable blood sugar on their medication. It is definitely not intended to reverse or eliminate diabetes. My patient Russ would be deep into diabetes on the ADA diet, enjoying his rolls, whole wheat bread, breakfast cereals, and birthday cake.

Once again, another example of the growing irrelevance of the "official" arbiters of health information for those of us looking for reversal of disease.

Study review: cerivastatin

I'd like to start an occasional series of blog posts on The Heart Scan Blog in which I review studies relevant to the whole heart scan score reversal experience.

In a previous post, Don't be satisfied with "deceleration,"I discussed the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), in which either atorvastatin (Lipitor), 80 mg, or pravastatin (Pravachol),40 mg, was given to 615 women. Both groups showed an average of 15% annual plaque growth, regardless of which agent was taken and regardless of the amount of LDL cholesterol reduction.

I cited another study in which 471 participants received either Lipitor, 80 mg, or Lipitor, 10 mg. The rate of annual score increase was 25-27%, regardless of drug dose or LDL lowering.

Here's yet another study, a small German experience in 66 patients, with a curious design and using the now-defunct statin drug, cerivastatin (Bayccol, pulled in 2001, nearly simultaneous with the publication of this study, due to greater risk of muscle damage, particularly when used in combination with gemfibrozil). Achenbach et al in Influence of lipid-lowering therapy on the progression of coronary artery calcification: A prospective evaluation reported on this trial in which all participants underwent heart scanning to obtain a heart scan score; no treatment was initiated based on the score. A second scan was obtained after the no treatment period, followed by treatment with cerivastatin, 0.3 mg per day. A third scan was finally obtained.

In year one without treatment, the average increase in heart scan scores was 25%. In year two with cerivastatin, the average increase in heart scan score was 8.8%. In 32 participants who achieved LDL<100 mg/dl on the drug, there was an average modest reduction in heart scan scores of 3.7% (i.e., -3.7%).

Now, that was eye-opening. Why did this small study achieve such startlingly different results from the other two studies that showed relentless progression despite even high doses of Lipitor? That remains unanswered. Was cerivastatin unique among statins? Did the unique two-phase trial design somehow change the outcome by triggering participants to change lifestyle habits after their first scan (since most exhibited an increase in score; they were not "blinded" to their scores). Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

This experience is unique, as you can see, compared to the two other studies. But it was also smaller. The results are also different than what I have seen in day-to-day practice when I've seen people treated with statin drugs alone (not cerivastatin, of course): rarely do heart scan scores stop increasing. While slowing does usually occur (18-24% per year rates of annual score increase are very common in people who do nothing but take a statin drug and make modest lifestyle changes), I have personally seen only two people stop their score with this strategy alone. Nobody has ever dropped their score taking a statin alone, in my experience.

You can also see the nature of clinical studies: single or limited interventions instituted in order to control for unexpected or complex effects. If three different treatments are used, then what desirable or undesirable effects, or lack of an effect, is due to which treatment agent?

My experience is that no single treatment stops or reduces heart scan scores. It requires a more rational effort that includes 1) identification of all causes of coronary plaque (e.g., low HDL, high triglycerides, Lp(a), small LDL, deficiency of vitamin D, etc, none of which are substantially affected by statin drugs), and 2) correction of all causes. That simple concept has served us well.

Dr. William Blanchet: A voice of reason

I don't mean to beat this discussion to a pulp, but looking back over the comments posted on www.theHeart.org forum, I am so deeply impressed with Dr. William Blanchet's grasp of the issues, that I posted his articulate and knowledgeable comments again.

Here is one post in which Dr. Blanchet, in response to accusations of trying to profit from heart scans, provides a wonderful summary of the logic and evidence behind the use of heart scans as the basis for heart disease prevention.


Yes, I have seen a dramatic reduction in coronary events.

Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk factors is low risk and most do not qualify for preventive treatment. EBT calcium imaging could identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school, a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Arteriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card.[I believe it's the study Dr. Blanchet was referring to.]

I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test. Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of
patients with less than 70% vessel obstruction will pass their stress test.

Regarding [the] question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologist's stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.



That's probably the best, most concise summary of why heart scanning makes sense that I've ever heard. And it comes from a primary care physician in the trenches. With just a few paragraphs, Dr. Blanchet, in my view, handily trumps the arguments of my colleagues arguing to maintain the status quo of cholesterol testing, stress tests, and hospital procedures.


Note:
Dr. Blanchett talks openly about his affiliation with an imaging center in Boulder, Colorado, Front Range Preventive Imaging. I'm no stranger to the accusations Dr. Blanchet receives about trying to profit from the heart scan phenomenon. Ironically, heart scanning loses money. It is a preventive test, not a therapeutic, hospital-based procedure. Free-standing heart scan centers that do little else (perhaps virtual colonoscopies) usually manage to pay their bills but make little profit. Hospitals that offer heart scans usually do so as a "loss-leader," i.e., an inexpensive test that brings you in the door in the hopes that you will require more testing.

Accusations of profiteering off heart scans are, to those in the know, ridiculous and baseless. On the contrary, heart scans are both cost-saving and life-saving.

Vitamin D2 rip-offs

Here's a sampling of prescription vitamin D2/ergocalciferol products available:






Prescription ergocalciferol (vitamin D2) (Drisdol brand), 50 caps for $130.84.










Alfcip brand of erogocalciferol (vitamin D), 30 capsules for $28.20.









Ergocalciferol (vitamin D2) as Drisdol oral solution, 1 bottle $146.26.










How about vitamin D3/cholecalciferol?



Carlson's brand cholecalciferol (vitamin D3), 120 capsules $5.09.









