Self-directed health: At-home lab testing

29. March 2009 William Davis (20)
I have a prediction.

I predict that more and more healthcare can and will be obtained directly by the individual--without doctors, without hospitals, without the corrupt profit-at-any-costs modus operandi of the pharmaceutical industry. I predict that, given the right tools, Joe or Jane Q. Public will have the choice to manage his or her own health using tools that are directly accessible, tools that include direct-to-consumer medical imaging (CT scans, ultrasound, MRI, etc.), nutritional supplements (a loosely-defined term, to our advantage), and direct-to-consumer laboratory testing.

Done responsibly, self-directed healthcare is superior to healthcare from your doctor. While no one expects you to remove your own gallbladder, you can manage cholesterol, blood sugar issues, vitamin D, low thyroid, and others--better than your doctor.

As everyone becomes more comfortable with the notion of self-directed health, you will see new services appear that help individuals manage their health. You will see prices for direct-to-consumer medical imaging and lab testing drop due to competition, something that doesn't happen in current insurance-based healthcare delivery. People are being exposed to larger deductibles and/or draw money from a medical savings account and will seek more cost advantages. Such direct-to-consumer competitive pricing will meet those needs. Overall, the presently unsustainable cost of healthcare will decline.

To help accelerate the shift of human healthcare away from conventional paths and divert it towards the individual, we have launched a panel of direct-to-consumer at-home laboratory tests that we are making available on the Track Your Plaque website.

On your own (except in California, which requires a doctor's order or prescription; and NY, the only state in the nation that prohibits entirely), you can now test, in the comfort of your own home with no laboratory blood draw required, parameters including:

--Thyroid tests--Free T3, free T4, TSH
--Lipids
--C-reactive protein
--Vitamin D
--Testosterone
--Progesterone

and others.

As the technology improves, more tests will become available for testing at home. (Lipoproteins are not yet available, but will probably be available within the next few years. That would be an enormous boon to those of us interested in supercharged heart disease prevention and reversal.)

Anyone interested in our at-home testing can just go to the Track Your Plaque lab test Marketplace.

When I first began the Track Your Plaque program around 8 years ago, I saw it as a way for people to learn how to control or reverse coronary atherosclerotic plaque, and I'd hoped that physicians would begin to see the light and become patient advocates in this process. But I have lost hope that most of my colleagues are interested in becoming your advocate in health. They are too locked into the "call me when you hurt" mentality. I now see Track Your Plaque as a way for people to seize control over coronary plaque with minimal assistance from their doctors. Indeed, some of our Members have achieved reduction of their plaque in spite of their doctors.

This is just the tip of the iceberg of what's to come. Brace yourself for a cataclysmic shift in returning health to you and away from those who would profit from your misfortune.

Vitamin D for Peter, Paul, and Mary

27. March 2009 William Davis (15)
Why is it that vitamin D deficiency can manifest in so many different ways in different people? One big reason is something called vitamin D receptor (VDR) genotypes, the variation in the receptor for vitamin D.

It means that vitamin D deficiency sustained over many years in:

Peter yields prostate cancer

Paul yields coronary heart disease and diabetes

Mary yields osteoporosis and knee arthritis.


Same deficiency, different diseases.

VDR genotype-determined susceptibility to numerous conditions have been identified, including Graves' thyroiditis, osteoporosis and related bone demineralization diseases, prostate cancer (Fok1 ffI genotype), ovarian cancer, rheumatoid arthritis, breast cancer (Fok1 ff), birth weight of newborns, melanoma and non-melanoma skin cancers, insulin resistance and metabolic syndrome, susceptibility to type I diabetes, Crohn's disease, and neurological or musculoskeletal deterioration with aging that leads to falls, respiratory infections, kidney cancer, even periodontal disease.


