When meat is not just meat


The edgy nutrition advocate, Mike Adams, over at NewsTarget.com came up with this scary photo tour of a processed meat product from Oscar Mayer: Mystery Meat Macrophotography: A NewsTarget PhotoTour by Mike Adams







Along with increasingly close-up photographs of this meat-product, Adams lists the ingredients in Oscar Mayer's Cotto Salami:


Beef hearts
Pork
Water
Corn syrup
Beef

Contains less than 2% of:
Salt
Sodium lactate
Flavor
Sodium phosphates
Sodium diacetate
Sodium erythorbate
Dextrose
Sodium nitrite
Soy lecithin
Potassium phosphate
Potassium chloride
Sugar


As I reconsider the role of saturated fat in diet, given the startlingly insightful discussion by Gary Taubes of Good Calories, Bad Calories, I am reminded that not all meat is meat, not all saturated fat sources are equal.

I am concerned in particular about sodium nitrite content, a color-fixer added to cured meats that caused a stir in the 1970s when data suggesting a carcinogenic effect surfaced. The public's effort to remove sodium nitrite from the food supply was vigorously opposed by the meat council and it remains in cured meats like sausage, hot dogs, and processed meats like Cotto Salami. A 2006 meta-analysis (combined analysis of studies) of 63 studies did indeed suggest that sodium nitrite was related to increased risk of gastric cancer. This argument is plausible from animal models of cancer risk, as 40 animal models have likewise suggested the same carcinogenic association.

Also, fructose? This is most likely added for sweetness. Recall that fructose heightens appetite and raises triglycerides substantially.

I personally have a natural aversion to meat. I don't like the taste, the look, smell, and the thought of what the animal went through to make it to the supermarket. But, considered from the cold, carnivorous viewpoint of the question, "Is meat okay to eat?", among the issues to consider is whether the meat has been cured or processed, and does that process include addition of sodium nitrite.

Cotto Salami and similar products are not, of course, what carnivorous humans in the wild ate. This is a processed, modified product created from factory farm animals raised in cramped conditions and fed corn and other cheap, available foods. It is not created from free-ranging animals wandering their pastures or pens, eating diets nature intended. This results in modified fat composition, not to mention hormones and antibiotics added. These are not listed on the ingredients. Wild meat does not contain fructose or color-fixers, either.

So don't mistake "meat" in your grocery store for meat. It might look and smell the same--until you look a little closer.



Copyright 2007 William Davis, MD

Don't lament no OTC mevacor

After Merck's third go at FDA approval for over-the-counter (OTC) status for its statin cholesterol drug, Mevacor (lovastatin), the FDA advisory board suggested that its request be denied. They expressed concern that too many people would not understand how the drugs would be used and that misuse would be common.

Similar sentiments were echoed by Dr. Sidney Wolfe, director of the Health Research Group at Public Citizen; the American Medical Association (though the AMA always fights anything that threatens to erode physician control over health); and the de facto spokesman for cardiologists, Dr. Steven Nissen of the Cleveland Clinic.

Although I am a supporter for tools and legislation that yield greater self-empowerment in health care to the public, there is no need to lament the failed OTC status for Mevacor. For one, Merck had no plans to reduce the price on its OTC preparation. For many people, this would have meant an increase in cost, since health insurers would surely not cover a non-prescription agent.

Second, OTC status sends the implicit message that cholesterol is the most common cause of heart disease; it is not. (Small LDL particles are the number one cause, a pattern only partially addressed by any statin drug and a pattern largely responsible for the failure of statin drugs to "cure" heart disease despite pharmaceutical manufacturer's attempts to increase doses to take up any slack in effect.)

Thirdly, you can achieve the same effect--no, a superior effect--by incorporating several simple strategies into your life. These strategies are superior to Mevacor because they do more than just reduce LDL cholesterol. You can achieve similar LDL-reducing effect to Mevacor, 20 mg, just by adding:

--2 tablespoons oat bran or ground flaxseed per day (choose flaxseed if you have sugar problems or small LDL; flaxseed contains no digestible sugars, only protein and fiber)
--Raw almonds or walnuts--at least a handful, though more is fine and will not make you fat. (It's nuts like party mixes, mixed nuts roasted in unhealthy oils, and honey-roasted nuts that make us fat, not raw.)
--Soy protein sources--probably the weakest effect of all foods listed, but a contributor that can be obtained in a variety of forms, such as tofu, soy protein powders, and soy milk.
--Other foods that reduce LDL include pectin sources (e.g., citrus rind), flavonoids (e.g., green tea); stanol esters found in butter substitute Benecol (recall that sterol-containing products like Take Control and the flood of new products on the market like HeartWise orange juice might have potential for allowing sterol esters to enter the blood, so I do NOT recommend them); and, of course, niacin.

Many of these strategies also reduce small LDL, raise HDL, reduce triglycerides, and reduce blood sugar, effects that go beyond that achieved with Mevacor. Of course, a combination strategy is not as easy as popping one pill a day, it's better for you.

I will certainly not shed any tears for Merck and its relentless efforts to gain a stronger foothold in the "transform conditions into diseases" marketing strategy, the same strategy that classifies shyness, toe fungus, and sadness into medical conditions necessitating medication. While I do generally support efforts to increase public access to strategies that increase their health care power, this one was not necessarily all good.

Members of Track Your Plaque can read the complete report, Unique nutritional strategies to Reduce cholesterol naturally on the Track Your Plaque website.



Copyright 2007 William Davis, MD

Damage control

Medical device manufacturer, Cordis, is launching a new marketing program to promote its Cypher drug-coated stent. You can view the details at www.CypherUSA.com , including the slick TV commercial that HeartHawk posted a blog about.

The campaign opens with:

When you open up your heart, you open up your life.

