Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl
BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl

In other words, small LDL constitutes 81% of all LDL particles (1811 All posts by william-davis

Dr. Michael Eades on the Paleolithic diet

18. February 2009 William Davis (16)

Dr. Michael Eades has posted an absolutely spectacular commentary on the Paleolithic diet concept:

Rapid health improvements with a Paleolithic diet

The post was prompted by publication of a study that tried to recreate a Paleolithic-like diet experience over a brief study period:

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.

Dr. Eades discussion is wonderfully insightful and comprehensive and there's little to say to improve on his discussion.

I'd make one small point: From what I see in my experience, the improvements in lipid patterns seen in the brief period of this study are very likely to have been primarily due to the removal of wheat. Followers of this blog know that wheat elimination is among the most powerful cholesterol-reducing strategies available.

What vitamin D form?

15. February 2009 William Davis (36)

In response to questions regarding why don't vitamin D tablets work, here are my observations.

When I first started correcting vitamin D levels around 3 1/2 years ago, people would begin with starting 25-hydroxy vitamin D blood levels of around 20 ng/ml.

Taking, say, 6000 units vitamin D as tablets over 3 months yielded blood levels of 24-30 ng/ml. Taking 6000 units in an oil-based form, and blood levels would commonly be 60-70 ng/ml.

In other words, tablets are very poorly absorbed. I also saw very erratic absorption with tablets, with tremendous variation in blood levels.

I witnessed this effect many times. I finally began telling patients to avoid the tablets altogether. It's simply not worth it. Taking dose X of tablets, you cannot predict what the blood level of vitamin D will be.

Now, you can sometimes make the tablets get absorbed by either taking with a teaspoon of oil (e.g., olive, flaxseed) or taking with an oil-rich meal. However, I am uncertain just how consistent the absorption is under these circumstances, not having done this enough times to know.

Oil-filled gelcaps are no more expensive than tablets (or perhaps a dollar more). Health food store employees and pharmacists don't know this. I have had many patients come to the office claiming they changed to tablets because that's all their health food store or pharmacy carried and the person behind the counter assured them it was the same. Blood level of vitamin D to confirm: right back down to the starting level or near it--little or no absorption.

The only way to know whether a preparation is absorbed is to check a blood level. But, in my experience, having checked vitamin D blood levels thousands of times, gelcaps never fail; tablets fail over 80% of the time.

Vitamin D for the pharmaceutically challenged

14. February 2009 William Davis (20)

Most Heart Scan Blog readers already know:

Your doctor has been brainwashed by the pharmaceutical industry.

Your doctor more than likely has spent the better part of his or her career in the Guantanamo Bay of healthcare, water-boarded by seductive sales representatives, enticed with promises of fame and riches, threatened with ostracism from the clubby internal halls of healthcare if--gasp!--he or she didn't subscribe to the "rule" that only drugs are good, anything else is bad.

The same FDA-approval-is-necessary-to-be-good brand of nonsense is gaining popularity among my colleagues who, having caught some mention (on the Today Show, Oprah, or similar source of medical information), hope to join the vitamin D hoopla.

People will proudly declare that they are taking a high dose of vitamin D: 50,000 units once per week.

No. They are taking a barely useful form: D2, ergocalciferol.

Studies examining the reliability of the D2 form differ:

There's the Heaney study suggesting that D2 is less effective than D3:
Vitamin D2 is much less effective than vitamin D3 in humans

Then there's the Holick study showing they are equivalent:
Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D.

My experience is more in line with the Heaney study: Little or no real effect with D2.

One particularly illustrative case I witnessed was a woman who was mistakenly prescribed D2 at 50,000 units per day. She told me that she'd been taking it for a year. I fully expected to see clear-cut signs of toxicity (e.g., high blood calcium levels). Curiously, she showed no signs of toxicity. Nor did she show any vitamin D at all in her blood: 25-hydroxy D level of zero--literally zero.

I've witnessed similar phenomena several times: plenty of vitamin D2 . . . very little vitamin D in the blood.

All in all, I suppose that D2 is better than No-D at all. But you are far better off joining the ranks of the pharmaceutically challenged and go with the stuff that really works: D3.

D3, or cholecalciferol, yields confident increases in blood levels. It is inexpensive, safe, and an exact copy of the human form of vitamin D. (Of course, gelcap or drops only, NEVER tablets.)

There is absolute NO reason to take vitamin D2, the form that sometimes works, sometimes doesn't, the facsimile plant form issued by the drug industry.

Why don't stents prevent heart attack?

12. February 2009 William Davis (11)

No study has ever documented that stents prevent future heart attack. But, in day-to-day practice, stents are frequently implanted for just this reason.

A little clarification. Stents do prevent heart attack--if the heart attack is already underway, either as an "acute myocardial infarction" or "unstable angina."

In other words, a plaque in a coronary artery can rupture just like a little volcano. Rather than spewing lava, the underlying plaque contents--fibrous tissue, inflammatory cells, cholesterol crystals, fatty material, debris--are exposed to flowing blood and trigger spasm of the artery and blood clot formation. A ruptured plaque is typically found in people who go to the emergency room with severe chest pain or have difficulty breathing.

A heart catheterization is performed, a severe (e.g., 90-100%--completely closed) is found. A stent in this situation is of clear-cut benefit.

What is not clearly beneficial is someone with no symptoms, symptoms only with physical activity that has been present for at least several months, or someone with a high heart scan score and no symptoms. In these circumstances, stent implantation does not reduce risk for future heart attack.

Why?

Take a look at this angiogram of a right coronary artery. You can seen plaque all along the artery (represented by areas that appear pinched off. There are at least 4 visible.)

Putting one 15 millimeter stent in the artery will only affect the area of artery stented. (Stents vary in length, but typically are 12-18 millimeters in length.) The right coronary artery is about 10 times or more this length. There are also two other arteries of similar length. A stent at one location will do nothing to affect the potential for rupture in any of the other plaque-laden areas.

Say a stent is implanted in the "worst" blockage in this right coronary artery, the plaque located at around 9 o'clock. What about all the other plaques? They can still rupture.

Why not put in many stents, say, 4 or 5, and stent all the visible plaques?

Two reasons: 1) Plaque you can't even see on an angiogram can still rupture, and 2) it is very costly (easily $30,000 at the very least), 3) incurs greater procedural risk, and 4) messes up the artery for future procedures, since a steel-lined artery that develops more disease in future will be more difficult to re-implant stents, bypass, or perform other procedural manipulations.

The point: Putting in stents does not reduce potential for plaque rupture in the entire artery.

What can prevent plaque rupture? That's the whole point of following an effective prevention program: prevent plaque rupture.

(Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

Top image courtesy National Heart, Lung, and Blood Institute.

Low thyroid: What to do?

8. February 2009 William Davis (25)

I've gotten a number of requests for solutions on how to solve the low thyroid issue if either 1) your doctor refuses to discuss the issue or denies it is present, or 2) there are government mandates against thyroid correction unless certain (outdated) targets are met.