Why is it that the dose of vitamin D necessary to reach a specific level differs so widely from one person to the next? VDR genotype, again. Variation in blood levels of 25-hydroxy vitamin D from a specific dose of vitamin D can vary three-fold, as shown by a University of Toronto study. In other words, a dose of 4000 units per day may yield a 25-hydroxy vitamin D blood level of 30 ng/ml in Mary, 60 ng/ml in Paul, and 90 ng/ml in Pete--same dose, different blood levels.

Should we all run out and get our VDR genotypes assessed? So far the data have not progressed far enough to tell us. If, for instance, you prove to have the high-risk Fok1 ff genotype, would you do anything different? Would vitamin D supplementation be conducted any differently? I don't believe so.

Virtually all of us should be supplementing vitamin D at a dose that generates healthy blood levels, regardless of VDR genotype. For those of us following the Track Your Plaque program for coronary plaque control and reversal, that means maintaining serum 25-hydroxy vitamin D levels between 60-70 ng/ml.

As the fascinating research behind VDR genotype susceptibility to disease unfolds, perhaps it will suggest that specific genotypes be somehow managed differently. Until then, take your vitamin D.

Blowup at Milwaukee Heart Scan

26. March 2009 William Davis (20)
A local TV investigative news report just ran a critical report of the goings-on at Milwaukee Heart Scan:

Andy Smith went to Milwaukee Heart Scan. "It passed the smell test like a road kill skunk. I mean it was bad," Smith explained.

Our hidden cameras went inside the high pressure sales pitch. "On a good day I sell eight, nine, 10 people. On a bad day probably three," sales manager Angelo Callegari told us.


What the heck happened?

Let me tell you a story.

Back in 1996, I learned of a new technology called UltraFast CT scanning, or electron-beam tomography (EBT), a variation on the standard CT technology that permitted very rapid scanning, sufficiently rapid to allow visualization of the coronary arteries. Back then, only a few dozen devices had been established nationwide.

But the technology was so promising and the initial data so powerful that I lobbied several hospital systems in town to consider purchasing one of the $1.8 million devices. I was interested in applying this exciting technology for early detection of coronary heart disease in Milwaukee. While administrators from several hospitals listened, they quickly lost interest when they figured out that the scanner was primarily a tool for prevention, and would not be directly useful to increase revenue-generating hospital procedures.

I floundered about for a year, trying to drum up support for obtaining a scanner. The manufacturer of the device, Imatron, put me in touch with a couple from Indiana who were also interested in setting up a scanner and had actually obtained the investment capital to do it. We met and, over the next year, got Milwaukee Heart Scan up and running. I served as Medical Director (but never an investor or owner).

Milwaukee Heart Scan was busy from day one, performing EBT heart scans, as well as CT coronary angiograms as long ago as the late 1990s, virtual colonoscopies, and other imaging tests. We all spent a great deal of time educating the public and physicians on what this technology meant for detection and prevention of disease.

Despite the public's perception that the owners, Nancy and Steve Burlingame, were making a bundle of money, in reality they could barely pay their expenses. As price competition heated up in Milwaukee with the lower-cost competing multidetector scanners cropping up, the Burlingames often did not pay themselves.

My interest was to keep this device afloat. I therefore told the Burlingames that they should pay their bills first--their staff, overhead, the scanner costs, and pay themselves--and not worry about reimbursing me for the (very modest) heart scan interpretation fees. For several years, I read thousands of scans without any compensation. But that was okay with me--I just wanted to be sure this device remained available.

But in 2008, some business people from Chicago contacted Steve Burlingame with prospects of applying a contract model of long-term scanning to patients,i.e.,getting people to sign a several-year contract for discounted imaging. They proposed that Milwaukee Heart Scan offer heart scans for free to get people in the door.

What was peculiar about all this is that none of the four physicians on staff at Milwaukee Heart Scan had any knowledge of these discussions at all, including myself. Personally, I figured something was afoot when I came in to read scans in the summer of 2008. While, ordinarily, there is a single stack of scans to read from the preceding few days, this time there were numerous stacks of scans, hundreds of scans in all. Not a word had been said to me or my colleagues. I quickly figured out (thanks to the staff filling me in) that they had been offering scans for free. Not surprisingly, many people took them up on the offer.