Lives hampered by angina. By shortness of breath. By restricted blood flow. These lives are changing. Because of a state-of-the-art advancement. One that can have a huge impact on arteries around your heart. The CYPHER® Stent. It can open up your arteries. Increase flow of blood and oxygen. And change your restricted life. To an active life worth living. Your new life is...

Life Wide Open


Direct-to-consumer drug advertising has been around for a few years. While it has increased awareness of drugs and the "conditions" they are supposed to treat, it has also highlighted the aggressive profit-motive of the drug industry. This is not health care for the needy and sick, but health care for profit.

So now we're beginning to see the emergence of direct-to-consumer (DTC) advertising for medical devices. There was also a brief, though unsuccessful, foray into DTC advertising for implantable defibrillators, of all things, by Medtronic a couple of years ago, also.

What is the purpose of Cordis' marketing effort? Is it to educate and inform the public who might unknowingly receive non-drug coated stents and be deprived of the restenosis-inhibiting advantage of a drug-coated device? Is it meant to right a systematic wrong, a failure of cardiologists to insert the technologically, biologically, and ethically superior coated stents?

I find that doubtful. A more likely motive is damage control. With some of the (both deserved and undeserved) negative press the drug-coated stents have received lately, Cordis, eager to protect their $20 billion (annual revenues, 2006) medical device franchise, came up with this DTC strategy. After viewing the smiling faces of people , elated because of their "wide open" arteries and lives, Cordis hopes to see people going to their doctors insisting on the stent that is "opening millions of lives," since, "when your arteries narrow, so does your life."

Cool, trendy, liberating. That's the message they wish to deliver. Cool music, beautiful people, flashy high-tech images. Who wouldn't want a Cypher stent?

Beyond damage control, it's a familiar marketing theme: You're slender, glamorous, and sexy if you drink Coke, you're a caring mother if you feed your children Jif peanut butter, you're health conscious and smart if you eat Total cereal . . . you're cool and know what you want from life if you insist on a Cypher stent.

I don't object to advertising. It's part of the capitalistic economic system. It drives awareness and grows businesses. I do get concerned when advertising is so slick and effective that the people who are not properly armed with information can be duped into thinking that they need something that they don't really need.

Or, for which there are powerful, viable alternatives. Even hear about "prevent the disease in the first place?"

Low expectations

The Framingham Risk Calculator is a standard method used by many physicians to predict risk for heart attack or death from heart disease over a 10-year period. Low-risk is defined as <10% risk of heart attack or cardiac death over 10 years; high-risk is defined as 20% or more over 10 years; intermediate-risk is in between.

Let's put it to the test:

Amy is a 53-year old businesswoman. She is 5 ft 4 inches, weighs 150 lbs. Her father had a heart attack in his early 50s followed by the usual list of hospital procedures including bypass surgery at age 60.

What is Amy's risk for heart attack or death from heart disease over the next 10 years? If we enter her data into the Framingham risk calculator, the following result is returned:

Information about your risk score:
Age: 53
Gender: female
Total Cholesterol: 198 mg/dL
HDL Cholesterol: 74 mg/dL
Smoker: No
Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No
Risk Score: 1% Means 1 of 100 people with this level of risk will have a heart attack in the next 10 years.


So, according to the Framingham calculation, Amy has <1% risk for heart attack or death from heart disease over the next 10 years. Most primary care physicians would, at most, prescribe a statin drug and talk about a reduction in saturated fat.

Thankfully, Amy didn't fall for that bit of conventional mis-information. She instead got a CT heart scan, principally because of her father's history. Her score: 117. At age 53, this put her into 90th percentile, in the worst 10% of scores for women in her age group (50-55). By heart scan criteria, her risk for heart attack is probably more like 4-5% per year, or approximately 40-50% over the next 10 years.

Let's do just a bit more math. If Amy hadn't known about her heart scan score and no preventive action was taken, the expected progression of her heart scan scores would likely be:

Start: 117
Year 1: 152
Year 2: 198
Year 3: 257
Year 4: 335
Year 5: 436
Year 6: 567
Year 7: 737
Year 8: 958
Year 9: 1245
Year 10: 1618

In fact, given Amy's starting heart scan score of 117, it is highly unlikely that she survives the next 10 years without heart attack or a fatal heart event. Yet the Framingham risk calculator puts Amy's risk at less than 1%. Could anything be more wrong?

The folly of the Framingham calculator was highlighted by a recent publication from the large Multi-Ethnic Study of Atherosclerosis (MESA), in which 3600 women (45-84 years), all of whom fell into the "low-risk" category by the Framingham calculator--just like Amy--were tracked over approximately 3 3/4 years. This study generated several observations:

1) 30% of the "low-risk" women had positive heart scan scores.
2) 5% of the "low-risk" women had scores of 300 or greater (very significant for a woman). 8.6% of these women experienced a cardiovascular event like heart attack or death over the period. Women with a heart scan score of 300 or greater had a 22-fold greater event risk compared to women with zero heart scan scores.
3) Women with heart scan scores of 1 to 299 had a cardiovascular event risk of approximately 5-fold greater risk over the period.


Across the U.S., 90% of women younger than 70 years old fall into the Framingham "low-risk" category. Yet this fiction is accepted as the prevailing standard, along with LDL and total cholesterol, for determination of risk in women and men.

In my view, using the Framingham risk calculator is a misguided, misleading path, one that will mis-classify a substantial number of women who could otherwise be spared from heart attack and catastrophe.

By the way, Amy is also the Track Your Plaque program record holder (by percentage drop), with a 63% drop in heart scan score over a 15 month period.

Niacin vs. low-carb weight loss

Niacin:

--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.
--Reduces total LDL.
--Reduces small LDL particles.
--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein).
--Reduces fibrinogen.
--Reduces inflammatory responses.