Oh, boy.

While I'm not encouraging anyone to break the laws or regulations of their country (and it's impossible to generalize, with readers of this blog originating from over 30 countries), here are some simple steps to consider that might help you in your quest to correct hypothyroidism:

--Measure your body temperature--First thing in the morning either while lying in bed or go to the bathroom and measure your oral temp. Record it and, if it is consistently lower than 97.0 degrees (Fahrenheit), show it to your doctor. This may help persuade him/her.(You can still be hypothyroid with higher temperatures, but if low temperatures are present, it is simply more persuasive evidence in favor of treatment).

--Supplement with iodine 150 mcg per day to be sure you are not iodine deficient. This is becoming more common in the U.S. as people avoid iodized salt. It is quite common outside the U.S. An easy, inexpensive preparation is kelp tablets.

--Show your doctor a recent crucial study: The HUNT Study that suggests that cardiovascular mortality begins to increase at a TSH of only 1.5 or greater, not the 5.5 mIU usually used by laboratories and doctors.

--Ask people around you whether they are aware of a health practitioner who might be willing to work with you, or at least have an open mind (sadly, an uncommon commodity).

Also, see thyroid advocate and prolific author, Mary Shomon's advice on how to find a doctor willing to work with you. Yes, they are out there, but you may have to ask a lot of friends and acquaintances, or meet and fire a lot of docs. It shouldn't be this way, but it is. It will change through public pressure and education, but not by next week.

Another helpful discussion from Mary Shomon: The TSH Normal Range: Why is there still controversy? You will read that even the endocrinologists (a peculiarly contentious group) seethingly debate what constitutes normal vs. low thyroid function.

Also, you might remind a resistant health practitioner that guidelines are guidelines--they are not laws that restrain anyone. They are simply meant to represent broad population guidelines that do not take your personal health situation into consideration.

Which statin drug is best?

8. February 2009 William Davis (7)

I re-post a Heart Scan Blog post from one year ago, answering the question: Which statin drug is best?

I still get this question from patients in the office and online, nearly always prompted by a TV commercial. So let me re-express my thoughts from a year ago, which have not changed on this issue.

The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this quesll restoration of vitamin D are in the thousands of units. (My personal dose for full restoration of vitamin judged by serum levels of 25-hydroxy vitamin D is 8000 units per day.)

The information coming from the Food and Nutrition Board is about as good as the information coming from the USDA (you know, that "government" agency meant to represent the interests of ConAgra, Cargill, and Big Farming) and the American Heart Association (that represents consensus opinion from data 20 years out of date and now arm-in-arm with Big Food like General Mills, Kraft, and Nabisco). These agencies and the advice they offer has, over the past few years, become increasingly irrelevant and outdated. It is the Information Age, in which ulterior motives are becoming more readily exposed, yet they still operate by the rules of the Industrial Age and deliver a message that serves their own purposes.

Ms. Austin fell for it.

The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals.

First of all, what is a "diet expert" doing advocating industrial foods? Cereals, in particular, are among the worst foods on the supermarket shelves, whether or not they are fortified. Candy bars can be fortified, too; that doesn't make them any better for you.

The vitamin D added to these foods is, more often than not, the ergocalcferol, or D2, form that is woefully ineffective. And the dose added is trivial, usually in the 100-200 unit range per serving. The same goes for the milk, an inadequate source that we don't even factor into total intakes because of the low quantity.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week.

Nope. This might be true for a young person below age 30 in a southern environment. It is NOT true for the majority of people in northern climates and anyone over age 30 or 40, since we lose most of the capacity to activate vitamin D in the skin as we age. A deep, dark Florida tan does not necessarily mean that vitamin D has been activated. See A tan does not equal vitamin D. Here in Wisconsin, where, despite this darn cold winter, does enjoy wonderfully warm and beautiful summers, the average vitamin D dose need ranges from 4000-8000 units per day in summer, slightly more in winter.

By the way, it is not calcium that is instrumental to bone health. It is vitamin D. Calcium is the passive bricks and mortar of bones, while vitamin D is the bricklayer, the determinant of calcium's fate, the master control of bone health. Calcium supplementation becomes almost immaterial when vitamin D is restored.

I praise Ms. Austin for her hard work, trying to help fat Americans lose weight. But please ignore her advice on vitamin D, along with the numbing repetition of this mis-information that will likely propagate from other exercise gurus, dietitians, and pseudoexperts.

A Tale of Two LDL's

15. January 2009 William Davis (10)

Kurt, a 50-year old businessman with a heart scan score of 323, had a :

--Conventional (calculated) LDL of 128 mg/dl
--Real measured LDL 241 mg/dl.

Laurie, a 53-year old woman who underwent a coronary bypass operation last year (before I met her), had a:

--Conventional LDL of 142 mg/dl
--Real measured LDL was 85 mg/dl.

(By "real, measured" LDL, I'm referring to LDL particle number in units of nmol/L obtained through NMR lipoprotein testing and dividing by 10, or just dropping the last digit to convert the value to mg/dl. This technique was arrived at by comparing the population distributions of these two parameters, LDL particle number and calculated LDL. This is the gold standard in my view. Similar numbers can be obtained by measuring apoprotein B, direct LDL, or calculated non-HDL, with diminishing reliability from first to last.)

In other words, Kurt's conventional LDL underestimated real LDL by 88%. Laurie's conventional LDL overestimated real LDL by 40%.

Interestingly, Laurie's doctor had insisted she take Lipitor for a high LDL cholesterol. Her real LDL was, in fact, low to begin with and benefits of a statin drug would be little to none. (Remember, in our Track Your Plaque approach, multiple other treatments are included, such as omega-3 fatty acids from fish oil, vitamin D normalization, and wheat elimination, strategies that yield benefits that others expect to obtain with statins.) Laurie's real cause of her heart disease proved to have nothing to do with LDL cholesterol, but involved lipoprotein(a) and thyroid issues.

Kurt proved to have a severe preponderance of small LDL particles--the worst kind of LDL, while Laurie had none--a benign pattern.

Then how can anyone make sense of the conventional, calculated LDL cholesterol that is generally (95% of the time) provided? If accuracy can stretch to plus or minus 80% . . . you can't. Conventional LDL is a miserably inaccurate number. The problem is that obtaining a superior number requires a step or two more testing and insight, something most busy primary care doc's simply don't have in the midst of a day filled with arthritis, bronchitis, diarrhea, belly aches, and seborrhea.

Yet conventional--I call it "fictitious"--LDL serves as the basis for this $27 billion (annual revenues) industry selling statin drugs.

This is meant to be neither an argument in favor of nor against statin drugs. However, it is plain as day that any study designed to reduce LDL cholesterol will be hopelessly clouded by calculated LDL imprecision. A calculated LDL of, say, 143 mg/dl might really be 187 mg/dl, or it might be 74 mg/dl--you can't tell by looking just at LDL. Yet billions of dollars of research and billions of dollars of healthcare costs are based on the treatment of this number.