Up until then, I had been readily willing to read heart scans without compensation, provided I could perform scan readings in a modest time commitment every week on the weeks it was my responsibility. But work several hours every day for free? Impossible.

My colleagues and I were deeply upset and concerned and insisted on a meeting with all the people involved, including the Burlingames, who had engineered this new sales program. We expressed serious reservations about what they were doing and insisted that they dramatically scale back the promises being made to people. I personally asked that they fire several of the people they had hired as sales people, given what we thought was unprofessional appearance and behavior.

The Burlingames and their new business partners essentially thumbed their noses at the physicians and ignored our advice. So, of the four physicians (one radiologist, three cardiologists), three of us resigned. (The one remaining cardiologist, I believe, didn't really understand what was going on.)

Apparently, after we left, the hard sales tactics continued. The news media got hold of the story through some understandably disgruntled people, and you know the rest.

The tragedy in all this is that, as wonderful as heart scans are, they don't make money for the people who invest in the technology. In the sad case of Milwaukee Heart Scan, it meant that my former friends, the Burlingames, turned to questionable tactics to make this technology pay.

Make no mistake: Heart scans remain a wonderful medical imaging modality. EBT, in particular, remains a fabulous technology that would--even today--remain the pre-eminent means to image coronary arteries, except that GE (who acquired Imatron some years ago) decided that a more direct path to bigger revenues was to purchase Imatron, then promptly scrap the entire operation, choosing to focus on multidetector technology exclusively.

Don't let the spotty past and petty ambitions cloud the fact that heart scans remain the best way to identify and track coronary plaque. Just don't get tempted by the offer of any free scans "without obligation."

Do you work for the pharmaceutical industry?

24. March 2009 William Davis (30)
In response to my post, Lovaza Rip-off, I received this angry comment:


Very high triglycerides, as you all know, is a very serious and life-threatening condition. Therefore, it is very important that any medication you take for treatment must be FDA proven and scientifically backed. This is true for a few reasons. First, there have been zero studies done to show the effects of Costco brand fish oil pills on patients with high triglycerides. So, you cannot assume, simply because the pills you are taking "claim" to have a certain amount of Omega 3 in the them, that they actually do (supplement labeling is self-submitted by the company, and not regulated by any external or 3rd party agency).

Secondly, the other components in fish oil, and maybe in Costco brand (no one knows because it isn't on the label) can actually inhibit the bioavailablity of Omega 3, most notably, Omega 6. And, nowhere on the Costco label does it tell you how much Omega 6 is in it. We also cannot underestimate the importance of purity with these compounds: a top selling brand of fish oil found stores like CVS was recently recalled because it was found to have large amounts of fire retardant in it! These supplements are NOT regulated by the FDA.

Thirdly, be careful when you compare costs. The cost of hospitalization due to acute pancreatitis (a risk of very high triglycerides) far outweighs the cost of taking Lovaza for even several years. If you have a real disease, you need a real drug. And, until Costco does a prospective long-term clinical trial to show that it lowers triglycerides, it should not be used in place of Lovaza.

Finally, I am a living example of how taking a high-potency supplement form of Omega 3 barely lowered my triglycerides, yet within 2 weeks of being on Lovaza there was a significant difference. I am now at my goal. So, before you knock a company, that, in my opinion, has saved my life, please do your research and do not mislead people into thinking that an Omega 3 is an Omega 3 is an Omega 3. If your insurance covers the most potent, the most pure, and the ONLY proven Omega 3 pill on the market, you should be thankful.


The comment was posted anonymously, so I don't know who it came from. But I can tell who I think it is: Someone who works for the drug industry.