Cholecalciferol, vitamin D3, is far less expensive than ergocalciferol, vitamin D2. Cholecalciferol is available as a supplement without prescription. Ergocalciferol is available only by prescription.

The price difference must mean that the plant-based form, ergocalciferol, must be far superior to the naturally-occurring human form, vitamin D3.

Of course, that's not true. Dr. Robert Heaney's study is just one of several documenting the inferiority of D2/ergocalciferol, Vitamin D2 Is Much Less Effective than Vitamin D3 in Humans. D2 exerted less than a third of the effect of D3.

In my experience, D2/ergocalciferol often exerts no effect whatsoever. One woman I consulted on came into the office having been prescribed Drisdol capsules, 50,000 units every day for the past 18 months (by mistake by her physician). Blood level of active 25-OH-vitamin D3: Zero.

But the pharmacy and drug manufacturer collected $1413 for her 18-month course. Cost for a 4000 unit per day dose of D3/cholecalciferol: $45--and it would have actually worked.

In my view, prescription vitamin D2 is yet another example of drug manufacturer scams, a product that provides no advantages, costs more, but yields bigger profits.

Yet this wonderful supplement called cholecalciferol, among which Carlson's is an excellent choice, is available to you inexpensively, without prescription, and actually provides the benefits you desire.

Stenosis detection vs. plaque detection

One of the most common misunderstandings encountered by both physicians and the public is that, to create an effective heart disease prevention program, we need tools for atherosclerotic plaque detection. What we do not need is a tool for stenosis detection. (Stenosis means percent blockage. A 50% stenosis means 50% of the diameter of an artery is reduced by atherosclerosis.)

This issue came to mind recently with the ongoing conversation at Heart.org forum, in which the conversation predictably degenerated into a "what good are heart scans when there are better tests to detect blockage" sort of mentality.
They are right: There are better tests to detect stenoses or blockages, such as stress tests, heart catheterization, and CT coronary angiography. If someone is having chest pain or breathlessness, these tests are useful to help understand why. These tests are preludes to stents, bypass surgery, and the like. They are the popular tools in hospitals, the ones that provide entry into the revenue-yielding world of heart disease procedures.

Plaque detection, on the other hand, is principally a tool for the person without symptoms. In this regard, it is more like cholesterol testing. I doubt my colleagues would bash cholesterol because it doesn't reveal blockages. Plaque detection identifies the person who has already started developing atherosclerosis.

Dr. William Blanchett of Colorado articulates this idea well:

EBT calcium imaging not only identifies the vast majority of individuals at risk, it also identifies individuals with minimal risk. In other words, it distinguishes those who are likely to benefit from treatment . . .and it identifies those unlikely to benefit from treatment. Furthermore, the greatest value of EBT calcium imaging is that with serial imaging you can determine who is and who is not responding to treatment.

Those patients not responding to the initial treatment are identified by progression of their calcified plaque on a subsequent scan are then placed on additional therapies. The net result is a remarkable reduction in heart attack rates.

Ahh, the voice of reason. Plaque detection empowers you in your prevention program. If you know how much plaque your begin with, you can track that value to know whether you have having a full effect or not. Stenosis detection, on the other hand, empowers your doctor and provides the irresistible impulse to stent.

Another common objection raised to plaque detection is "why bother if you're going to give everybody a statin anyway?" We know the origins of that argument, don't we? If the only strategy known to your doctor is cholesterol reduction with statin drugs, then perhaps that's right. But, with awareness of all the things that go beyond statin drugs, often make them unnecessary, then knowledge of who should engage in an intensive program of prevention or not is enabled by plaque detection.

Is an increase in heart scan score GOOD?

In response to an earlier Heart Scan Blog post, I don't care about hard plaque!, reader Dave responded:

Hello Dr Davis,

Interesting post about hard and soft plaque. I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).

After the first scan we started aggressively going after my LDL, HDL and Trig...196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 [The Track Your Plaque target values]-

So the increase is a surprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.



Dave's doctor then responded to him with this comment:

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago. Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT [i.e., calcium score]. It is only the safe, calcified plaque that can be measured with the EBT. [Emphasis mine.] For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque. There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque. We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above."


Huh?

This bit of conventional "wisdom" is something I've heard repeated many times. Is it true?

It is absolutely NOT true. In fact, the opposite is true: Dave's substantial increase in heart scan score from 235 to 419 over 22 months, representing a 78% increase, or an annualized rate of increase of 37%. This suggests a large increase in his risk for heart attack, not a decrease. Big difference!

Dr. Paulo Raggi's 2004 study, Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy in 495 participants addresses this question especially well. Two heart scans were performed three years apart, with a statin drug initiated after the first scan, regardless of score.

During the period of study, heart attacks occurred in 41 participants. When these participants were analyzed, it was found that the average annual increase in score over the three year period was 42%. The average annual rate of increase in those free of heart attack was 17%. The group with the 42% annual rate of increase--all on statin drugs--the risk of heart attack was 17.2-fold greater, or 1720%.

The report made several other important observations:

--20% of the heart attack-free participants showed reduction of heart scan scores, i.e., reversal. None of the participants experiencing heart attack had a score reduction.
--Only 2 of the 41 heart attacks occurred in participants with <15% per year annual growth, while the rest (39) showed larger increases.
--The intensity of LDL reduction made no difference in whether heart attacks occurred or not. Those with LDL<100 mg/dl fared no better than those with LDL>100 mg/dl.

Dr. Raggi et al concluded:

"The risk of hard events [heart attack] was significantly higher in the presence of CVS [calcium volume score] progression despite low LDL serum levels, although the interaction of CVS change and LDL level on treatment was highly significant. The latter observation strongly suggests that a combination of serum markers and vascular markers [emphasis mine] may constitute a better way to gauge therapeutic effectiveness than isolated measurement of lipid levels."