This reminds me of the mark-to-market accounting magic that helped topple Wall Street.

I don't think that the statin world is poised for such a huge downfall. But I do see this as a source of enormous dilution of the effects of statin drugs. People who barely stand to benefit get the drugs, while others who might truly benefit are treated inadequately. It provides fuel to the growing idea that reducing LDL cholesterol fails to truly provide benefit.

I am no lover of statin drugs nor drugs in general. But I am a fan of knowing the truth. Despite my bashing of the drug industry (and make no mistake: the drug industry is a cutthroat, profit-seeking, do-anything-to-increase-sales industry), I do believe that there is a role for statin drugs (though far smaller than $27 billion per year). But the usual method of selecting people for treatment is pure fiction. The ATP-III cholesterol treatment guidelines? An anemic attempt to apply structure to meaningless values.

You and I do not need to subscribe to this sort of non-quantitative nonsense.

All posts by william-davis

Niacin scams

12. January 2009 William Davis (0)

In the Track Your Plaque program, we often resort to niacin (vitamin B3 or nicotinic acid) to:

--Raise HDL cholesterol
--Reduce the proportion of small LDL particles
--Shift HDL towards the healthy larger fraction (HDL2b or "large")
--Reduce lipoprotein(a), the most aggressive risk factor known

But niacin comes with a crazy "hot flush," a warm, prickly feeling that usually envelops the upper chest, neck and face that is, without a doubt, annoying. Around 1 in 20 people simply cannot tolerate any amount of niacin >100 mg, while others have no problem even into the 3000 mg per day or more range. (Tolerance to niacin is genetically determined, governed by the rapidity of metabolism to the niacin metabolite, nicotinuric acid.)

The niacin flush has spawned an entire panel of niacin-like scams, agents that sound like niacin or may even contain niacin, but exert no beneficial effect whatsoever:

Flush-free niacin--I have previously posted on this useless but ubiquitous preparation that often costs several times more than conventional niacin. Flush-free niacin, or inositol hexaniacinate, does indeed contain niacin, but it is not released in the human body. You simply pass it out down the toilet, where this preparation belongs in the first place.

Nicotinamide--Also called niacinamide. While the nicotinamide/niacinamide forms of vitamin B3 can be used to treat B3 deficiency ("pellagra"), they do not reproduce the lipid and lipoprotein effects of niacin. For our purposes, they are useless.

Niacin-containing heart-healthy supplements--These are the multi-supplements that contain a little of everything that might be beneficial for the heart, but none at a dose that provides genuine benefit. Don't throw your money away.

There's also a prescription niacin, Niaspan, that costs 20-fold more than the best over-the-counter preparation, Sloniacin. Niaspan has yielded hundreds of millions of dollars for the pharmaceutical industry. Your money, in my view, is far better spent on Sloniacin (around $12-14 per bottle of 100 tablets of 500 mg).

For more on niacin, here's an article I wrote for the Life Extension Magazine people a while back: Using Niacin to Improve Cardiovascular Health.

Deja vu all over again?

10. January 2009 William Davis (8)

HeartHawk brought a report and debate on The Heart.Org website to my attention:

Screening for risk factors or detecting disease? Debate divides the CV community. After landing on theheart.org, paste this onto your URL address:article/883239.do. (Full address: http://www.theheart.org/article/883239.do. I don't know why, but I couldn't go there directly.)

Some interesting comments:

Dr. Jay Cohn (University of Minnesota):

"They're saying that we can't identify disease very effectively so let's just stick with risk factors, which we know are very poorly predictive and nonspecific. It boggles my mind as to why they won't open up their minds to the importance of moving forward in finding better strategies to identify the disease that we are treating. It's very strange. They criticize these disease markers because they are not predictive of events, but they are looking at very short-term outcomes. We're interested in lifetime risk. We're screening people in their 40s who are concerned about morbid events in their 60s and 70s, and no trials are going to track them that long."

"You have to accept the pathophysiologic reality that heart attacks don't occur in the absence of coronary disease, and coronary disease doesn't occur in the absence of endothelial dysfunction and vascular disease, all of which now can be identified."

". . . Can we as a society and as a profession accept the idea that there is a link between the vascular abnormalities and the events? "And that that linkage is tight enough that it should allow us to accept slowing of progression of the vascular abnormalities as an adequate marker for slowing disease progression, without waiting for events to occur? As soon as you use the word surrogate, people jump up and say we have all these markers that we know don't work well—things like premature ventricular contractions [PVCs] on the electrocardiogram, LDL, HDL—but those are not the markers we're talking about. We're talking about structural and functional changes in the blood vessel and in the heart."

Wow. The idea may be starting to catch on.

As an interesting aside, Cohn et al use a 10-test panel to screen for vascular disease:

"Named for the center's benefactor, the Rasmussen score includes tests for large and small artery elasticity (compliance), resting blood pressure, blood-pressure response to moderate treadmill exercise, optic fundus photography, carotid intimal-media thickness (IMT), microalbuminuria, electrocardiography, left ventricular (LV) ultrasonography for LV volume and mass, and brain natriuretic peptide (BNP). Each test result is scored out of 10 for low, intermediate, or high risk, and the combined results yields a score that Cohn et al believe is more predictive than any of the existing standalone tests."

The counterarguments in this debate were provided by Dr. Philip Greenland (Northwestern University), who repeated his oft-used argument that, while he accepts that vascular disease can be identified, no one has proven that measuring it improves outcomes:

"We do have that evidence for risk-factor screening. Even though people criticize risk-factor assessment because it is not sensitive enough or not accurate enough, the interesting and curious thing is that we actually have evidence that if you go to the trouble of screening for risk factors and treating them, patients have better outcomes. We do not have that evidence for any of these other tests."

An interesting debate ensues that includes Track Your Plaque friend, Dr. William Blanchet, who characteristically argues persuasively in favor of broad screening for coronary disease with coronary calcium scoring:

"If we were doing our jobs in primary prevention, we would not need to look at improved intervention and secondary prevention to reduce coronary death."

Here's a shock: Dr. Melissa Shirley-Walton, the cardiologist who previously preached the "cath lab on every corner" argument seems to have undergone a change of heart:

"What if I walked up to a gentleman and said, "you are at risk for CAD, take a statin", to which he replies, "I'm afraid of those meds". BUT if he sees his calcium score........he is then convinced to be pro-active. What is so wrong with that? What is so wrong with allowing him to spend 250.00 US out of pocket in order to save the US 150,000.00 US later on?

No hard endpoints you say with intensive therapy for primary prevention? What about extrapolating from trials for secondary prevention like HATS? ARBITER2? And what exactly is the true definition of secondary prevention? Is it truly primary prevention if we already have intima thickness abnormalities, or fatty streaks? That would more likely fall under secondary prevention by today's new standards.