This is a common phenomenon: Large corporations are fearful of the comments that are generated on internet conversations and other media. On the internet, there are actually people whose job it is to do "damage control." I suspect this came from one of them.

Why bother? Surely there are better things to do? Well, that's easy. There are billions of dollars at stake. Lovaza, in particular, is sold on the perception that it is somehow superior. If word gets out that maybe you can achieve the same results at a fraction of the cost . . .

Perhaps the "commenter" should also question whether omega-3 fatty acids can come from eating fish.

As part of my cardiology practice, I provide consultation on complex hyperlipidemias, or unusual lipid abnormalities. I have many patients with something called familial hypertriglyceridemia, a genetic condition that permits triglyceride levels of 500, 1000, even many thousands of mg/dl, levels that, as the anonymous commenter points out, can be dangerous.

I virtually never prescribe Lovaza for these people. In their treatment program, I use simple fish oil supplements, such as that from Costco, Sam's Club, or other retailers. I have not witnessed a single failure in treating these people and reducing triglycerides. People with lesser triglyceride abnormalities likewise respond very nicely to inexpensive fish oil that we can buy at the health food store. (I do rely on useful services like Consumer Reports and www.consumerlab.com to reassure us that no pesticide residues, mercury, or other contaminants are in the brands we use.) Excellent, high-quality fish oil supplements are sold by Carlson, Life Extension, Barlean's, even the Members' Mark brand from Sam's Club.

So, the notion that only prescription fish oil is capable of reducing triglycerides is, in a word, nonsense.

Take that back to your CEO.

Cholesterol effects of carbohydrates

24. March 2009 William Davis (31)
Let's take a hypothetical person, say, a 50-year old male. 5 ft 10 inches, 160 lbs, BMI 23.0. He's slender and in good health.

Our hypothetical man eats a simple diet of vegetables, some fruit, nuts, and meats but avoids processed industrial foods. By macronutrient composition, his diet is approximately 30% protein, 40-50% fat, 20-30% carbohydrate. His starting lipid panel:

Total cholesterol 149 mg/dl
LDL cholesterol 80 mg/dl
HDL 60 mg/dl
Triglycerides 45 mg/dl

His starting lipids are quite favorable (though I don't often see this kind of starting panel nowadays except in athletes). We begin here because this hypothetical man is going to serve as our test subject.

We ask our hypothetical man to load his diet up on "healthy whole grains." He complies by eating whole grain cereals for breakfast, whole wheat toast; sandwiches made with whole grain bread; dinners of whole wheat pasta; snacks of granola bars, whole wheat pretzels and crackers.

Three months later, his lipids show:

Total cholesterol 175 mg/dl
LDL cholesterol 130 mg/dl
HDL 45 mg/dl
Triglycerides 150 mg/dl


You can see that LDL cholesterol has increased, HDL has dropped, and triglycerides have increased. This wave of change is the hallmark of carbohydrate excess, but more specifically of overreliance on wheat products. Beyond his lipid panel, the man has gained 10 lbs, all concentrated in a soft roll around his abdomen, his blood sugar is now in the "borderline range" of between 110 and 126 mg/dl, i.e., pre-diabetic.

If we were to examine this man's advanced lipoproteins (e.g., NMR from Liposcience, or VAP from Atherotech), we would see that there has been an explosive increase in small LDL particles, along with a shift of large HDL to small, and the appearance of multiple abnormal classes of particles called VLDL and IDL (signalling abnormally slowed clearance of dietary by-products from the blood).

Familiar scenario? The "after-carbohydrate" situation is the rule among the people who I first meet who claim to be eating a "healthy" diet, though their patterns are usually much worse, with higher LDL, lower HDL, and much higher triglycerides, an exaggeration of our hypothetical man's abnormalities.

What if our hypothetical man now goes to his conventionally thinking (read "taught medicine by the pharmaceutical industry") physician? What will likely be the advice he receives? Reduce his saturated fat intake, eat plenty of healthy whole grains, take a statin drug.