This study demonstrates an important principle: Rising heart scan scores signal potential danger, regardless of LDL cholesterol treatment. Yes, LDL reduction does achieve a modest reduction in heart attack, but it does not eliminate them--not even close.

These are among the reasons that, in the Track Your Plaque program, we aim to correct more than LDL cholesterol. We aim to correct ALL causes of coronary plaque, factors that can be responsible for continuing increase in heart scan score despite favorable LDL cholesterol values.

So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

Just don't let your doctor's ignorance permit the heart attack that is clearly in the stars. Take preventive action now.

The Heart.org online debate

There's a fascinating and vigorous debate going on at the Heart.org website among Dr. Melissa Shirley-Walton, the recently publicized proponent of "a cath lab on every corner": Dr. William Blanchet, a physician in northern Colorado; and a Track Your Plaque Member who calls himself John Q. Public.

John Q. has been trying to educate the docs about the Track Your Plaque program. Unfortunately, Dr. Shirley-Walton essentially pooh-poohs his comments, preferring to lament her heavy work load. In her last post, when she discovered that John Q. was not a physician, she threatened to block his posts and delete all prior posts.

However, Dr. Blanchet has emerged as a champion of heart scanning, intensive lipid management, and lipoproteins, much similar to our program. In fact, many of Dr. Blanchet's comments were so similar to mine that John Q. asked me if it was really me! (It is definitely not.)


Here's a sampling of some of the discussion going on now:


Dr. Blanchett started out the discussion by saying:

Stent Insanity
I have no trouble agreeing with the argument that we have initiated the widespread use of DES without adequate study regarding outcomes. Shame on us.

That said, we are ingoring the DATA that shows that most heart attacks occur as a result of non-obstructing plaque and all the talk about which stent to use ignors the majority of individuals at risk. In addition, for a decade we have known that stenting does not improve net outcomes anyway.

What ever happened to effective primary prevention? We discarded EBT calcium imaging like moldy cabbage without even looking at the outcomes DATA. With direction provided by EBT calcium imaging and effective primary prevention, I have been able to reduce myocardial infarction by 90% in my very large Internal Medicine practice. Through effectively identifying patients at risk and measuring success or failure of treatment with serial EBT, I have made the argument as to which stent to use moot. No symptomatic angina and rare infracts equals little need for any stent.

Is anybody listening? Certainly not the cardiologists whose wealth and fortunes are based on nuclaer imaging, angiography and stenting.



Dr. Shirley-Walton, skeptical of Dr. Blanchet's claim of >90% reduction of heart attacks using a prevention program starting with a heart scan:

To rely soley upon a calcium score will deprive you of a lot of information that could be otherwise helpful in the management of your patients.

Without seeming sarcastic, I must refute : "of 6,000 patients I've seen 4 heart attacks in 3 years". Although I certainly hope your statistics are accurate, I will suggest the following:

You've not seen all of the heart attacks since up to 30% of all heart attacks are clinically silent. So unless you are echo'ing or nuclear testing all of these patients in close followup, you aren't certain of your stats.

Secondly, in order to attribute this success to your therapy, you would have to have nearly 100% compliance. In the general population, compliance is often less than 50% with any regimen in any given year of treatment. If you can tell us how you've achieved this level of compliance, we could all take a lesson.




Dr. Blanchett, commenting on his use of heart scanning as a primary care physician:

CAC [coronary artery calcium] is an inexpensive and low radiation exam to identify who is at increased risk for heart attacks.

A study of 222 non-diabetic patients admitted with their first MI found 75% of them did not qualify for cholesterol modifying therapy prior to their initial MI (JACC 2003:41 1475-9). In another study of 87,000 men with heart attacks, 62% had 0 or 1 major risk factors (Khot, et al. JAMA. 2003). Almost all individuals with 0 or 1 risk factor are Framingham "Low risk" and therefore will not qualify for cholesterol lowering therapies. (JAMA. 2001;285:2486-2497)


Risk factors alone are not sufficient. In my practice, of the last 4 patients who have died from heart attacks, none qualified for preventive therapies by NCEP guidelines.

Studies have shown that CAC by EBT provides an independent and incremental predictor of heart attack risk. (1. Kondos et al, Circulation 2003;107:2571-2176, 2. Am Heart J 141. 378-382, 2001, 3. St Francis Heart Study Journal of the American College of Cardiology July, 2005) The old saw that CAC simply reflects risk factors and age is just wrong.


Although CT angiography shows great promise to reduce unnecessary conventional angiography and is helpful in emergency room chest pain evaluation, I do not see CT angiography as a screening study in asymptomatic individuals. 10 times more radiation than EBT calcium imaging plus the risk of IV dye exposure makes CT angiography inconsistent with the principles of a screening test. Taken in the context of a primary care physician's evaluation of heart attack risk, EBT calcium imaging has great value.

Coronary calcium changes management by: 1. Identifying those at risk who do not show up with standard risk stratification (St Francis Heart Study: Journal of the American College of Cardiology July, 2005). 2. Motivating patients to be compliant with therapies (Atherosclerosis 2006; 185:394-399). 3. By measuring serial calcium, we can see who is and who is not responding to our initial treatment so that we can further refine our therapeutic goals (Atherosclerosis, 2004;24:1272).

When used in the primary care preventive setting, CAC imaging is indeed of great incremental value. In my practice, in improves my outcomes so greatly that it compels Melissa Walton-Shirley to question my veracity.



Dr. Melissa Walton-Shirley:

Ahhhhhh.......the aroma of profit making, I thought I smelled it. [Accusing Dr. Blanchett of referring patients for heart scans for personal profit.]