So, I'm all for any visual aid that will encourage compliance with life style change, necessary medical therapy and followup. If the patient is willing to spend 250.00$ to get a calcium score, so be it. Better yet, why not lower the price so everyone can have the option if they are motivated enough to seize an opportunity?"

I have to admit that I thought that Dr. Blanchet was wasting his time trying to persuade Shirley-Walton et al, but perhaps he is having an impact, though having hammered away at them for the last year or so.

These arguments, for me, eerily echo many previous debates I've heard. But I am encouraged by the more favorable treatment the notion of atherosclerosis screening is receiving. Just 5 years ago, all coronary calcium scoring would have received from the conventionalists is "more clinical studies are needed."

So perhaps the cardiology and medical worlds are inching slowly towards broad acceptance of screening for coronary and vascular disease.

BUT, screening is not sufficient. What do you do with the information?

Here is where the conventional-thinkers stop. The question that seems to occupy them: Perhaps we should screen people for hidden coronary and vascular atherosclerosis so we can better decide who needs a statin drug or a procedure.

I would pose a different challenge: We should screen people for hidden coronary and vascular atherosclerosis so we can better decide who needs to engage in an intensive program of disease reversal using natural means and as little medication and procedures as possible.

Well, perhaps in time.

Lead to Gold: The alchemy of transforming nutritional-supplement-to-medication

9. January 2009 William Davis (25)

Here's a recipe to make hundreds of millions of dollars. Others have done it and you can do it, too!

1) Identify a nutritional supplement that works.

Find some agent deemed to fall within the broad allowances of the 1994 Dietary Supplement Health and Education Act . However, because this agent is already in the public domain and is essential non-patent-protectable, you may need to develop some patent protectable aspect of its production, application, or encapsulation. This patent-protected aspect may or may not provide genuine advantage, but that's not your concern. Your concern is protecting your investment and providing the appearance of exclusivity.

2) Identify a medical indication for your product.

Choose a disease or condition that is likely to yield unquestioned efficacy, e.g., omega-3 fatty acids to reduce high triglycerides in people with familial hypertriglyceridemia (triglycerides >500 mg/dl). While this will restrict your ability to make market claims, it will not restrain your ability to sell or allow use of your agent for "off-label" applications. In fact, there are methods to surreptitiously promote the use of your product for off-label use, such as hiring experts to discuss the science behind your product with doctors who can prescribe your product. Ideally, your product's primary indication will provide a substantial market on its own to justify your investment. However, the eventual off-label sales can be substantial, even outstripping the sales generated through your primary indication.

3) Obtain at least $230 million to pay for the clinical trials required to obtain FDA approval.

You will also have to raise the capital to build the business to manufacture, distribute, and sell your product.

4) After FDA approval is obtained, your business is up and running, and distribution begins, start bashing the non-FDA-approved nutritional products that stand to compete in your market.

You could point out that only your product has actually passed through the rigorous FDA process. You could make claims regarding purity, potency, "approved by your doctor," etc., whether or not there is any truth behind the claim.

5) Buy that second vacation home in Aspen and the corporate jet you've been dreaming about! After all the risks you've taken, you deserve it!

That's it, plain and simple. It is a tried-and-true formula that has been applied many times.

It is a formula like this that brought Lovaza-brand omega-3 fatty acids to market, Niaspan brand of niacin, ergocalciferol form of vitamin D, Folbee (prescription combination B vitamins), with a slightly different spin for Synthroid (since the Armour Thyroid it is meant to replace is not a nutritional supplement, but a low-cost, generic thyroid replacement).

Whatever you do, don't EVER run a head-to-head comparative trial of your agent versus the nutritional supplement competition. For instance, NEVER compare Lovaza to supplemental fish oil capsules, matched milligram-for-milligram for EPA and DHA content. NEVER compare Niaspan to over-the-counter Sloniacin. NEVER compare Armour Thyroid to Synthroid. You never know what you might find. (Psssssttt! They might be equivalent!)

The formula is not a foolproof road paved with riches, however. There have been market failures, as well. Folbee, for instance, is hardly a household name. So there's risk involved, no question about it. But, should it all work out, the payoff can be big, VERY big, as it has been for Niaspan and Lovaza.

So, start thinking about how you might follow this formula for:

1) Cholecalciferol (vitamin D3)--e.g., for osteopenia, low HDL, or high c-reactive protein
2) Vitamin K2--also for osteopenia
3) Magnesium--for suppression of ventricular arrhythmias (especially Torsade de Pointes)
4) Iodine--for goiter and iodine deficiency
5) Vitamin C--for uric acid reduction

Who said you can't turn lead into gold?

Irvingia and Leptin Resistance: Fact or fiction?

7. January 2009 William Davis (0)

Another interview with Livin' La Vida Low Carb's Jimmy Moore

7. January 2009 William Davis (4)

I recently provided another interview for Livin' La Vida Low Carb's Jimmy Moore.

You may remember Jimmy as the irrepressible host of the Livin' La Vida Low Carb Show who lost around 200 lbs, dropping from 410 to 230 lbs on a low-carbohydrate diet.

In this hour-long interview, we discussed some of the dietary strategies that we use in the Track Your Plaque program.

Jimmy's website is definitely worth exploring. It's loaded with great interviews, including with Good Calories, Bad Calories author, Gary Taubes.

"Millions of needless deaths"

6. January 2009 William Davis (4)

"Millions of needless deaths" is the title of an editorial by Life Extension Magazine's Bill Faloon.

". . . If vitamin D’s only benefit was to reduce coronary heart attack rates by 142%, the net savings (after deducting the cost of the vitamin D) if every American supplemented properly would be around $84 billion each year. That’s enough to put a major dent in the health care cost crisis that is forecast to bankrupt Medicare and many private insurance plans."

Although I don't agree with all the over-the-top commentary that issues from Mr. Faloon or Life Extension (although I sit on their Medical Advisory Board), I agree with virtually all of the issues he raises with vitamin D.

Despite the enormously compelling observations of vitamin D potential effects in populations, the medical community's reluctance comes from the lack of treatment data. In other words, what we lack are long-term data on vitamin D supplementation vs. placebo on rate of heart attack, vitamin D vs. placebo on risk of colon cancer, etc.

The data that exists connecting vitamin D levels with cardiovascular risk originate from three population observations:

1) The NHANES data in 16,000 participants showed 20% increased risk of cardiovascular events in those with vitamin D levels <20>20 ng/ml after factoring in all standard risk factors.

Another NHANES analysis showed the high prevalence of vitamin D deficiency in those with cardiovascular disease.

2) A German study of 2500 participants that showed showed the lowest quartile of vitamin D levels (<13.3>28.4 ng/ml.