Although my illustrative man is hypothetical, I've seen this scenario play out many thousands of times. It happens in real life all the time. It is predictable, it is highly manipulable. Sadly, it is rarely recognized for what it is: the result of excess carbohydrates, or what I call "Carbohydrate Intolerance Syndrome."

The misinterpretation of this condition has created 1) an epidemic of diabetes and pre-diabetes, 2) a nation of frustrated obese Americans, 3) a $27 billion per year statin industry, 4) another growth opportunity for the drug industry in diabetes drugs.

Wheat Belly Revisited

23. March 2009 William Davis (24)
Do you have a wheat belly?

When I first coined this phrase back in July, 2007, I had witnessed the phenomenal health effects of wheat elimination in several hundred patients.

In the nearly two years that have passed since my original post, I have witnessed hundreds more people who have done the same: eliminate pretzels, crackers, breads of all sorts, bagels, pasta, muffins, waffles, pancakes, etc.

If anything, I am convinced now more than ever that wheat is among the most destructive foods in the human diet. At least 70% of people who eliminate wheat from their diet obtain at least one, if not several, substantial health benefits.

Now, if I were trying to sell you something, say, an alternative to wheat, then you should be skeptical. If I tell you that drug or nutritional supplement X is great and you should take it, only to follow it with a sales pitch, you should be skeptical.

What am I selling? Nothing. I gain nothing by telling everyone to avoid wheat. In fact, I wish it wasn't true. Wheat foods taste good. Wheat flour makes great comfort foods. In years past, I spent many hours sitting at the bagel shop reviewing papers over a cup of coffee and a bagel. No longer.

So here, back by popular demand, the original Wheat Belly post:



Wheat Belly

You've heard of "beer bellies," the protuberant, sagging abdomen of someone who drinks excessive quantities of beer.

How about "wheat belly"?

That's the same protuberant, sagging abdomen that develops when you overindulge in processed wheat products like pretzels, crackers, breads, waffles, pancakes, breakfast cereals and pasta.



(By the way, this image, borrowed from the wonderful people at Wikipedia, is that of a teenager, who supplied a photo of himself.)

It represents the excessive visceral fat that laces the intestines and triggers a drop in HDL, rise in triglycerides, inflames small LDL particles, C-reactive protein, raises blood sugar, raises blood pressure, creates poor insulin responsiveness, etc.

How common is it? Just look around you and you'll quickly recognize it in dozens or hundreds of people in the next few minutes. It's everywhere.

Wheat bellies are created and propagated by the sea of mis-information that is delivered to your door every day by food manufacturers. It's the same campaign of mis-information that caused the wife of a patient of mine who was in the hospital (one of my rare hospitalizations) to balk in disbelief when I told her that her husband's 18 lb weight gain over the past 6 months was due to the Shredded Wheat Cereal for breakfast, turkey sandwiches for lunch, and whole wheat pasta for dinner.

"But that's what they told us to eat after Dan left the hospital after his last stent!"

Dan, at 260 lbs with a typical wheat belly, had small LDL, low HDL, high triglycerides, etc.

I hold the food companies responsible for this state of affairs, selling foods that are clearly causing enormous weight gain nationwide. Unfortunately, the idiocy that emits from Nabisco, Kraft, and Post (AKA Philip Morris); General Mills; Kelloggs; and their kind is aided and abetted by organizations like the American Heart Association, with the AHA stamp of approval on Cocoa Puffs, Cookie Crisp Cereal, and Berry Kix; and the American Diabetes Association, whose number one corporate sponsor is Cadbury Schweppes, the biggest soft drink and candy manufacturer in the world.

As I've said many times before, if you don't believe it, try this experiment: Eliminate all forms of wheat for a 4 week period--no breakfast cereals, no breads of any sort, no pasta, no crackers, no pretzels, etc. Instead, increase your vegetables, healthy oils, lean proteins (raw nuts, seeds, lean red meats, chicken, fish, turkey, eggs, Egg Beaters, low-fat yogurt and cottage cheese), fruits. Of course, avoid fruit drinks, candy, and other garbage foods, even if they're wheat-free.