Weight loss achieved through a low-carbohydrate (read "wheat-free") diet:

--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.
--Reduces total LDL.
--Reduces small LDL particles.
--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein).
--Reduces fibrinogen.
--Reduces inflammatory responses.


Curious, isn't it? Niacin achieves virtually the same effect as weight loss achieved through a low-carbohydrate diet, particularly if free of wheat products. The only major difference is that niacin also reduces lipoprotein(a), though even that distinction shrinks if monounsaturated fat sources like almonds are included in a low-carbohydrate program.

So which should you do first if you have any of the above patterns? Well, it's a question of 1) severity, 2) how carbohydrate-rich your starting diet is, 3) how much weight you could stand to lose, and 4) how urgent your program is (determined largely by your heart scan score).

Niacin can also be very helpful if you've taken full advantage of weight loss through a carbohydrate-restricted program, yet still retain some of the abnormal lipoprotein patterns that could continue to grow coronary plaque. For instance, if HDL cholesterol rises from 28 to 40 mg/dl by eliminating wheat and reducing carbohydrates and losing weight, niacin could raise HDL to 50 mg/dl or higher.

As much as I love and use niacin for its broad array of plaque-controlling effects, a low-carbohydrate, wheat-free diet can achieve many of the same effects. Use this strategy to full advantage.

Explosive plaque growth

Every once in a while, we will see someone experience more-than-expected rate of coronary plaque growth, a sudden jump in heart scan scores. I'm talking about increases in score of 50%, even 100%, sometimes despite favorable lipid and lipoprotein patterns.

It's not always easy to pin this phenomenon down, since we often detect it after a year or more on a repeat heart scan. It would be wonderfully insightful to perform heart scans more frequently and track plaque growth more precisely, but of course, radiation exposure is the most important limiting factor, as is cost.

So this list is, admittedly, speculative. It is based on observation, on presumptive associations between events and heart scan scores. But, judging from what we do confidently know about coronary atherosclerotic plaque, I think these observations make physiologic sense.

These are the sorts of increases in heart scan score that can scare the heck out of you, silent yet explosive growth of coronary atherosclerotic plaque that can grow with no warning whatsoever.



Image courtesy Wikipedia and the United States Geological Survey.









Factors which I have observed to possibly be responsible for explosive plaque growth include:

--Overwhelming tragedy such as death of a loved one, financial ruin, divorce. One of my early and catastrophic failures was a young man in his early 40s who, in the space of just a few months, suffered the loss of his mother, a brother, and his mother-in-law, while working a high-stress job. His heart scan score doubled from around 100 to 200 in one year, despite perfect lipoproteins. He had a heart attack shortly after the second score, despite a normal stress test just months earlier. (Pessimism is tragedy's weak cousin, but one that still holds power to corrupt our otherwise best efforts at plaque reversal.)

--Substantial weight gain. In the early years of the Track Your Plaque program, before it was even called "Track Your Plaque," I witnessed a man more than double his score from 1100 to 2400 in 18 months just by allowing himself to gain 40 lbs. (I don't know what became of him. His life apparently suffered other disasters, as well, and we lost track of him.)

--Poorly-controlled diabetes. High blood sugars out of control have yielded explosive growth.

--Kidney disease--However, I am uncertain of how much this overlaps with a deficiency of vitamin D's active form, 1,25-OH-vitamin D3, the form that is often deficient in people with dysfunctional kidneys.

--An inflammatory disease that is out of control, e.g., rheumatoid arthritis.

--This is very speculative, but I've witnessed explosive growth after vaccine administration that yielded strange viral-like symptoms. In this one instance, the man was getting heart scans (on his own) every three to six months and described a severe illness following a vaccine administered in preparation for travel out of the U.S.

--Unrecognized low thyroid function--i.e., hypothyroidism. This is easily corrected with thyroid hormone replacement.


These factors can also be relative and they can be overcome. Look at our current Track Your Plaque reversal record-holder: a 53-year old woman who dropped her heart scan score an amazing 63% despite the loss of a loved one during the 15 months of her program. Despite an overwhelming tragedy, she overcame the potential adverse effects and set a record, probably a record for the entire world.

Dr. Cannell on "How much vitamin D?"

In his most recent Vitamin D Council Newsletter (reprinted in its entirety below, minus clickable links, as Dr. Cannell apparently lost his webmaster and this issue of the newsletter is therefore not posted on the Vitamin D Council website; if you would like to either donate money to the Vitamin D Council or pitch in with help with his website, go to www.vitamindcouncil.com), Dr. John Cannell once again enlightens us with some new insights into vitamin D and its enormous role in health. In this issue, he discusses the role of vitamin D in people diagnosed with cancer (treatment, not prevention).

While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels.

Dr. Cannell cites a recent study from vitamin D research expert, Dr. Bruce Hollis:

In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it: would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. (I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. 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):631-634.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

In answer to the question, "How much vitamin D should someone with cancer take?," Dr. Cannell advises:
"Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight.

Dr. Cannell, no stranger to the resisitance among many practicing physicians unaware of the expanding and robust literature on vitamin D, advises people with cancer that:
In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.



For readers wishing to read the entire text of Dr. Cannell's newsletter, it is reprinted below:

The Vitamin D Newsletter
January, 2008


The January newsletter is coming early as I will be out of touch for awhile. If you remember, the last newsletter was on preventing cancer, not treating it. Below is a sampling of the tragic emails the last newsletter generated:


"Dr. Cannell, I was just diagnosed with breast cancer, how much vitamin D should I take?"

"My mother has colon cancer, how much vitamin D should she take?"

"I've had prostate cancer for four years, is there any reason to think vitamin D would help?"

