All posts by william-davis

From Mukuddem-Petersen J, Oosthuizen1 W, Jerling JC. J Nutr 2005.

If you haven't yet done so, adding raw nuts to your health program yields a broad panel of health benefits.

Contrary to conventional advice, nuts can be eaten in unlimited quantities. Provided they are raw--unroasted, unsalted (since salting only accompanies roasted nuts), not roasted in unhealthy oils like hydrogenated cottonseed or soybean (very common)--they do not make you fat, regardless of the quantity consumed. Beer nuts, honey-roasted nuts, mixed nuts roasted in unhealthy oils with salt added are either fattening or exert other unhealthy effects (e.g., hypertension, rise in Lp(a), and cancer from the hydrogenated fats).

Some notable observations from the chart:

--Hazelnuts and macadamians are the richest in monounsaturates
--Walnuts are the richest in the omega-6 linoleic acid, while also richest in the "omega-3" linolenic acid.
--From a fat composition standpoint, raw cashews and dry roasted peanuts aren't so bad.
--Pistachios figure pretty favorably in this analysis, rich in monounsaturates.
--Coconuts are unusually rich in saturated fat, though about half is lauric acid--an issue for future conversation.

Here's a listing of the fiber composition of nuts per 1 oz serving (about a handful):

Almonds (24 nuts) 3.5 g
Brazilnuts, dried (6-8 nuts) 2.1 g
Cashew nuts, dry roasted, with salt added (18 nuts) 0.9 g
Hazelnuts or filberts 2.7 g
Macadamia nuts, dry roasted, with salt added (10-12 nuts) 2.3 g
Mixed nuts, dry roasted, with peanuts, with salt added 2.6 g
Peanuts, all types, dry-roasted, without salt 2.3 g
Pecans (20 halves) 2.7 g
Pine nuts, dried 1.0 g
Pistachio nuts, dry roasted, with salt added (47 nuts) 2.9 g
Walnuts, English (14 halves) 1.9 g

Data courtesy USDA Nutrient Database

Note that almonds are the winners with 3.5 grams fiber per ounce, pistachios a close second. Pine nuts and cashews place last on the fiber content chart.

Not addressed by the charts is protein content of nuts, as well as the low sugar content, all additional beneficial aspects of nuts. Nuts are also a moderate source of magnesium (though seeds like pumpkin and sunflower shine in the magnesium content area).

Rather than micromanage the specific fat and fiber content of your diet, why not get a little of the good of everything on the list and just mix and match the nuts? (Mixed and matched on your own, of course, not a hydrogenated cottonseed oil nut mixture).

Here, I re-post a conversation I've posted before, that of the scam product, "no-flush" niacin, also known as "flush-free" niacin.

I find this issue particularly bothersome, since I have a patient or two each and every week who forgets the explicit advice I gave them to avoid these scam products altogether. Despite costing more than conventional niacin, they exert no effect, beneficial or otherwise. Niacin--the real thing--exerts real and substantial beneficial effects. No-flush or flush-free does nothing except drain your wallet. I continue to marvel at the fact that supplement manufacturers persist in selling this product. Ironically, it commands a significant premium over other niacin forms.

They are outright scams that should be avoided altogether.

My former post, No-flush niacin kills:

Gwen was miserable and defeated.

No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor).

No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small.

Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events.

Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about.

When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended.

What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed.

So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague.

No-flush niacin does not work. Period.

Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin.

Copyright 2008 William Davis, MD

I've recently had several hospital employees tell me that their hospitals offered CT coronary angiograms without charge to their employees.

Among these hospital employees were several women in their 30s and 40s.

Why would young, asymptomatic, pre-menopausal women be subjected to the equivalent of 100 chest x-rays or 25 mammograms? Is there an imminent, life-threatening, symptomatic problem here?

All of these women were without symptoms, some were serious exercisers.

There is NO rational justification for performing CT coronary angiography, free or not.

What they really want is some low-risk, yet confident means of identifying risk for heart disease. Cholesterol, of course, is a miserable failure in this arena. Framingham risk scoring? Don't make me laugh.

Step in CT coronary angiography. But does CT coronary angiography provide the answers they are looking for?

Well, it provides some of the answers. It does serve to tell each woman whether she "needs" a heart procedure like heart catheterization, stent, or bypass surgery, since the intent of CT angiography is to identify "severe" blockages, sufficient to justify heart procedures.

Pitfalls: Because of the radiation exposure, CT angiography is not a procedure that can be repeated periodically to reassess the status of any abnormal findings. A CT angiogram every year? After just four years, the equivalent of 400 chest x-rays will have been performed, or 100 mammograms. Cancer becomes a very real risk at this point.