I will tell you that I was a little hurt when I was called "a typical cardiologist with a butcher block mentality" after my primary pci piece for med-gen Med was reviewed by the track your placque [sic] folks.

Though, it's clear that they misunderstood and thought I was cathing for dollars, instead my intention was to "push" for primary PCI for AMI, it left me seething until the blessing of a busy schedule and a forgetful post menopausal brain took its toll.
None the less, an honest open discussion is always welcome here but I would appreciate it if everyone would just divulge their affiliations up front so that the context of their opinions could be better understood.

I also insist that the compliance described by you William B. is rather astounding and a bit unbelieveable, however if it's accurate, you are to be congratulated.




Dr. Blanchett, in response to Dr. Shirley-Walton's statement that she relies on stress testing:

I think that the threshold of comfort you get from stress test stratification is different than what I consider acceptable. It is hard for me to tell a bereaved spouse that the departed did everything I suggested and still died from a MI. Coronary calcium imaging provides me the tool that I need.

Are you aware that there are a number of studies that show a dramatic increase in risk of MI in individuals with an annualized increase in calcified plaque burden of >14%? I consider this to be a valuable measure of inadequacy of medical management. A stress test does not become positive until we have catastrophically failed in medical management. Consequently, even in the patient with “high risk” stratification, one can justify a calcium score to establish a baseline to measure adequacy of primary prevention. Calcium scores by EBT cost about 1/5th the cost of a nuclear stress test and subject the patient to 1/10th the radiation of nuclear imaging and provides more precise information.

Regarding John Q, I do not think that non-medical prospective should be excluded from this blog. I think we as physicians benefit from hearing how the non-physician public views medicine. I have become much better at what I do by listening to my patients and learning from them.


Dr. Blanchett continues:

Yes, I have seen a dramatic reduction in coronary events. Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk facto is low risk and most are do not qualify for preventive treatment. EBT calcium imaging could have identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Ateriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card


Melissa, I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test.
Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of patients with less than 70% vessel obstruction will pass thier stress test.


William, regarding your question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologists stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.



John Q. Public jumps into the fray with:

Fascinating, isn't it, that there appear to be two doctors, William Blanchet in this forum and Dr. William Davis, FACC, of cureality.com that both claim to have dramatically reduced risk of heart attack among their patients and/or actual calcium plaque score regression and BOTH are ardent proponents of CT Calcium Scoring?


Despite Dr. Blanchet's persuasive arguments backed up with numerous scientific citations and John Q.'s support, I sense they had no effect whatsoever on Shirley-Walton's way of thinking.

Such are the deeply-entrenched habits of the cardiology community. It will be many years and impassioned pleas to see things in a different light before the wave of change seizes hold.

To learn how to eat . . . try fasting

Curious thing about fasting: It teaches you how to eat.

In previous posts, I've discussed the potential benefits of fasting: reduction of blood pressure, reduction of inflammatory responses, drop in blood sugar, weight loss, and reduced heart attack risk. In my recent Heart Scan Blog post, Fasting and Heart Disease, I discussed the just-released results of a study in people who fast for religious reasons and experience less heart disease.

Fasting can mean going entirely without food and just making do with (plenty of) water, or it can mean variations on "fasting" such as vegetable juice fasts, soy milk fasts, etc.

How can fasting teach you any lessons about food and eating?

People who fast will tell you that the experience:

--Helps you appreciate food tastes when you resume eating. After a fast, flavors are stronger; sensations like sweet, sweet, or salty are sharper; you become reacquainted with the variety of wonderful food textures.

--Makes you realize how you ate too much before your fast. After a fast, you are satisfied with less. You will eat more for taste and enjoyment, less for satiety and mindless indulgence.

--Makes you more mindful of the act of eating. For many of us, eating is an automatic activity that provides fleeting satisfaction. After a fast, each bite of food brings its own special enjoyment.

--Reveals to you how awful you felt when many foods were eaten. For example, many people are physically slightly ill after eating pancakes, pizza, or other highly processed foods but cease to recognize it. Remove the offensive foods entirely and you might realize just how bad you felt.

--Takes away fear of hunger. Many people have a gut-wrenching fear of hunger. It's probably partly instinctive, that animal-like fear of not knowing when your next meal is coming, partly the abnormal, artificial drive to eat ignited by processed foods like wheat and corn syrup.

--Makes you realize just how much of your day is spent in some activity associated with food. Shopping, eating, cleaning up afterwards, thinking and talking about food all occupy an extraordinary portion of everyone's life. A fast can open your eyes to just how much time is spent in these pursuits. Sometimes, gaining an awareness of a mindless, repetitive behavior can provide the first step towards changing direction.


Most people consider a fast for rapid weight loss. But fasting is far more than that. Perhaps fasting has become an integral part of many religious practices because of its capacity for enlightenment, reawakening, revelation, but not of only the spiritual, but also of how far many of us have strayed in diet.

Fasting is what Omnivore's Dilemma author Michael Pollen might describe as looking the pig you're about to eat in the eye, an opportunity to open your eyes to what it is you 've been doing all these years.
All posts by william-davis

Emmer, einkorn, and agribusiness

10,000 years ago, Neolithic humans did not obtain wheat products from the bagel shop, grocery store, or Krispy Kreme. They obtained wheat by locating a nearby wild-growing field of wild emmer or einkorn wheat grass, then harvesting it with their stone sickles.

Neolithic humans, such as the Natufians of the Fertile Crescent, carried their freshly-cut wheat home, then ground it by hand using homemade mortar and pestle. As yeast-raised bread was still some 5000 years in the future, emmer and einkorn wheat was not used to bake bread, but was consumed as a porridge in bowls. Einkorn has the simplest genetic code of 14 chromosomes, while emmer has 28 chromosomes.