"Dr. Cannell, my son has leukemia, should I give him vitamin D?"


It's one thing to talk about evidence vitamin D may prevent cancer but something quite different to discuss evidence vitamin D might help treat cancer. I used to think the answers to all the above questions were the same. Like anyone else, people with cancer should be screened for vitamin D deficiency and be treated if deficiency is present. Simple. However, it's not that simple. The real questions are, What are reasonable 25-hydroxy-vitamin D [25(OH)D] levels for someone with a life-threatening cancer? How much vitamin D do they need to take to obtain such levels? Is there any evidence, of any kind, that vitamin D will help treat cancer? The risk/benefit analysis of taking vitamin D is quite different if you are in perfect health than if your life, or your child's life, is on the line.

Remember, unlike cancer prevention, not one human randomized controlled trial exists showing vitamin D has a treatment effect on cancer. By treatment effect, I mean prolongs the lives of cancer patients. However, as I cited in my last newsletter, Dr. Philippe Autier of the International Agency for Research on Cancer, and Dr. Sara Gandini of the European Institute of Oncology, performed a meta-analysis of 14 randomized controlled trials showing even low doses of vitamin D extend life but they looked at all-cause mortality, not just cancer (Arch Intern Med. 2007;167(16):1730-1737). However, some epidemiological studies indirectly address the treatment issue and are quite remarkable. The first are a series of discoveries by Professor Johan Moan, Department of Physics at the University of Oslo, with Dr. Alina Porojnicu as the lead author on most of the papers.

Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19

Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70.

Porojnicu AC, et al. Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8.

Porojnicu A, et al. Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8.

Porojnicu AC, et al. Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4.

Porojnicu AC, et al. Seasonal and geographical variations in lung cancer prognosis in Norway. Does Vitamin D from the sun play a role? Lung Cancer. 2007 Mar;55(3):263-70.

What Professor Moan's group discovered, repeatedly, is quite simple, whether it be cancer of the breast, colon, prostate, lung, or a lymphoma. You live longer if your cancer is diagnosed in the summer. And it is not just Moan's group who has found this. A huge English study recently confirmed Moan's discovery.

Lim HS, et al. Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6.

What do these studies mean? Something about summer has a treatment effect on cancer. Whatever it is, you live longer if you are diagnosed in the summer but die sooner if you are diagnosed in the winter. What could it be about summer? Exercise? Fresh air? Melatonin? Sunlight? Pretty girls? Remember, these patients already had cancer. Whatever it is about summer, it is not a preventative effect that Professor Moan discovered, it is a treatment effect. Something about summer prolongs the life of cancer patients.

Dr. Ying Zhou, a research fellow, working with Professor David Christiani at the Harvard School of Public Health, went one step further. The stuffy Harvard researchers assumed summer worked its magic, not by pretty girls, but by summer sunlight making vitamin D. So they looked at total vitamin D input, from both sun and diet, to see if high vitamin D input improved the survival of cancer patients. Yes, indeed, remarkably. They found that early stage lung cancer patients with the highest vitamin D input (from summer season and high intake from diet) lived almost three times longer than patients with the lowest input (winter season and low intake from diet). Three times longer is a huge treatment effect, a treatment effect that most conventional cancer treatment methods would die for.

Zhou W, Vitamin D is associated with improved survival in early-stage non-small cell lung cancer patients. Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2303-9.

And that's not all, Marianne Berwick and her colleagues, at the New Mexico Cancer Institute, found malignant melanoma patients with evidence of continued sun exposure had a 60% mortality reduction compared to patients who did not. That implies a robust treatment effect from sunlight.

Berwick M, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005 Feb 2;97(3):195-9.

I will not list the thousands of animal studies that indicate vitamin D has a treatment effect on cancer as almost all of them studied activated vitamin D or its analogs, drugs that bypass normal regulatory mechanisms, cannot get autocrine quantities of the hormone into the cell, and that often cause hypercalcemia. However, Michael Holick's group found that simple vitamin D deficiency made cancers grow faster in mice. That is, vitamin D has a cancer treatment effect in vitamin D deficient mice. Professor Gary Schwartz, at Wake Forest, recently reviewed the reasons to think that vitamin D may have a treatment effect in cancer.

Tangpricha V, et al. Vitamin D deficiency enhances the growth of MC-26 colon cancer xenografts in Balb/c mice. J Nutr. 2005 Oct;135(10):2350-4.

Schwartz GG, Skinner HG. Vitamin D status and cancer: new insights. Curr Opin Clin Nutr Metab Care. 2007 Jan;10(1):6-11.

Finally, one human interventional study exists. In 2005, in an open trial, Professor Reinhold Vieth and his colleagues found just 2,000 IU of vitamin D per day had a positive effect on PSA levels in men with prostate cancer.

Woo TC, et al. Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy. Nutr Cancer. 2005;51(1):32-6.

So we come back to the crucial question. If you have cancer, how much vitamin D should you take, or, more precisely, what 25(OH)D level should you maintain? We don't know. You can correctly say that definitive studies have not been done and, incorrectly, conclude physicians treating cancer patients should do nothing. I say incorrectly because standards of medical practice have always demanded that doctors make reasonable decisions based on what is currently known, doing a risk/benefit analysis along the way to decide what is best for their patients based on what is known today. If a patient has a potentially fatal cancer, the doctor cannot dismiss a relatively benign potential treatment modality just because definitive studies have not been done, and passively watch his patient die. Standards of care require doctors consider what is known now, using information currently available, perform a risk/benefit analysis, and then act in the best interest of their patient.

Luckily, such doctors recently obtained some guidance. In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D?

Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it, would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production.

Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. [ I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.)

Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below.

Hollis BW, et al. 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.

If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.