3) The Health Professionals' Follow-Up Study of 18,000 males showed a 2.4-fold increase in cardiovascular events in those with vitamin D levels <15>30 ng/ml.

While we lack treatment data (vitamin D vs. placebo) in a large population, we do have data that Suzie Rockway, Mary Kwasny (both from Rush University, Chicago) and I generated on the effect of vitamin D as a part of a broader treatment program on coronary calcium scores:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.
Davis W, Rockway S, Kwasny M. Amer J Ther 2008 (Dec 15).

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

I also summed up the data as of early 2008 in a Life Extension article:

Vitamin D's Crucial Role in Cardiovascular Protection

I do agree with Mr. Faloon: It's time to take the vitamin D issue very seriously. Personally, I think it is foolhardy to not correct vitamin D deficiency, even in the absence of long-term treatment data.

Should we subject people living in tropical climates with vitamin D blood levels of 90 ng/ml to long-term observation? Though that has not yet been done, it has been done--in effect--through observations on the prevalence of diabetes, heart disease, and various cancers by latitude: the farther away from the equator, the greater the prevalence of these diseases.

That's more than good enough for me.

Thiazide diuretics: Treatment of choice for high blood pressure?

5. January 2009 William Davis (14)

Thiazide diuretics are a popular first-line treatment for hypertension among the primary care set.

This practice became especially well-established with the 2002 publication of the ALLHAT Study (Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic:The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)).

ALLHAT showed that an inexpensive diuretic like chlorthalidone (a weak diuretic in the thiazide class, similar to hydrochlorothiazide) as first-line treatment for hypertension achieved equivalent reductions in cardiovascular events (cardiovasular death and heart attack) as non-thiazide antihypertensives, lisinopril (an ACE inhibitor) and amlodipine (a calcium channel blocker, better known as Norvasc).

After 7 years of treatment, there was 14% death or heart attack among all three groups--no difference.

This was interpreted to mean that inexpensive thiazide diuretics like chlorthalidone offer as much benefit as other blood pressure medications at reduced cost.

On the surface, that's great. Anything that detracts from the ubiquitous pharmaceutical industry propaganda of bigger, better, more expensive drugs to replace old, inexpensive, generic drugs is fine by me.

But you knew there'd be more to this issue! If we accept that thiazides are equivalent to other single-drug treatments for high blood pressure, what do we do with the following issues:

--Thiazides deplete body potassium-This effect can be profound. In fact, built into the ALLHAT mortality rate is an expected death rate from potassium depletion. When potassium in the body and blood go low, the heart becomes electrically unstable and dangerous rhythms develop.

--Thiazides deplete magnesium--Similar in implication to the potassium loss, magnesium loss also creates electrical instability in the heart, not to mention exaggeration of insulin resistance, rise in triglycerides, reduction in HDL.

--Thiazides reduce HDL cholesterol

--Thiazides increase triglycerides

--Thiazides increase small LDL particles--You know, the number one cause for heart disease in the U.S.

--Thiazides increase uric acid--Uric acid is increasingly looking like a coronary risk factor: The higher the uric acid blood level, the greater the risk for heart attack. Thiazides have long been known to increase uric acid, occasionally sufficient to trigger attacks of gout (uric acid crystals that precipitate in joints, like rock candy). (Fully detailed Special Report on uric acid coming this week on the Track Your Plaque website.)

What about the advice we commonly give people to hydrate themselves generously? Yet we give them diuretics? Which is it: More hydration or less hydration? You can't have both.

Do thiazides exert an apparent cardiovascular risk reduction in a society due to its flagrant sodium obsession?

Thus, there are a number of inconsistencies in the thinking surrounding thiazides. In my experience, I have seen more harm done than good using these agents. While I cannot fully reconcile the reported benefit seen in ALLHAT with what I see in real life, all too often I see people having to take another drug to make up for a side-effect of a thiazide diuretic (e.g., high-dose prescription potassium to replace lost potassium, allopurinol to reduce uric acid, etc.). I have seen many people get hospitalized, even suffer near-fatal or fatal events from extremely low potassium or magnesium levels.

My personal view: ALLHAT or no, avoid thiazide diuretics like the plague. Sure, it might save money on a population basis, but I suspect that the ALLHAT data are deeply misleading.

What's better than a thiazide, calcium blocker, or ACE inhibitor? How about vitamin D restoration, thyroid normalization, wheat elimination?

"High-dose" Vitamin D

30. December 2008 William Davis (43)

I stumbled on one of the growing number of local media stories on the power of vitamin D.

In one story, a purported "expert" was talking about the benefits of "high-dose" vitamin D, meaning up to 1000, even 2000 units per day.

I regard this as high-dose---for an infant.

Judging by my experiences, now numbering well over 1000 patients over three years time, I'd regard this dose range not as "high dose," nor moderate dose, perhaps not even low dose. I'd regard it as barely adequate.

Though needs vary widely, the majority of men require 6000 units per day, women 5000 units per day. Only then do most men and women achieve what I'd define as desirable: 60-70 ng/ml 25-hydroxy vitamin D blood level.

I base this target level by extrapolating from several simple observations:

--In epidemiologic studies, a blood level of 52 ng/ml seems to be an eerily consistent value: >52 ng/ml and cancer of the colon, breast, and prostate become far less common; <52 ng/ml and cancers are far more likely. I don't know about you, but I'd like to have a little larger margin of safety than just achieving 52.1 ng/ml.

--Young people (not older people >40 years old, who have lost most of the capacity to activate vitamin D in the skin) who obtain several days to weeks of tropical sun typically have 25-hydroxy vitamin D blood levels of 80-100 ng/ml without adverse effect.

More recently, having achieved this target blood level in many people, I can tell you confidently that achieving this blood level of vitamin D achieves:

--Virtual elimination of "winter blues" and seasonal affective disorder in the great majority
--Dramatic increases in HDL cholesterol (though full effect can require a year to develop)
--Reduction in triglycerides
--Modest reduction in blood pressure
--Dramatic reduction in c-reactive protein (far greater than achieved with Crestor, JUPITER trial or no)
--Increased bone density (improved osteoporosis/osteopenia)
--Halting or reversal of aortic valve disease

(I don't see enough cancer in my cardiology practice to gauge whether or not there has been an impact on cancer incidence.)

My colleagues who have bothered to participate in the vitamin D conversation have issued warnings about not going "overboard" with vitamin D, generally meaning a level of >30 ng/ml.

I know of no rational basis for these cautions. If hypercalcemia (increased blood calcium) is the concern, then calcium levels can be monitored. I can reassure them that calcium levels virtually never go up in people (without rare diseases like sarcoid or hyperparathyroidism). Then why any hesitation in recreating blood levels that are enjoyed by tropical inhabitants exposed to plentiful sun that achieve these extraordinary health effects?

For the present, I have applied the target level of 60-70 ng/ml without apparent ill-effect. In fact, I have witnessed nothing but hugely positive effects.