A third variety of wheat appeared on the scene around 9000 years ago, a natural hybridization between emmer and goat grass, yielding the 42-chromosome Triticum aestivum species. Egyptians learned how to cause wheat to rise around 3000 BC, yielding bread, rather than the unleavened flatbreads of their predecessors.

From the original three basic varieties of wheat available to Neolithic man, over the past 30 years wheat has exploded to over 25,000 varieties. Where did the other 24,997+ strains come from?

In the 1980s, thousands of new wheat strains arose from hybridization experiments, many of them conducted in Mexico. Then, in the late 1980s, genetic engineering quietly got underway in which geneticists inserted or deleted single genes, mostly designed to generate specific characteristics, such as height, yield per acre, drought resistance, but especially resistance to various pesticides and weed killers. The fruits of these efforts were introduced into the market in 1994. Most of the genetically modified foods were thought to be only minor modifications of the unmodified original and thus no safety testing in animals or humans was conducted.

We now have many thousands of wheat strains that are different in important ways from original emmer, einkorn, and Triticum aestivum wheat. Interestingly, it has been suggested that einkorn wheat fails to provoke the same immune response characteristic of celiac disease provoked by modern wheat gluten, suggesting a different amino acid structure in gluten proteins. Another difference: Emmer wheat is up to 40% protein, compared to around 12% protein for modern wheat.

In other words, the wheat of earlier agricultural humans, including the wheat of Biblical times, is NOT the wheat of 2010. Modern wheat is quite a different thing with differing numbers of chromosomes, different genes due to human manipulation, varying gluten protein composition, perhaps other differences.

Somewhere in the shuffle and genetic sleight-of-hand that has occurred over the last 30 years, wheat changed. What might have been the "staff of life" has now become the cause of an incredible array of diseases of "wheat" intolerance.

Near-death experience with nattokinase

This is a true story that I personally witnessed.

A 60-some year old man heard that nattokinase "thinned the blood." So he had been taking it for the past 6 months.

One week before he came to see me, he abruptly became quite breathless. He was unable to walk more than 20 feet or bend over to tie his shoes due to the breathlessness.

He came to see me in the office. I was alarmed by how breathless he was without signs of heart failure or other obvious explanation. I sent him for an immediate CT pulmonary angiogram. Within 30 minutes, we had the diagnosis: a large "saddle" pulmonary embolus, meaning a large blood clot that straddled the right and left main pulmonary arteries. One wrong move and . . . bang! He would have been dead within a couple of minutes, since a large clot can completely occlude the large arteries feeding the lung, essentially corking any blood circuiting through the lungs and back to the left side of the heart. (Causing, incidentally, electromechanical dissociation, in which the heart keeps beating for a few minutes but no blood is being pumped. CPR can keep you alive for a few minutes, then it's over.)

When I advised the patient of the diagnosis (after initiating the REAL anticoagulants), he said, "But I was taking nattokinase!"

Exactly. Blood clots are no laughing matter. They are potentially fatal events. Betting your life on some company's advertisement is nothing short of foolish.

Anyone who reads The Heart Scan Blog knows that I am an avid supporter of nutritional supplements. I even write articles and consult for the supplement industry. But I truly despise hearing unfounded marketing claims that some supplement companies will make in the pursuit of a fast buck.

There is no doubt that we need better, safer methods to deal with dangerous blood clots, whether in the lung, pelvis, or other areas. But, before anyone takes a leap based on the extravagant marketing claims made by a supplement manufacturer, you want to be damn sure there are real data--not marketing claims, REAL data--before you use something like nattokinase in place of a proven therapy.

Don't confuse the very interesting, though unpalatable, natto with nattokinase. Natto contains vitamin K2 and some other interesting compounds, including nattokinase.

Blame the gluten?

Wheat is among the most destructive components of the human diet, a food that is responsible for inflammatory disease, diabetes, heart disease, several forms of intestinal diseases, schizophrenia, bipolar illness, ADHD, behavioral outbursts in autistic children . . . just to name a few.

But why?

Wheat is mostly carbohydrate. That explains its capacity to cause blood sugar to increase after eating, say, a turkey sandwich on whole wheat bread. The rapid release of sugars likely underlies its capacity to create visceral fat, what I call "wheat belly."

But neither the carbohydrate nor the other components, like bran and B vitamins, can explain all the other adverse health phenomena of wheat. So what is it in wheat that, for instance, worsens auditory hallucinations in paranoid schizophrenics? Is it the gluten?

First of all, what is gluten?

Gluten protein is the focus of most wheat research conducted by food manufacturers and food scientists, since it is the component of wheat that confers the unique properties of dough, allowing a pizza maker to roll and toss pizza crust in the air and mold it into shape. The distinctive “doughy” quality of the simple mix of wheat flour and water, unlike cornstarch or rice starch, for instance, properties that food scientists call “viscoelasticity” and “cohesiveness,” are due to the gluten. Wheat is mostly carbohydrate, but the 10-15% protein content is approximately 80% gluten. Wheat without gluten would lose its unique qualities that make it desirable to bakers and pizza makers. Gluten is also the component of wheat most confidently linked to immune diseases like celiac.

The structure of gluten proteins has proven frustratingly elusive to characterize, as it changes over time and varies from strain to strain. But an understanding of gluten structure may be part, perhaps most, of the answer to the question of why wheat provokes negative effects in humans.

The term “gluten” encompasses two primary families of proteins, the gliadins and the glutenens. The gliadins, one of the protein groups that trigger the immune response in celiac disease, has three subtypes: a/ß-gliadins, ?-gliadins, and ?-gliadins. The glutenins are repeating structures, or polymers, of more basic protein structures.