So my answer to "How much should I take if I have cancer?" is "Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight. And this may not be enough; cancer patients may use it up faster (increased metabolic clearance) and children may do the same due to their young and vital enzymes. Or you may need less, because you get more sun than you think, more from your diet, or because you are taking a modern medicine that interferes with the metabolism of vitamin D. An even easier way to do it is go to a sun tanning booth every day and obtain and keep a dark, full-body, tan. Then you don't have to worry about blood levels but I'd get one anyway, just to be sure it was above 60 ng/ml.

Given what Hollis discovered, given the well-known potent anti-cancer properties of activated vitamin D, given epidemiological evidence that summer extends the life of cancer patients, given a meta-analysis of randomized controlled trials showed that vitamin D prolongs life, given animal data that simple vitamin D has a treatment effect on cancer, and given a patient with a life-threatening cancer, what would a reasonable physician do? Simply let their patient die while muttering something about the lack of randomized controlled trials?

No, they would simply check a 25(OH)D level every month and advise cancer patients to take enough vitamin D or frequent sun tanning parlors enough to keep their level above 60 ng/ml. Toxicity does not start until levels reach 150 ng/ml but if you take more than 2,000 IU per day have your doctor order a blood calcium every month or two along with the 25(OH)D. Both you and he will feel better and because if you have cancer, you are probably taking lots of other drugs and little is known about how modern drugs interact with vitamin D metabolism. By getting your level above 60 ng/ml, all you are doing is getting your level to where most lifeguards' levels are at the end of summer, to levels our ancestors had when they lived in the sun, to levels regular users of sun-tan parlors levels achieve, and most importantly, to levels where vitamin D's pharmacokinetics are normalized.

In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.

What are the potential benefits? It probably depends on a number of things. Did your cancer cells retain the enzyme that activates vitamin D? Many do. Did your cancer cells retain the vitamin D receptor? Many do. If your cancer cells get more substrate [25(OH)D], will that substrate induce the cancer cells to make more vitamin D receptors or more of the activating enzyme? Some cancer cells do both. In practical terms, vitamin D is theoretically more likely to help your cancer the earlier you start taking it. However, no one knows. Certainly there is no reason, other than bad medicine, for cancer patients to die vitamin D deficient. Unfortunately, most do.

Tangpricha V, et al. Prevalence of vitamin D deficiency in patients attending an outpatient cancer care clinic in Boston. Endocr Pract. 2004 May-Jun;10(3):292-3.

Plant AS, Tisman G. Frequency of combined deficiencies of vitamin D and holotranscobalamin in cancer patients. Nutr Cancer. 2006;56(2):143-8.

It is very important that readers understand I am not suggesting vitamin D cures cancer or that it replace standard cancer treatment. Oncologists perform miracles every day. Do what they say. The only exception is vitamin D. If your oncologist tells you not to take vitamin D, ask him three questions. 1) How do you convert ng/mls to nmol/Ls? How many IU in a nonogram? 3) How do you spell "cholecalciferol?" If he doesn't know how to measure it, weigh it, or spell it, chances are he doesn't know much about it.

All of the epidemiological and animal studies in the literature suggest cancer patients will prolong their lives if they take vitamin D. I can't find any studies that indicate otherwise. However, none of the suggestive studies are randomized controlled interventional trials; they are all epidemiological or animal studies, or, in the case of Vieth's, an open human study. However, if you have cancer, or your child does, do you want to wait the decades it will take for the American Cancer Society to fund randomized controlled trials using the proper dose of vitami

Wheat-free 2007


Long ago, most of us made the change of reducing saturated fat in our diet. Few people now rely on butter (despite the idiotic butter vs. margarine controversy), full-fat dairy products, fried foods, and greasy meats. That's a healthy change, since saturated fat has conclusively been tied to various cancers, high blood pressure, rise in LDL, and is calorie-dense.

But if there were just one change you were to make beyond a reduction in saturated fat, a change that would translate into dramatic health benefits, it would be a drastic reduction, even elimination, of wheat products.

People do indeed eat enormous quantities of wheat flour-containing products. U.S. per capita consumption of wheat flour was 110 pounds in the early 1970s, and rose to 141 pounds in 1991. It's even higher now. 20% or more of most people's caloric intake every day is provided by wheat flour products.

Wheat containing foods are tasty and convenient. Witness the popularity of bagel shops, the goodie counter at Starbuck's, the proliferation of crackers, breads, and breakfast cereals at the grocery store. Patients are horrified when I suggest that they find a substitute for the sandwiches they eat every day. Even Mom said they were okay!

You're unlikely to hear much about this from the popular press. The wheat industry is enormous and exerts extraordinary clout, just like the drug industry. Texas alone farms 6 million acres of wheat, yielding over $2 billion for the state's economy. The "wheat chain" is complex and far-reaching: growers, processors, food manufacturers, the transportation industry, retailers, chemical producers, and on and on. Wheat futures are traded on the Chicago Board of Trade. Wheat is a major export industry for the U.S.

Of course, these are not evil people, intent on corrupting your health. In fact, most of them are probably working under the perception that they are raising a healthy product. The point is that the notion that wheat is healthy is deeply entrenched in the minds and economy of the U.S. Don't expect to hear unbiased commentary on the health effects of wheat products from most media sources.

What can you expect if you sharply reduce or eliminate wheat? The majority of people:

--Feel like a cloud has been lifted from their thinking.
--Don't experience the afternoon blah or tired feeling after lunch.
--Lose weight, sometimes substantial quantities.
--Raise HDL.
--Reduce small LDL.
--Reduce triglycerides, particularly if they start >100 mg/dl.
--Reduce blood sugar.

The reduction in small LDL can be especially impressive.