Most people will report that a cloud has been lifted from their brains. Thinking is clearer, you have more energy, you don't poop out in the afternoon, you sleep more deeply, some rashes disappear. You will also notice that hunger ratchets down substantially. Most people lose the insatiable hunger pangs that occur 2-3 hours after a wheat-containing meal. Instead, hunger is a soft signal that gently prods you that it's time to consider eating again.

You will also make considerable gains towards gaining control over your risk for heart disease and your heart scan score, a crucial step in the Track Your Plaque program.

Thank you, Crestor

20. March 2009 William Davis (9)
I'm sure everyone by now has seen the Crestor ads run by drugmaker, AstraZeneca. TV ads, magazine ads, and the Crestor website all echoing the same message:

"While I was busy building my life, something else was busy building in my arteries: dangerous plaque."

While previous drug trials with Mevacor, Pravachol, Zocor, and Lipitor have focused mostly on examining whether the drugs reduced incidence of cardiovascular events, Crestor studies have also focused on effects on atherosclerotic plaque volume. The best example is the ASTEROID trial that demonstrated approximately 7% reduction in plaque volume by intracoronary ultrasound.

So the AstraZeneca decision makers took the leap from cholesterol reduction to plaque reduction.

I'm sure this switch wasn't taken lightly, but was the topic of discussion at many meetings before the decision to make plaque reduction the focus of hundreds of millions of dollars of advertising. After all, billions of dollars are at stake in this bloated statin market.

Ordinarily, I couldn't care less about how the drug manufacturers conduct their advertising campaigns. But this one I paid attention to because the Crestor ads are helping fuel a new way of thinking about coronary heart disease: It's not about the cholesterol; it's about the atherosclerotic plaque that accumulates in arteries.

It's not cholesterol that grows, limits coronary blood flow, and causes angina. It's not cholesterol that "ruptures" its internal contents to the surface within the interior of the blood vessel and causes blood clot and heart attack. It's not cholesterol that fragments from the carotid arteries and showers debris to the brain, causing stroke. It's all plaque.

I took the same leap years ago, though not backed by hundreds of millions of dollars of marketing money. When I first called my book Track Your Plaque, some of the feedback I got from editors included comments like "I thought this was a book about teeth!" Even now, the word "plaque" in the book title and website is responsible for confusion.

But AstraZeneca is helping me clear up the confusion. As the word plaque gains hold in public consciousness, it will become increasingly clear that cholesterol reduction is not what we're after. We are looking for reduction of plaque.

If you are trying to develop an effective means to reduce or reverse coronary heart disease, then there are two simple equations to keep in mind:


Plaque = coronary heart disease

Cholesterol ? coronary heart disease


Plaque is the disease, cholesterol is not. Cholesterol is simply a crude risk for plaque.

While I'm no friend to the drug industry nor to AstraZeneca, some good will come of their efforts.

Supermarkets and buggy whips

17. March 2009 William Davis (17)
Will supermarkets eventually phase out, joining the history books as a phenomenon of the past? Or are supermarkets here to stay, an emblem of the industrialization of our food--easy access to foods that are convenient, suit the undiscriminating masses, stripped of nutritional value despite the prominent health claim on the package front?

Anna left an insightful comment on the last Heart Scan Blog post, Sterols should be outlawed, along with some useful advice on how to avoid this trap for poor health called a supermarket:


I rarely shop in regular supermarkets anymore (farm subscription for veggies, meat bought in bulk for the freezer, eggs from a local individual, fish from a fish market, freshly roasted coffee from a local coffee place, etc.). What little else I need comes from quirky Trader Joe's (dark chocolate!), the fish market, farmer's markets, a small natural foods store, or mail order.