Beyond gluten, the other 20% or so of non-gluten proteins in wheat include albumins, prolamins, and globulins, each of which can also vary from strain to strain. In total, there are over 1000 other proteins that serve functions from protection of the grain from pathogens, to water resistance, to reproductive functions. There are agglutinins, peroxidases, a-amylases, serpins, and acyl CoA oxidases, not to mention five forms of glycerinaldehyde-3-phosphate dehydrogenases. I shouldn’t neglect to mention the globulins, ß-purothionin, puroindolines a and b, tritin, and starch synthases.

As if this protein/enzyme smorgasbord weren’t enough, food processors have also turned to fungal enzymes, such as cellulases, glucoamylases, xylanases, and ß-xylosidases to enhance leavening and texture. Many bakers also add soy flour to enhance mixing and whiteness, which introduces yet another collection of proteins and enzymes.

In short, wheat is not just a simple gluten protein with some starch and bran. It is a complex collection of biological material that varies according to its genetic code.

While wheat is primarily carbohydrate, it is also a mix of gluten protein which can vary in structure from strain to strain, as well as a highly variable mix of non-gluten proteins. Wheat has evolved naturally to only a modest degree, but it has changed dramatically under the influence of agricultural scientists. With human intervention, wheat strains are bred and genetically manipulated to obtain desirable characteristics, such as height (ranging from 18 inches to over 4 feet tall), “clinginess” of the seeds, yield per acre, and baking or viscoelastic properties of the dough. Various chemicals are also administered to fight off potential pathogens, such as fungi, and to activate the expression of protective enzymes within the wheat itself to “inoculate” itself against invading organisms.

From the original two strains of wheat consumed by Neolithic humans in the Fertile Crescent 9000 years ago (Emmer and Einkorn), we now have over 200,000 strains of wheat virtually all of which are the product of genetic manipulations that have modified the protein structure of wheat. The extraordinary complexity of wheat proteins have therefore created a huge black box of uncertainty in pinpointing which protein causes what.

But there's an easy cure for the uncertainty: Don't eat it.

Glycemic gobbledygook

The concept of glycemic index is meant to help determine what foods raise blood sugar a lot vs. what foods raise blood sugar a little. Dr. Jennie Brand-Miller's searchable database can be found here.

I have to admit that glycemic index provided me with a sense of false assurance for some years. It screwed up my health until I came to understand the issues a lot better.

For those of you just starting out in nutritional conversations, glycemic index (GI) represents a comparison of the blood glucose area-under-the-curve (AUC) over 2 hours after consuming 50 grams of the food in question compared to the AUC of glucose or white bread. Volunteers involved in developing these values are healthy people who are generally of normal weight.

Glucose, by definition, has a GI of 100. An equal quantity of sucrose (50% glucose, 50% fructose) has a GI of 60, lower than glucose. An equal quantity of whole wheat bread has a GI of 68-77 (Yes: The GI of whole wheat is higher than sucrose). Non-carbohydrate foods, such as eggs or avocado, have no GI since they do not impact on blood glucose.

Because the GI is also sensitive to how much carbohydrate is contained, the concept of Glycemic Load (GL) was introduced:

GL = (GI x amount of carbohydrate) / 100

GL is therefore the GI that incorporates the glycemic potential of the food of interest. GI does not vary with portion size; GL varies with portion size.

Let's take whole wheat pasta, a food regarded by most people as a healthy choice. Whole wheat pasta has a GI of 55--fairly low--and a GL of 29. A serving of 180 g (approximately 6 oz cooked) provides 50 g carbohydrates.

People who advocate that low-glycemic index foods would say that this is a desirable profile and should therefore replace high-glycemic index foods.

I say WRONG. First of all, most of us are not slender 20-somethings. We will therefore not show the same response as a young, slender person (like the GI volunteers), but will show exagerrated blood sugar responses. So this much low-glyemic index whole wheat pasta will typically yield a blood sugar of 120-200 mg/dl in non-diabetic people, high enough to trigger glycation. Sure, a high-glycemic index food, such as white flour birthday cake with plenty of sugary icing, might trigger a blood sugar of 140-250 mg/dl, much worse. But that doesn't make the lower blood sugar following pasta any less bad--it's still terrible.

Another issue: GI is assessed over a 2-hour timeline. What if blood sugar remains high in a sustained way, say, over 6 hours? That's precisely what whole wheat pasta will do: Keep blood sugar high for an extended period.

So not only does a low-glycemic index food like pasta increase blood sugar in most of us extravagantly, it does so in a sustained way.

Lastly, low-glycemic index pasta still triggers small LDL particles to an extreme degree, as I discussed in the previous Heart Scan Blog post, Small LDL: Complex vs. simple carbohydrates.

Don't be false reassured by the notion of low GI or GL. In fact, I'd go so far as to say that NO glycemic index is a GOOD glycemic index (or load). The foods we want to dominate our diet are the foods that aren't even listed in the GI database.

Man walks after removing wheat

No, this isn't some National Enquirer headline like "Woman delivers alien baby."

Tom is a 26-year old man with a complex medical condition, a malformation he was born with and has had reconstructed. Aside from this, he leads a normal life: works, is married, and is, in fact, quite intelligent.

He came to me for an opinion regarding his overall health. Tom was worried that his congenital condition would impair his long-term health and longevity prospects, so he wanted to optimize all other aspects of his health.

But, when I examined Tom, he could barely get himself up on the exam table without wincing in pain. When I asked him to walk, he hobbled a few steps, again clearly in pain. When I asked him what hurt, he said "everything." He said that all his joints hurt just to move.