Vitamin D Home Test

29. December 2008 William Davis (13)

The ever-resourceful Dr. John Cannell of the Vitamin D Council has announced the availability of an at-home, self-ordered vitamin D test kit for $65. The Vitamin D Council newsletter is reprinted below.

(However, please note that, as wonderful as the advice Dr. Cannell provides, I don't agree on several small points, such as the lack of need for vitamin D if you use a tanning bed or obtain "sufficient" sun; I have seen many people with dark tans, virtually all over 40 years old, who are still severely deficient. I attribute this to the lost capacity for vitamin D activation as we age.)

I have not used this service. Should anyone choose to try it, please let us know how it goes.

The Vitamin D Newsletter
December 28, 2008

The Vitamin D Council is happy to announce that we have partnered with ZRT Laboratory to provide an inexpensive, $65.00, in-home, accurate, vitamin D [25(OH)D] test. The usual cost for this test is between $100.00 and $200.00.

If you read this newsletter, you know about our interest in accurate vitamin D testing. In the next few weeks, you may read about the Vitamin D Council's quest for accurate vitamin D blood tests in the national media. Before we partnered with ZRT, we verified, repeatedly, that ZRT provides accurate and reliable vitamin D tests and that their method corresponds very well to the gold standard of vitamin D blood tests, the DiaSorin RIA.

Our ZRT service is not just inexpensive, it means no more worrying about your doctor ordering the right test or interpreting it correctly. You buy the test kit on the internet or by phone, a few days later the kit comes in the mail, you or a nurse friend do a finger stick, collect a few drops of blood, and send the blotter paper back to ZRT in the postage paid envelope provided with the kit. A week later you get results back in the mail and know accurate 25-hydroxy-vitamin D levels of you and your family.

For every test you order, ZRT will donate $10.00 to the Vitamin D Council. Please read the new page hyperlinked below on our website as it both explains the procedure and how to order the test.

http://www.vitamindcouncil.org/health/deficiency/am-i-vitamin-d-deficient.shtml

Executive summary: keep your family's 25-hydroxy-vitamin D blood test above 50 ng/ml, year around. Most adults need at least 5,000 IU per day, especially this time of year. Most children need at least 1,000 IU per day per every 25 pounds of body weight. Bio Tech Pharmacal provides high quality and inexpensive vitamin D. Currently Bio Tech Pharmacal is providing vitamin D for numerous scientific studies. To see their prices and for ordering, click the hyperlink below.

http://www.bio-tech-pharm.com/catalog.aspx?cat_id=2

As a gift to our readers for the New Year, Thorne publications have provided a free download to a basic paper about vitamin D. I wrote it earlier this year for educated lay people as well as health care practitioners. Please read this paper carefully, your family's well-being, even lives, may depend on you understanding it.

http://www.thorne.com/altmedrev/.fulltext/13/1/6.pdf

Seasons Greetings
John Cannell, MD
vitamindcouncil.org

Where do Track Your Plaque membership revenues go?

26. December 2008 William Davis (9)

People pay about $90 per year to become Members on the Track Your Plaque website. This provide access to our in-depth Special Reports, guides, webinars, and our proprietary software data tracking tools. Members can also participate in online discussions, such as those in the Track Your Plaque Forum and chats.

Why is there a charge for membership in the program and where does the money go?

Money raised from membership fees goes towards:

1) The costs of doing business, e.g., server fees, software purchases, legal fees. Hosting webinars, for instance, costs us about $99 per month for the GoToWebinar software service.

2) Software development--Our most recent round of software data tracking tools, for instance, cost us nearly $30,000. That may not be a lot from big business standards, but it is onerous enough that obtaining membership dues really helps.

3) Graphics development--A website without graphics would be awfully dull, regardless of the quality of the textual content. Some of the newest tools on the Track Your Plaque website require photography and graphics work, which can add up very quickly.

Where membership fees do NOT go:

1) In our pockets--In fact, except for the various contractors who are paid for their services (e.g., software developers), NOBODY on the Track Your Plaque staff are paid: not me, nor any of the behind-the-scenes staff. Some of the staff overlap with my office staff, but they are paid purely out of the office revenues, not out of Track Your Plaque membership dues.

2) Towards overhead costs beyond those listed above--For example, membership fees do not pay for office lease, utilities, phones, etc.

We rely on membership fees because we have chosen to remain as free of commercial bias as possible. We host no advertising, we have no behind-the-scenes corporate or institutional agendas, we show no favoritism to any business or commercial operation. We believe this permits editorial freedom that few other health websites can enjoy. (In fact, I know of no other that is so free of commercial bias, outside of small blogs or narrow-interest websites.)

If you want to see what damage commercial bias can create, just go to a health website like WebMD. I challenge you to find information that is not flagrantly biased by commercial influence, namely that of the drug industry. (According to the WebMD SEC filings, in fact, the great majority--approximately 80%--of their $331 million revenues (2007) were derived directly or indirectly from the drug industry.) This commercial bias reaches into all of WebMD's related businesses, including MedicineNet.com, RxList.com, Medscape.com, and several others.

Preventing heart disease is not a money maker, sad to say. It is, from the perspective of conventional heart care, a big money loser. Undergo a heart catheterization, hospitalization, stent or bypass for anywhere from $14,000 to well over $100,000---or pay $90 for in-depth health information that dramatically reduces the potential need for the hospital and its procedures, minimizes need for prescription medication (statins alone, of course, are a $27 billion annual revenue phenomenon), and achieves all this by maximizing nutrition, self-purchased nutritional supplements, and inexpensive heart scans. Nobody is going to make a bundle off of this approach.

So that is why we charge a membership fee. I often get a laugh from some of the comments of people on this blog or even in my office who believe that we are rolling in money from the website from membership dues. The opposite is true: We don't pay ourselves. Virtually every penny is reinvested back into the website to better serve the Members.

Thumb your nose at swine flu

29. April 2009 William Davis (35)

Judging from what we know about vitamin D, it is highly probable that it confers substantial protection from viral infections, including swine flu.

Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) first connected the dots, identifying the possibility of an influence of vitamin D on incidence of flu.

In 2006, Dr. Cannell reports noticing that the patients in his psychiatric ward in northern California were completely spared from the influenza epidemic of that year, while plenty of patients in adjacent wards were coming down with flu. Dr. Cannell proposed that the apparent immunity to flu in his patients may have been due to the modest dose of 2000 units vitamin D per day he had prescribed that the patients in other wards had not been given. (Since the hospital was run by the state of California, Dr. Cannell apparently had only so much leeway with vitamin D dosing.) While it’s not proof, it’s nonetheless a fascinating and compelling observation.

A similar conclusion was reached in a recent analysis of the National Health and Nutrition Examination Survey demonstrating that the higher the vitamin D blood level, the less likely respiratory infections were.