For most people, reducing or eliminating wheat is a sacrifice, a major change in food choices and even a loss of convenience. But the health benefits for most people can be dramatic.

Is vitamin D a "vitamin"?

Vitamins are crucial participants in the body's reactions and are obtainable from food. Vitamin C, for example, comes from citrus fruits and vegetables. Vitamin K comes from green vegetables. The B vitamins are found in meats, soy, dairy products, and grains. Vitamin A comes from carrots, squash, and other orange and green colored vegetables.

How about vitamin D? What foods contain vitamin D? The list includes:


Food International Units(IU) vitamin D per serving

Cod liver oil, 1 Tablespoon 1,360
Salmon, cooked, 3½ ounces 360
Mackerel, cooked, 3½ ounces 345
Tuna fish, canned in oil, 3 ounces 200
Sardines, canned in oil, drained, 1¾ ounces 250

Milk, nonfat, reduced fat, and whole, vitamin D fortified, 1 cup 98
Margarine, fortified, 1 Tablespoon 60
Pudding, prepared from mix and made with vitamin D fortified milk, ½ cup 50
Cheese, Swiss, 1 ounce 12

Ready-to-eat cereals fortified with 10% of the DV for vitamin D, ¾ cup to 1 cup servings (servings vary according to the brand) 40

Egg, 1 whole (vitamin D is found in egg yolk) 20
Liver, beef, cooked, 3½ ounces 15

(Modified from the Office of Dietary Supplements, National Institutes of Health)


You'll note that the only naturally-occurring food sources of vitamin D are the modest quantities in fish, egg yolks, and liver. All the other vitamin D-containing foods like cereal, milk, and other dairy products have vitamin D only because humans add it.

It takes me (personally) 6000 units of vitamin D per day to bring my blood level to an acceptable 50 ng/ml. To obtain this from eating salmon, I would have to eat 58 ounces, or 3 1/2 pounds of salmon--every day. Or, I could eat 30 cans of tuna fish.

If I didn't want to eat loads of fish every day, I could drink 60 glasses of milk every day. After I recovered from the diarrhea, my vitamin D might be adequate, provided the milk indeed contained the amount stated on the label (which it often does not when scrutinized by the USDA).

If vitamin D is a vitamin, how are humans supposed to get sufficient quantities? I don't know anybody who can eat 3 1/2 lbs of salmon per day, nor drink 60 glasses of milk per day. But aren't vitamins supposed to come from food?




The problem is that vitamin D is not really a vitamin, it's a hormone. If your thyroid hormone level was low, you'd gain 20, 30, or more pounds in weight, your blood pressure would skyrocket, you'd lose your hair, become constipated, develop blood clots, be terribly fatigued. In other words, you'd suffer profound changes. Likewise, if thyroid hormone levels are corrected by giving you thyroid hormone, you'd experience profound correction of these phenomena.

That's what I'm seeing with vitamin D: restoration of this hormone to normal blood levels (25-OH-vitamin D3 50 ng/ml) yields profound changes in the body.

If there's one thing that I've come across lately that packs extraordinary potential to help us in reducing heart scan scores, it's the vitamin--sorry, the hormone--cholecalciferol, or D3.

Heart scan curiosities 3


Note the shape of the chest in this 64-year old man. The front of his chest (upper portion of scan) is concave. In other words, if you were looking at this man (shirtless, of course) face to face, his chest would bow inward, rather than the usual outward configuration. The official name for this is "pectus excavatum".





Compare this to the normal chest in the second image, in which the chest is convex. Face to face, the chest would bow slightly outward.















What does it matter? The pectus excavatum in and of itself has no importance, just a curiousity. (I personally find this surprising, given the fact that the heart actually appears squashed by the sternum, or chest wall.) However, it is commonly associated with a "floppy" mitral valve (also called mitral valve prolapse), a common congenital disorder of the mitral valve often accompanied by a slender build, loose joints, and even a nervous disposition. Occasionally, in its more severe forms, the aorta is also enlarged. (This man's aorta is not enlarged.)

So, while we can't actually visualize the mitral valve by a CT heart scan, we can surmise that he likely has a floppy mitral valve, is slender, is probably a nervous sort, and has long limbs with loose joints. He probably required braces as a child, since many people have a phenemenon of "crowded teeth". The roof of his mouth, or hard palate, probably unusually high up in the mouth. He probably has a "weak chin", meaning a less prominent protuberance of his chin. His fingers and toes are likely unusually long and slender.

It could mean that some attention and exploration of how floppy his mitral valve might be could be useful, e.g., an ultrasound or echocardiogram. He might even require oral antibiotics at the time of any oral or some gastrointestinal procedures, since floppy valve are more susceptible to blood infections when potentially "dirty" orifices are instrumented.

All that from a heart scan!

Gratitude

The holidays and the end of the year may be a good time to reflect on how grateful we should be for having the freedom to discuss the ideas we share on this Blog, the Track Your Plaque website, online and offline.

Although I rant and rave against the status quo in heart disease, the shameful profiteering of my colleagues and hospitals, the cut-throat marketing practices of drug and device manufacturers, I am truly grateful that, in the U.S., I have the extraordinary freedom to say these things. You have the freedom to agree or disagree and none of us pays a price for truth.

I've been reflecting myself a great deal on this idea of happiness and gratitude being a critical component of coronary plaque regression and dropping your heart scan score. (See The Heart Scan Blog from earlier this week.) The more I think about this, the more I think that it is indeed true: Harboring anger and resentment, regrets, irritability, all those petty emotions that most of us know are not good for us, erode our chances for success in dropping your heart scan score.

We could rationalize it this way: Anger and other negative emotions are adrenaline-driven states, also characterized by activation of the "sympathetic" nervous system. (Despite its name, the sympathetic system is not sympathetic, as in compassionate; its the "fight-or-flight" activator that accelerates heart rate and blood pressure.)