He told me that his several doctors over the years didn't know why he was in such pain: It wasn't rheumatoid arthritis, gout, pseudogout, or any of the other inflammatory joint diseases that might account for virtually incapacitating this 26-year old man. Even the rheumatologists were stumped. It was also unrelated to his repaired congenital condition. So Tom went on with his life, barely able to even go for a walk with his wife without pain, slowing him down to the pace of an 80-year old.

So I suggested that he eliminate all wheat products. "I don't know for a fact whether it will work, Tom. But the only way to find out is to give it a try. Why not try a 4-week period of meticulously avoiding wheat? Nothing bad will come of it."

He and his wife look perplexed, but were so desperate for a solution that they agreed to give it a try.

Tom returned 6 weeks later. He walked into the room briskly, then bounded up on the exam table. He told me that, within days, all his joint pains had completely disappeared. He could walk, stretch, do all the normal physical things with none of the pain he had suffered previously.

Tom told me, "I didn't think it could be true. I thought it was just a coincidence. So I had a sandwich about 2 weeks into it. In about 5 minutes, I got about half my pains back."

Tom now remains wheat-free and pain-free, thankfully with no discernible joint impairment.

So, yes, Tom walked freely and without pain simply by eliminating wheat from his life.

Is it an immune phenomenon? Does wheat gluten trigger some inflammatory reaction in some people? There is surely something like this underlying experiences like Tom.

Wheat contains far more than gluten. Modern wheat is a collection of hundreds of different proteins, though gluten is the most plentiful, the one that confers the "viscoelasticity" of dough. But there's plenty more to wheat than gluten or celiac disease.

AGEing gracefully

Advanced Glycation End-products, or AGEs, have the potential to change our entire conversation about diet.

AGEs come from two principal sources:

1) Endogenous--Glucose-protein interactions that arise from high blood glucose levels

2) Exogenous--From diet

The first is sensitive to glucose levels: the higher the glucose level, the greater the AGE formation. The second depends on the quantity of AGE in the food consumed.

A compelling body of evidence points towards AGEs as an agent of aging, as well as kidney dysfunction, dementia, and atherosclerosis. Some of the observations made include:

--If AGEs are infused into an experimental animal, it develops atherosclerosis, kidney disease, and other "diseases of senescence" within weeks to months.

--In endothelial cells (cells lining arteries), AGE induces expression of adhesion molecules and inflammatory signals. In fibroblasts, AGE provokes collagen production. In smooth muscle cells, AGE triggers migration and proliferation. In monocytes and macrophages, AGEs induce chemotaxis and release of inflammation mediators. In short, AGEs have been implicated in just about every step leading to atherosclerosis.

--In humans, greater quantities of AGEs are present in diabetics, pre-diabetics and people with insulin resistance. We all know that these people develop atherosclerosis, kidney disease, cataracts, and other conditions at an accelerated rate.

--Foods containing greater quantities of AGEs cause endothelial dysfunction, i.e., artery constriction via blockade of nitric oxide and other mechanisms.

Short of taking agents that block AGE activity, how can you minimize the absorption or production of AGEs? There are two general strategies:

1) Keep blood glucose low--The Whitehall study demonstrated increased cardiovascular mortality with a postprandial (actually 2-hour post- 50-gram glucose challenge) blood sugar of 83 mg/dl. Lower blood glucose, less glycation. Less carbohydrates in the diet, the lower the blood sugar, the less the glycation. Studies like Whitehall demonstrate that glycation begins with glucose values within the normal range. Thus, aging occurs even with normal glucose levels. It occurs faster with higher glucose levels.

2) Choose and prepare foods with lower AGE content. Food content of AGEs is a major determinant of blood AGE levels. Fats and meats are the primary dietary source of AGEs, particularly if cooked at high temperature (broiling, frying). While this does not mean that meats and fats need to be avoided, it can mean that limiting serving size of meats and fats, while being selective in how they are prepared, are important. This can mean cutting your meats in thinner slices or smaller pieces to permit faster cooking, eating rare when possible (not poultry, of course), avoiding cooking with sauces that contain sugar (which enhances AGE formation). Is this an argument in favor of sashimi?

Minimizing exposure to AGEs, endogenous or exogenous, has the potential to slow the aging process, or at least to lessen the likelihood of many of the phenomena of aging.

More on this to come.

Small LDL: Simple vs. complex carbohydrates

Joseph is a whip-smart corporate attorney, but one who accepts advice at his own pace. He likes to explore and consider each step of the advice I give him.

Starting (NMR) lipoprotein panel on no treatment or diet change:

LDL particle number 2620 nmol/L (which I would equate to 262 mg/dl LDL cholesterol)
Small LDL 2331 nmol/L--representing 89% of LDL particle number, a severe dominance of small LDL

I advised him to eliminate wheat, cornstarch, and sugars, while limiting other carbohydrate sources, as well. Joseph didn't like this idea very much, concerned that it would be impractical, given his busy schedule. He also did a lot of reading of the sort that suggested that replacing white flour with whole grains provided health advantages. So that's what he did: Replaced all sugar and refined flour products with whole grains, but did not restrict his intake of grains.

Next lipoprotein panel with whole grains replacing white refined flour:

LDL particle number 2451 nmol/L
Small LDL 1998 nmol/L--representing 81.5% of LDL particle number.

In other words, replacing white flour products with whole grain products reduced small LDL by 14%--a modest improvement, but hardly great.

I explained to Joseph that any grain, complex, refined, or simple--will, just like other sugars and carbohydrates, still provoke small LDL. Given the severity of his patterns, I suggested trying again, this time with full elimination of grains.