Personally, I used to suffer through 2 or 3 episodes of a runny nose, sore throat, hacking cough, fevers and feeling crumby every winter. Over the last 3 years since I’ve supplemented vitamin D, I haven’t been sick even once. The past two years I didn’t bother with the flu vaccine, since I suspected that my immunity had been heightened: no flu either winter.

And so it has been with the majority of my patients. Since I began having patients supplement vitamin D to achieve normal blood levels (we aim for 60-70 ng/ml), viral and bacterial infections have become rare.

New research is uncovering myriad new ways that vitamin D enhances natural immune responses to numerous infections, including tuberculosis, bacteria such as those causing periodontal disease and lung infections, and viruses like the influenza virus. Enhanced immunity against cancer is also an intensive area of research on vitamin D.

Will vitamin D supplementation sufficient to achieve desirable blood levels confer sufficient immunity to swine flu should it come to your door? From what we know and what we’ve seen in the few years of vitamin D experience, I think it will in the majority. But I do believe that we should still heed public health warnings to avoid contact with others, minimize exposure to crowds, avoid travel to affected areas, etc.

Will the real LDL please stand up?

26. April 2009 William Davis (13)

The results of the latest Heart Scan Blog poll are in.

The question: How has your LDL been measured? The 187 responses broke down as:

I have only had a conventional calculated value
108 (57%)

NMR LDL particle number
35 (18%)

Apoprotein B
21 (11%)

Direct LDL cholesterol
21 (11%)

Non-HDL cholesterol
8 (4%)

I don't know what you're talking about
23 (12%)

Remember the TV game show, To Tell the Truth? Celebrities would have to guess which of three guests represented the real person, such as the notorious con man, Frank Abagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")

The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!"

If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:

--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation.

--Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL.

--Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.

--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.

--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL.

While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.

Vitamin D and inflammation

25. April 2009 William Davis (9)

We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack.

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.

In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.

Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.

Zitterman A, Frisch S et al.

BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis.
OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects.
DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program.
RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group.

(Calcitriol = 1,25-dihydroxy vitamin D.)

Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.

Even monkeys do it

24. April 2009 William Davis (6)

It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound.

A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku:

“Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.”

Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."
In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning.

Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves.

Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication.

If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?

Image courtesy Wikipedia

Cath lab energy costs

22. April 2009 William Davis (6)

In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory.

A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).

All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging.

Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath.

Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing.

At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs.

If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold.

By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluids.

That's just one procedure. The amount of trash generated by these procedures is staggering, much of it plastic. I don't know how much of the U.S.'s annual plastic trash burden of 62 billion pounds (source: EPA) originates from the the cath lab, but I suspect it is a big number in total.

So if you are truly interested in reducing your carbon footprint and doing your part to be "green," avoid a trip (or many) to the cath lab.

Wag the Dog

20. April 2009 William Davis (7)

What if the system to provide heart care has already gotten as big as it should be?

Worse (for hospitals), what if it’s already far larger than it needs to be? Can the system continue to increase revenues if they’ve already attained titanic proportions and outgrown demand? After all, darn it, there are only so many sick people around.

Hospital administrators might have to face an unpleasant choice: downsize to strip excess capacity and suffer the consequences in a competitive market, or . . . fabricate demand for their services.

Like the Dustin Hoffman and Robert DeNiro characters in the movie, Wag the Dog, about how two media-manipulators divert public attention away from a Presidential sex scandal by fabricating a war, spin is everything. It’s enough to sidetrack public attention from a scandal, obscure a truth, send us on a useless detour.

If healthcare for the heart isn’t driven by need, but many still desire to reap the benefits of the procedure-focused system, why not increase the perceived need?

That’s precisely the course that many hospital systems have chosen to follow. If the market you serve has been tapped to its full potential, then grow the market.

Imagine if a company like General Motors were to operate this way. In 2006, for instance, GM sold 9.1 million automobiles. If GM executives were to decide that they’d like to outstrip Toyota by boosting sales by 10% to 10 million, how would they do it? They would first have to determine whether it was feasible to grow demand for their product. If deemed possible, the company would need to ramp up manufacturing capacity to anticipate increased demand. If they miscalculate, GM could be stuck with a costly surplus and have to swallow the costs, maybe selling leftovers at a loss. (We don’t mean to pick specifically on GM; they’re a fine company as far as we’re concerned. This is just a hypothetical illustration.)

But what if a company could concoct some sort of scheme to persuade the car-buying public that they just had to have their cars or trucks? In other words, they could, in effect, create demand for their products.

As perverse as it sounds, that is exactly what occurs in healthcare for heart disease. The system long ago exceeded the necessary level of infrastructure to maintain a high-quality level of care accessible to most Americans. Instead, it continues to grow through a distortion of perception, delivering more services of increasing complexity to larger and larger numbers of people.

The size of the market is therefore a manipulable thing, something that can be massaged and cultivated. There are a variety of clever ways to exaggerate the need for heart procedures.

Why not raise the alarm for heart disease every chance you get? When a local sports figure survived a heart attack here in Milwaukee, St. _____ marketing department was right there, broadcasting the process in TV ads after his recovery. What could be more American than baseball, apple pie . . . and St. _____ Hospital? After his hospital discharge, the 57-year old local icon was shown on the sidelines with his team, back on the job, and at home with family, all beaming, just three months after a bypass operation. “I received only the very best care at St. _____ Hospital. They treated me like family. St. _____ doctors and nurses are the best!” Predictably, a two-month long spike in hospital testing followed filled with people worried whether they, too, might be in imminent danger. Several local cardiologists boasted of the many sports figures who came through the stress testing and heart catheterization labs, though virtually all checked out to be fine.

Though it can serve a legitimate purpose in some situations, stress tests are the ultimate example of a heart scam built on the perception of danger. Pull people in with promises of reassuring them whether or not they have heart disease, only to provide murky results that usually do no such thing. The pitfalls of the test are turned to advantage. The all too common equivocal or mildly abnormal result can be converted into a hospital procedure. (Imagine you could perform such alchemy on the uncertain calculations on your income taxes.)

With millions of stress tests performed every year and the push to perform more and more screening tests, the market has, in effect, been expanded—even though no increase in the disease itself has actually occurred.

Beware: As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine.

Heart scan book

20. April 2009 William Davis (0)

There are only two books on heart scans available.

One, of course, is Track Your Plaque.

The other is the basic book on heart scans, What Does My Heart Scan Show?

Lost in the navigation column to the left on this blog is the link to get the electronic version of the book. In case you didn't know, we make this available for free.

If you're interested, just go here. This book can provide many basic answers to the questions that often arise regarding heart scans, such as the expected rate of increase in score, how your score compares to other people, when should a stress test be considered. Many heart scan centers use this book for educational purposes to help patients understand the importance of their heart scan scores.

(The sign-up for the book requires that an e-mail address be entered.)

The hard copy of What Does My Heart Scan Show? is available from Amazon, also, for $12.99.