Happiness, contentment, and gratitude are "parasympathetic" states characterized by slower heart rates, deeper respiration, greater variation in beat-to-beat heart rates (a powerful predictor for health and the basis for the HeartMath program of Lew Childre), lower blood pressure, and even a subtle change in brain waves. In other words, happiness is not just a mental and emotional state, it is a constellation of physical phenomena.

Even though I pick on Dr. Dean Ornish for his stubborn adherence to the outdated low-fat mantra, I do agree with him on the value of happiness. His book, Love and Survival, articulates this concept. Ornish has even said on several occasions that it wasn't the diet that was most important but the connection and warmth that was created by the comraderie created by participation in the Ornish Program group sessions.

I am personally grateful that the concepts I promote are gaining a following and that I can say so without fear of prosecution. I am grateful that Track Your Plaque followers are not just sharing our concepts, but obtaining genuine and powerful health advice that will help keep them home and healthy, away from hospitals, procedures, and the dangers of heart disease.

I hope you share in my gratitude and are thankful for all the truly wonderful things that surround us. I wish you all a wonderful holiday and long, healthy life filled with gratitude.

A Track Your Plaque failure

We recently had a man suffer a heart attack after beginning the program. Let me tell you the details.

Jerry's heart scan score 781, age 53. Multiple lipoprotein abnormalities: HDL 32 mg/dl, triglycerides 279 mg/dl, nearly all of his LDL was in small particles with an "effective" LDL (LDL particle number), and very high IDL. So Jerry added fish oil 6000 mg per day, niacin, and vitamin D to the statin drug prescribed by his primary physician. Jerry added oat bran, ground flaxseed, and tried to eat fish at least once per week.

However, Jerry continued to smoke. He'd smoked for 40 years (!), up to 2 packs per day, and just reasoned that it was too late to quit. He also continued to indulge in the packaged, processed foods that were part of his convenience story business.

Jerry's stress test was normal--no chest pain, normal EKG, normal images of blood flow, though he was somewhat breathless, likely from his lung disease from smoking.

Two months into his program, he abruptly experienced severe crushing pain in his chest. Because he was traveling, he ended up in a small local hospital. A failed angioplasty led to urgent coronary bypass surgery.

Jerry's alive. Now he's a non-smoker. He's got the pursed lips and peculiar breathing pattern that smokers get, but he's breathing.

Lesson: In the face of the most powerful program for heart disease known, it can still be overpowered by Twinkies, Hoho's, pretzels, chips--and cigarettes.

The new year is approaching. Be grateful for another year of healthy life and commit to a new year of even greater health. If you're a smoker, there's no choice: you've got to quit.

Are you more like a dog or a rabbit?

Dr. William Roberts, editor of the American Journal of Cardiology and cardiovascular pathologist, is a perennial source of clever ideas on heart disease.
In a recent editorial, Dr. Roberts comments:








"Because humans get atherosclerosis, and atherosclerosis is a disease only of herbivorers, humans also must be herbivores. Most humans, of course, eat flesh, but that act does not make us carnivores. Carnivores and herbivores have different characteristics. (1) The teeth of carnivores are sharp; those of herbivores, flat (humans have some sharp teeth but most are flat for grinding the fruits, vegetables, and grains we are built to eat). (2) The intestinal tract of carnivores is short (about 3 times body length); that of herbivores, long (about 12 times body length). (Since I am 6 feet tall my intestinal tract should be about 60 feet long. As a consequence, if I eat bovine muscle [steak], it could take 5 days to course through those 20 yards.) (3) Body cooling for carnivores is done by panting because they have no ability to seat; although herbivores also can pant, they cool their bodies mainly by sweating. (4) Drinking fluids is by lapping them for the carnivore; it is by sipping them for the herbivore. (5) Vitamin C is made by the carnivore's own body; herbivores obtain their ascorbic acid only from their diet. Thus, although most human beings think we are carnivores or at least conduct their lives as if we were, basically humans are herbivores. If we could decrease our flesh intake to as few as 5 to 7 meals a week our health would improve substantially."



You can always count on Dr. Bill Roberts to come up with some clever observations.

I think he's right. Some of the most unhealthy people I've known have been serious meat eaters. Most of the vegetarians have been among the healthiest. (I say most because if a vegetarian still indulges in plenty of junk foods like chips, crackers, breakfast cereals, breads, etc., then they can be every bit as unhealthy as a meat eater.)

Should you become a vegetarian to gain control over coronary plaque and other aspects of health? I don't believe you have to. However, modern livestock raising practices have substantially modified the composition of meats. A steak in 2006, for instance, is not the same thing as a steak in 1896. The saturated and monounsaturated fat content are different, the pattern of fat "marbling" is different, the lean protein content is different. Meat is less healthy today than 100 years ago.

Take a lesson from Dr. Roberts' tongue-in-cheek but nonetheless provocative thoughts. Pardon me while I chew on some carrots.

Are happy people more likely to reduce heart scan scores?

I was talking to Darryl, a patient today: 71 years old with a heart scan score of 378, as well as an enlarged aorta (4.5 cm).

We had identified numerous lipoprotein abnormalities 12 months ago and advised him on a program for correction. His patterns included small LDL, high triglycerides, sky-high IDL (VERY important when you have an enlarged aorta), and lipoprotein(a). Blood pressure was also high, another crucial fact to correct when the aorta is enlarged.

Anyway, Darryl corrected lipoproteins to perfection: basic lipids were substantially better than 60-60-60; lipoprotein(a) was reduced well into the desirable range; IDL was eliminated; blood pressure was 108/64. Repeat heart scan score: 354.