Next lipoprotein panel with elimination of whole grains:

LDL particle number 1320 nmol/L
Small LDL 646 nmol/L
--48.9% of total LDL particle number, but a much lower absolute number, a reduction of 67.6%.

This is typical of the LDL responses I see with elimination of wheat products on the background of an overall carbohydrate restriction: Big drops in precisely measured LDL as LDL particle number (i.e., an actual count of LDL particles, not LDL cholesterol) and big drops in the number of small LDL particles.

You might say that wheat elimination and limitation of carbohydrate intake can yield statin-like values . . . without the statin.

Is Cocoa Puffs no longer heart healthy?

Until recently, Cocoa Puffs enjoyed the endorsement of the American Heart Association (AHA) as a heart-healthy food.

For a price, the AHA will allow food manufacturers to affix a heart "check mark" signifying endorsement by the AHA as conforming to some basic "heart healthy" requirements.

Odd thing: The list of breakfast cereals on the check mark program has shrunk dramatically. When I last posted about this, there were around 50-some breakfast cereals, from Cocoa Puffs to Frosted Mini Wheats. Now, the list has been trimmed down to 17:

Berry Burst Cheerios-Triple Berry
Cheerios
Cheerios Crunch
Honey Nut Cheerios
Kashi Heart to Heart Honey Toasted Oat Cereal
Kashi Heart to Heart Oat Flakes & Wild Blueberry Clusters
Kashi Heart to Heart Warm Cinnamon Oat Cereal
Multi Grain Cheerios
Oatmeal Crisp Crunchy Almond
Oatmeal Crisp Hearty Raisin
Quaker Cinnamon Life
Quaker Heart Health
Quaker Life
Quaker Life Maple & Brown Sugar
Quaker Oat Bran
Quaker Oatmeal Squares - Brown Sugar
Quaker Oatmeal Squares - Cinnamon


According to sales material targeted to food manufacturers, the American Heart Association boasts that "The American Heart Association’s heart-check mark is the most recognized and trusted food icon today . . . Eighty-three percent of consumers are aware of the heart-check mark. Sixty-six percent of primary grocery shoppers say the heart-check mark has a strong/moderate influence on their choices when shopping."

So, is Cocoa Puffs no longer heart healthy?

I suspect that agencies like the AHA, the USDA, the American Diabetes Association as starting to understand that they have blundered big time by pushing low-fat, having contributed to the nationwide epidemic of obesity and diabetes, and that it is time to quietly start backpedaling.

While it's a step in the right direction, judging from the above list of breakfast cereal "survivors" of the check mark program, the criteria may have been tightened . . . but not that much.

Fractures and vitamin D

This is a bit off topic, but it's such an interesting observation that I'd like to pass it on.

Over the past several years, there have been inevitable bone fractures: People slip on ice, for instance, and fracture a wrist or elbow. Or miss a step and fracture a foot, fall off a ladder and fracture a leg.

People will come to my office and tell me that their orthopedist commented that they healed faster than usual, often faster than anyone else they've seen before. My son was told this after he shattered his hand getting slammed against the boards in hockey; his orthopedist took the screws and cast off much sooner than usual since he judged that healing had occured early. (My son was taking 8000 units vitamin D in gelcap form; I also had him take 20,000 units for several days early after his injury to be absolutely sure he had sufficient levels.)

My suspicion is that people taking vitamin D sufficient to enjoy desirable blood levels (I aim for a 25-hydroxy vitamin D level of 60-70 ng/ml) heal fractures much faster, abbreviating healing time (crudely estimated) by at least 30%.

For any interested orthopedist, it would be an easy clinical study: Enroll people with traumatic fractures, randomize to vitamin D at, say, 10,000 units per day vs. placebo, watch who heals faster gauged by, for instance, x-ray. My prediction: Vitamin D will win hands down with faster healing and perhaps more assured fusion of the fracture site.

T3 for accelerating weight loss

Supplementation of the thyroid hormone, T3, is an underappreciated means to lose weight.

Thyroid health, in general, is extremely important for weight control, since even subtle low thyroid hormone levels can result in weight gain. The first step in achieving thyroid health is to be sure you are obtaining sufficient iodine. (See Iodine deficiency is real and Healthy people are the most iodine deficient) But, after iodine replacement has been undertaken, the next step is to consider your T3 status.

I've seen T3 ignite weight loss or boost someone out of a weight loss "plateau" many times.

Endocrinologists cringe at this notion of using T3. They claim that you will develop atrial fibrillation (an abnormal heart rhythm) and osteoporosis by doing this. I have yet to see this happen.

Adding T3 revs up metabolic rate at low doses. The idea is to push free T3 hormone levels to the upper limit of normal, but not to the hyperthyroid range. While an occasional person feels a little "hyper" like they've had a pot of coffee, most people just feel energized, clear-headed, and happier. And weight trends down much more readily.

Taking T3 by itself with no effort at weight loss generally yields only a modest weight reduction. However, T3 added to other weight reducing efforts, such as wheat elimination and exercise, accelerates the weight loss effect considerably. 5 lbs lost will likely be more like 8 to 10 lbs lost; 10 lbs lost will likely be more like 15 to 20 lbs, etc.

It's also my suspicion that more and more people are developing a selective impairment of T3, making it all the more important. I believe that you and I are being exposed to something (perchlorates, bisphenol A, perflurooctanoic acid, and others?) that may be impairing the 5'-deiodinase enzyme that converts the T4 thyroid hormone to the active T3. Relative lack of T3 leads to slowed metabolism, weight gain, and depressed mood. While avoiding or removing the toxin impairing 5'-deiodinase would be ideal, until we find out how to do this, taking T3 is a second best.

The tough part: Finding a prescriber for your T3.