Lies, damned lies, and statistics

18. April 2009 William Davis (8)

In the last Heart Scan Blog post, I discussed the question of whether statin drugs provide incremental benefit when excellent lipid values are already achieved without drugs.

But I admit that I was guilty of oversimplification.

One peculiar phenomenon is that, when plaque-causing small LDL particles are reduced or eliminated and leave relatively benign large LDL particles in their place, conventional calculated LDL overestimates true LDL.

In other words, eliminate wheat from your diet, lose 25 lbs. Small LDL is reduced as a result, leaving large LDL. Now the LDL cholesterol from your doctor's office overestimates the true value.

Anne raised this issue in her comment on the discussion:

I eliminated wheat - and all grains - from my diet nearly three years ago (I eat low carb Paleo). My fish oils give me a total of 1680 mg EPA and DHA per day, and my vitamin D levels since last year have varied between 50 ng/ml and 80 ng/ml. However, my lipid profile is not like either John's or Sam's:

LDL cholesterol 154 mg/dl
HDL cholesterol 93 mg/dl
Triglycerides 36 mg/dl
Total cholesterol 255 mg/dl

My cardiologist and endocrinologist are happy with my profile because they say the ratios are good, no one is asking me to take a statin. My calcium score is 0.

However, if we were to measure LDL, not just calculate it from the miserably inaccurate Friedewald equation, we would likely discover that her true LDL is far lower, certainly <100 mg/dl. (My preferred method is the bull's eye accurate NMR LDL particle number; alternatives include apoprotein B, the main apoprotein on LDL.)

So Anne, don't despair. You are yet another victim of the misleading inaccuracy of standard LDL cholesterol determination, a number that I believe should no longer be used at all, but eliminated. Unfortunately, it would further confuse your poor primary care doctor or cardiologist, who--still believe in the sanctity of LDL cholesterol.

By the way, the so-called "ratios" (i.e., total cholesterol to HDL and the like) are absurd notions of risk. Take weak statistical predictors, manipulate them, and try to squeeze better predictive value out of them. This is no better than suggesting that, since you've installed new brakes on your car, you no longer are at risk for a car accident. It may reduce risk, but there are too many other variables that have nothing to do with your new brakes. Likewise cholesterol ratios.

Aspirin, Lipitor, and a low-fat diet

17. April 2009 William Davis (0)

Despite all the hoopla heart disease receives in the media, I continue to marvel at how many people I meet who still think that aspirin, Lipitor, and a low-fat diet constitute an effective heart attack prevention program.

It doesn't. No more than washing your hands prevents all human infections. It helps, but it is a sad substitute for a real prevention program.

Of course, aspirin, Lipitor, and a low-fat diet is the same recipe followed by the unfortunate Tim Russert and his doctors. You know how that turned out. Mr. Russert's experience is far from unique.

What is so magical about aspirin, Lipitor and a low-fat diet?

There is a simple rationale behind this approach. Aspirin doesn't reduce atherosclerotic plaque growth, but it inhibits the propagation of a blood clot on top of a coronary plaque that has "ruptured," thereby reducing likelihood of heart attack (which occurs when the clot fills the artery). So aspirin only provides benefit if and when a plaque ruptures.

Lipitor and other statin drugs reduce LDL cholesterol, promote a modest relaxation of constricted plaque-filled arteries (normalization of endothelial dysfunction), and exerts other effects, such as inflammation suppression.

A low-fat diet is intended to reduce saturated fat that triggers LDL cholesterol formation and to encourage intake of whole grains that reduce cardiovascular events and LDL cholesterol.

If that is the extent of your heart disease prevention program, you will have a heart attack, bypass surgery, or stent--period. It may not be tomorrow or next Friday, or even next month. Aspirin, Lipitor, and a low-fat diet may delay your heart attack or procedure for a few years, but it will not stop it.

Some flaws in the aspirin, Lipitor, low-fat program:

--Aspirin can only exert so much blood clot-blocking effect. It can be overwhelmed by many other factors, such as increased blood viscosity, increased fibrinogen (a blood clotting protein that also triggers plaque), and plaque inflammation.
--Lipitor reduces LDL, but does not discriminate between the relatively harmless large LDL and the truly plaque-triggering small LDL--it reduces all LDL, but small LDL can still persist, even at extravagant levels since neither aspirin nor Lipitor specifically reduces small LDL, while a low-fat diet increases small LDL.
--Low-fat diet--A diet reduced in fat and loaded with plenty of "healthy whole grains" will trigger increased small LDL (an enormous effect), c-reactive protein, high blood sugar, resistance to insulin, high blood pressure, and an expanding abdomen ("wheat belly").

Aspirin, Lipitor and a low-fat diet do not address:

--Vitamin D deficiency
--Omega-3 fatty acid deficiency and the eicosanoid path to inflammation
--High triglycerides
--Small LDL particles
--Distortions of HDL "architecture"
--Lipoprotein(a)--the worst coronary risk factor nobody's heard of
--Thyroid status

In other words, the simple-minded, though hugely financially successful, conventional model of heart disease prevention is woefully inadequate.

Don't fall for it.

Statin drugs for everybody?

17. April 2009 William Davis (10)

Who is better off?

John takes Crestor, 40 mg per day:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl

Or Sam:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl

who obtained these values through vitamin D normalization (to increase HDL); wheat elimination (to reduce triglycerides and LDL); and omega-3 fatty acids (to reduce triglycerides).

Believe the drug industry (motto: If some statin is good, more statin is better!), then John is clearly better off: He has obtained all the "benefits" of statin drugs. They refer to the "pleiotropic" effects of statin drugs, the presumed benefits that extend outside of cholesterol reduction. The most recent example are the JUPITER data that demonstrated 55% reduction in cardiovascular events in people with increased c-reactive protein (CRP). Media reports now unashamedly gush at the benefits of Crestor to reduce inflammation.

However, on Sam's program, elimination of wheat and vitamin D both exert anti-inflammatory effects on CRP, typically yielding drops of 70-90%--consistently, rapidly, and durably.

So which approach is really better?

In my experience, there is no comparison: Sam is far better off. While John will reduce his cardiovascular risk with a statin drug, he fails to obtain all the other benefits of Sam's broader, more natural program. John will not enjoy the same cancer protection, osteoporosis and arthritis protection, relief from depression and winter "blues," and increased mental and physical performance that Sam will.

If our goal is dramatic correction of cholesterol patterns and reduction of cardiovascular risk, for many, many people statin drugs are simply not necessary.

Stents, defibrillators, and other profit-making opportunities

Will radiation kill you?

Are you using bogus supplements?

It really helps to have someone to lean on

Five foods that can booby trap your heart disease prevention program

Breakfast of champions?

In heart disease prevention, shoot for perfection

The epidemic of small LDL

A great discussion on vitamin D

MSNBC Report: We need more heart procedures!

CIS: Carbohydrate intolerance syndrome