When I do need to go into one of the many huge supermarkets near me, not being a regular shopper there, I never know where anything is, so I have to ramble a bit around the aisles before I find what I'm looking for (and I almost always can grab a hand basket, instead of a trolley cart).

It's almost like being on another planet! There's always so many new products (most of them I hesitate to even call food). It's really a shock to the senses now to see how much stuff supermarkets sell that I wouldn't even pick up to read the label, let alone put in a cart or want to taste. I'm not even tempted by 99% of the tasting samples handed out by the sweet senior ladies in at Costco anymore (only thing I remember tasting at Costco in at least 6 mos was the Kerrygold Irish cheese, because I know their cows have pasture access and it's real food).

What's really shocking to me is how large some sections of the markets have become in recent years. While Americans got larger, so did some sections of the supermarket (hint - good idea to limit the consumption of products from those areas). Meat and seafood counters have shrunk, though. Produce areas seem to be about the same size as always (but more of it is pre-prepped and RTE in packaging.

But the chilled juice section is h-u-g-e! And no, I don't think there is a Florida orange grove behind the cases. Come on, how much juice do people need? Juice glasses used to be teeny tiny, for a good reason. To me it looks like a long wall stocked full of sugar water. Avoiding that section will put a nice dent in the grocery expenses.

The yogurt case is also e-n-o-r-m-o-u-s! Your 115 yo Bulgarian "grandmother" wouldn't know what to make of all these "pseudo-yogurts"! Chock full of every possible variety, but very little fit to eat. The only yogurts I'll look at are made with plain whole milk, without added gums, emulsifiers, or non-fat milk solids, and live cultures (I mostly buy yogurt now and then to refresh my starter culture at home). I can flavor them at home if needed. The sterols are showing up in processed yogurts, too, along with patented new strains of probiotic cultures (I'll stick to my old fashioned, but time-proven homemade lacto-cultured veggies and yogurt instead).

I found the same "cooler spread" in the butter & "spread" section. The spread options were just grotesque sounding. Actually, the butter options weren't much better, as many were blended with other ingredients to increase spreadability, reduce calories or cholesterol/saturated fat, etc. A few plain butters were enhanced with "butter flavor" - say what? And on no package could it be determined if the butter came from cows that were naturally fed on pasture or on grain in confined pens.


Well said, Anna.

There's a huge supermarket about 1 mile away from my house similar to the one Anna describes with aisle after aisle of eye-catching cellophane-wrapped foods. I go there about every 3 or 4 months, and then I only go to get something I need in a pinch. Every time I go, I too am reminded just how many products there are that look more like junk food than real food.

But there's no real money in real food. Who gets rich off of selling green peppers, tomatoes, and eggs?

Supermarkets sell these modern industrial foods because people buy it: Look around you. You don't get to be a 250 lb 5 ft 2 inch-woman by eating too many cucumbers.

Like Anna, I drive an additional several miles to Trader Joes', buy at farmers' markets whenever possible, buy some odds and ends like wine and cheese and raw nuts at specialty stores. I grow my own basil in a big pot I keep in the kitchen and we are just about to start turning over the soil in the back yard for our vegetable garden. I don't need nor do I miss having the choice among 40 different chips, 25 brands of ready-made microwavable dinners, an entire aisle of breakfast cereasl (all of which are virtually the same with different names and labels), or 75 varieties of salad dressing.

The supermarket for me--and I hope for many of you--has become a place rarely frequented, and only for the odd forgotten item. Oh, I forgot the dog chewies the grocery does have--my dogs love them. So perhaps they are good for something after all.

Sterols should be outlawed

14. March 2009 William Davis (10)
While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Texas today, tomorrow . . . the world?

10. March 2009 William Davis (0)
Texas state representative, Rene Oliveira, has introduced legislation that mandates heart scans for adults in the state of Texas.