There's nothing spectacular about Darryl's story, except that, despite these issues, Darryl was a happy man. He smiled throughout our conversation. He has told me on several occasions how grateful he is for the life he has.

Darryl is not wealthy. He retired around 4 years ago and fills his day with helping his wife, walking outdoors, helping out at his church, and contributing to the care of his grandchildren. Through all this Darryl is incurably, unfailingly, and irrepressibly happy.

It made me think back through all the other people who've also had great succes in their Track Your Plaque program. It struck me that, for the most part, they too were a happy bunch: generally optimistic, happy, not overly stressed nor prone to extremely stressful responses to stressful situations. All seem to also be grateful for the good in their lives, though most had no more money than the average person and had their share of difficulties in life. In fact, I can only recall one person who reversed coronary plaque who was an angry, pessimistic personality. Just one.

Could it be that happy, optimistic people are more likely to reverse coronary plaque? It would, after all, be consistent with all the other observations that type A personalities have more heart attack, etc.

Anyway, this is just an informal observation but one that seems very consistent. Track your plaque--and be happy!

Don't overdo the vitamin D

As time passes and I advise more and more people to supplement vitamin D, I gain increasing respect for this powerful "vitamin". I am convinced that vitamin D replacement is the reason for a recent surge in our success rates in dropping CT heart scan scores. I believe it is also explains the larger drops we've been witnessing lately--20-30%.

But vitamin D can be overdone, too. Too much of a good thing . . .

Despite being labeled a "vitamin", cholecalciferol is actually a hormone. Vitamins are obtained from food and you can thereby develop deficiencies because of poor intake. Deficiency of vitamin C, for instance, arises from a lack of vegetables and fruits.

Vitamin D, on the other hand, is nearly absent from food. The only naturally-occuring source is oily fish like salmon and sardines. Milk usually has a little (100 units per 8 oz) because milk producers have been required by law to put it there to reduce the incidence of childhood rickets.

A woman came to me with a heart scan score of nearly 3800, the highest score I've every seen in a woman. (Record for a male >8,000!) She was taking vitamin D by prescription from her family doctor but at a dose of 150,000 units per week, or approximately 21,000 units per day. This had gone on for about 3-4 years. This may explain her excessive coronary calcium score. Interestingly, she had virtually no lipoprotein abnormalities identified, which by itself is curious, since most people have some degree of abnormality like small LDL. Obviously, I asked her to stop the vitamin D.

Should you be afraid of vitamin D? Of course not. If your neighbor is an alcoholic and has advanced cirrhosis, does that mean you shouldn't have a glass or two of Merlot for health and enjoyment? It's a matter of quantity. Too little vitamin D and you encourage coronary plaque growth. Too much vitamin D and you trigger "pathologic calcification", or the deposition of calcium in inappropriate places and sometimes to extreme degrees, as in this unfortunate woman.

Ideally, you should have your doctor check your 25-OH-vitamin D3 blood levels twice a year in summar and in winter. We aim for a level of 50 ng/ml, the level at which the phenemena of deficiency dissipate.

"It must have been the statin"

After four years of trying, Randy finally reduced her heart scan score. It not only dropped, it plummeted. After four previous scans that showed 25% or more increases, she'd finally dropped her score 23%. (I Blogged about Randy's case a few weeks ago.)

Randy also works for a cardiologist. When she told him that she had reversed her coronary plaque and reduced her heart scan score by 23%, he said, "It must have been the statin agent."

Randy was indeed on a statin drug at a low dose. But she also had taken great efforts in exercise, food choices, fish oil, and vitamin D. In fact, her score had progressed dramatically while she was taking the drug. Put simply, it was not the statin.

But that is the mindset of the conventionally thinking cardiologist. Stent, bypass, or statin drug--what else is there? Even with crystal clear evidence for coronary plaque regression, they refuse to acknowledge that tools that are not in their everyday consciousness could have achieved so spectacular a result.

Given a choice, 9 out of 10 cardiologists would rather put a stent in and walk away $2000 richer for an hour of work. Don't allow them to have this choice. Take control now.

Statin Drugs May Help the Healthy:
Cholesterol-Lowering Statin Drugs May Benefit People Without Heart Disease


That's the headline on WebMD, reporting the findings of a recent study published in the Archives of Internal Medicine. In reality, it wasn't really a study at all, but a re-analysis of previously published data, a so-called meta-analysis.

Nonetheless, the University of Toronto group re-analyzed the results of several studies, pooling data on 28,000 people, none of whom had known coronary disease. The results were similar to the results of the studies that were reported individually: a 29% reduction in heart attack and other "events" in people taking statin drugs.

What's surprising to me is this notion that statins, or any other treatment for that matter, prevent heart attack in people without heart disease. This is idiotic. Of course they had coronary heart disease. You can't have a heart attack in the absence of coronary disease. (There are very rare exceptions, like cocaine users, who experience coronary spasm from the drug).

What the study shows is that people with unrecognized heart disease experienced a reduction in heart attack. What it also means is that many, many people truly without heart disease were unnecessarily treated. As you'd predict, the drug manufacturers love this sort of broad, untargeted use of their drugs. It's an approach that brings in billions of dollars of revenues. The article on WebMD, in fact, was accompanied by three ads for various cholesterol drugs on this single page story.

What if only people with heart disease, as identified by CT heart scan scores, were treated? You would indeed witness an even larger reduction in heart attack risk, because the group receiving treatment both has the disease and is thereby at greater risk. Treatment should yield even greater risk reduction than treating broad groups who superficially appear to not have heart disease.

Ignore this nonsense about statin drugs reducing heart attack risk in people without heart disease. If you don't look for it, you won't know you have it. Once again, you can be lots smarter than the media. Get a heart scan and find out if your risk is worth reducing.

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