Rep. Oliveira

A press release from the SHAPE Society ( Society for Heart Attack Prevention and Eradication) reads:

Assessment of heart attack risk on the basis of traditional risk factors alone such as high cholesterol and high blood pressure and so forth, while useful, misses many who are at high risk and also incorrectly flags some for high risk who are in fact at very low risk of near term heart attack; on the other hand detection of atherosclerosis by non-invasive imaging, as suggested by the SHAPE group, accurately identifies plaque and improves the ability to identify at-risk individuals who could benefit from aggressive preventive intervention while sparing low-risk subjects from unnecessary aggressive medical therapy," said Dr. P.K. Shah, Director of Cardiology at Cedars Sinai Heart Institute in Los Angeles, a leading member of the SHAPE Task Force who is also an active member of the American Heart Association. "Sadly, these vulnerable patients go undetected until struck by a heart attack, because insurance companies don't cover the newer heart attack screening imaging tests."


Rep. Oliveira, whose coronary disease was first uncovered by a heart scan and prompted a bypass operation, states:

"It is about time that we cover preventive screening for the number one killer in Texas, and take action to reduce healthcare costs through preventive healthcare. Right now, we are extending the lives of those who can afford the procedure while hundreds of thousands of Texans with hidden heart disease go undetected because of antiquated thinking. The time has come for this change."


Is this what we've come to? Since practicing physicians are either so entranced by the drug and procedural solutions to heart disease, do we need to resort to heart scan by legislation?

It does indeed appear that we've come to this point. Should this trend catch on, it will surely mean an upfront increase in healthcare costs to cover the expense of heart scans. But in the long run, it will mean reduction in healthcare costs--dramatic reduction--if heart scans prompt effective preventive action.
Cureality | Real People Seeking Real Cures

Kitchen sink approach for Lp(a)

29. August 2008 William Davis (12)

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

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

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

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

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

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

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

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

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

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

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

Making Dr. Friedewald an honest man

28. August 2008 William Davis (3)
Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

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

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

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

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

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

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

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

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

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

Some basic vitamin D issues

24. August 2008 William Davis (7)
The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

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

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

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

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


Twinb asked:

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

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


Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

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


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

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


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

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

“How much vitamin D should I take?”

22. August 2008 William Davis (17)
It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

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

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

Utter nonsense.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

You probably don't take enough fish oil

20. August 2008 William Davis (17)
The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:


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

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

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

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

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

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



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

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

But what dose is sufficient? What dose is ideal?

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

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

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

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

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

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

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

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

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

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

Vitamin D and HDL

19. August 2008 William Davis (23)
Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

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

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies


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

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

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

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

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

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

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

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

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

Why? How?

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

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

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

Weight loss and blood pressure

15. August 2008 William Davis (6)
Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

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

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

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

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

Why the age-dependent difference?

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

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

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

13. August 2008 William Davis (6)
Brad needed to lose weight.

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

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

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

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

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

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

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

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

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

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

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

I call these changes "transitional" changes in lipids.

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

Divorce court for the doctor-patient relationship?

10. August 2008 William Davis (4)
The doctor-patient relationship has gone sour.

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

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

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

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



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

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

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


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

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

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

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

But a caveat: The patient MUST be informed.

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

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

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

It will be a startling change.

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


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

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

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

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

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

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

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

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

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

Wow. A woman after my own heart.

How much fish oil is enough?

9. August 2008 William Davis (7)

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

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

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

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




Several observations jump out:

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

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

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




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

Taken at face value, this study would argue that:

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

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


We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.
All posts by william-davis

Are you hungry?

6. December 2011 William Davis (43)
Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

30. November 2011 William Davis (22)
If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

19. November 2011 William Davis (29)
At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

14. November 2011 William Davis (73)
More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

2. November 2011 William Davis (0)
Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

30. October 2011 William Davis (53)
Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

21. October 2011 William Davis (39)
Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

19. October 2011 William Davis (33)
Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

14. October 2011 William Davis (21)
Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

14. October 2011 William Davis (6)
A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI."

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.