CT angiography is also not quantitative. Sure, it can provide a crude estimation of the percent blockage--the value your cardiologist seeks to "justify" a stent. But it does NOT provide a longitudinal (lengthwise) quantification of plaque volume, a measure of total plaque volume that can be tracked over time.

What's a woman to do? Simple: Get the test that, at least in 2008, provides the only means of gauging total lengthwise coronary plaque volume: a simple CT heart scan, a test performed with an equivalent of 4 - 10 chest x-rays, or 1 - 2.5 mammograms.

Perhaps, in future, software and engineering improvements will be made with CT coronary angiography that reduce radiation to tolerable levels and allows the lengthwise volume measurement of plaque. But that's not how it's done today.

Beware the dreaded Wheat Deficiency Syndrome.

Like any other syndrome, you can recognize this condition by its many tell-tale signs:

--Flat abdomen
--Rapid weight loss
--High energy
--Less mood swings
--Better sleep
--Diminished appetite
--Reduced blood sugar
--Reduced blood pressure
--Reduced small LDL and total LDL
--Increased HDL
--Reduced triglycerides
--Reduced C-reactive protein and other inflammatory measures

Of course, you could choose to cure yourself of this syndrome simply by taking the antidote: foods made with wheat flour, like bread, breakfast cereals, pastas, pretzels, crackers, and muffins.

All the signs of the syndrome will then disappear and you can have back your protuberant abdomen, irrational mood swings, exagerrated appetite, higher blood sugar, etc.

The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.

Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

That's easy: NONE.

(Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)

In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms.

This question is a common point of confusion.

In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur.

However, EVERY heart scan score above zero is a reason to engage in a program of prevention.

At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.

There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention.

Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life.

Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.

What exactly could Mr. Russert have done to prolong his life? Several basic strategies:

--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half.

--Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.

Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end.

Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"

In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely.

Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.

The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water.

The full text of the study from the EWG can be viewed here.

They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified."

"EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."

For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.

The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.

So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.

If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:

VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl

HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl

Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.

What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.

But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.

Image courtesy Wikipedia.

Copyright William Davis, MD 2008

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.

In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.

Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.

Copyright 2008 William Davis,MD

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.

These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.

Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.

--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.

Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.

All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)

For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.

Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.

How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.

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

DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)

Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)

Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

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

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.

Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.

This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.

Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglycer All posts by william-davis

Can I eat quinoa?

29. July 2011 William Davis (15)

. . . or beans, or brown rice, or sweet potatoes? Or how about amaranth, sorghum, oats, and buckwheat? Surely corn on the cob is okay!

These are, of course, non-wheat carbohydrates. They lack several crucial undesirable ingredients found in our old friend, wheat, including no:

Gliadin--The protein that degrades to exorphins, the compound from wheat digestion that exerts mind effects and stimulates appetite to the tune of 400 additional calories (on average) per day.
Gluten--The family of proteins that trigger immune diseases and neurologic impairment.
Amylopectin A--The highly-digestible "complex" carbohydrate that is no better--worse, in fact--than table sugar.

So why not eat these non-wheat grains all you want? If they don't cause appetite stimulation, behavioral outbursts in children with ADHD, addictive consumption of foods, dementia (i.e., gluten encephalopathy), etc., why not just eat them willy nilly?

Because they still increase blood sugar. Conventional wisdom is that these foods trend towards having a lower glycemic index than, say, table sugar, meaning it raises blood glucose less.

That's true . . . but very misleading. Oats, for instance, with a glycemic index of 55 compared to table sugar's 59, still sends blood sugar through the roof. Likewise, quinoa with a glycemic index of 53, will send blood sugar to, say, 150 mg/dl compared to 158 mg/dl for table sugar--yeah, sure, it's better, but it still stinks. And that's in non-diabetics. It's worse in diabetics.

Of course, John Q. Internist will tell you that, provided your blood sugars after eating don't exceed 200 mg/dl, you'll be okay. What he's really saying is "There's no need for diabetes medication, so you're okay. You will still be exposed to the many adverse health consequences of high blood sugar similar to, though less quickly than, a full diabetic, but that's not my problem."

In reality, most people can get away with consuming some of these non-wheat grains . . . provided portion size is limited. Beyond limiting portion size, there are two ways to better manage your carbohydrate sensitivity to ensure that metabolic distortions, such as high blood sugar, glycation, and small LDL particles, are not triggered.

More on that in the future.

Lipoproteins . . . zero!

27. July 2011 William Davis (23)

With the recent refinements in our approach to correction of the lipoprotein abnormalities that lead to coronary plaque and heart disease risk, I have been witnessing more and more people achieve:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L

For instance, Ted, a 58-year old man I saw in the office today started with:

Small LDL 1673 nmol/L
Lipoprotein(a) 219 nmol/L

In other words, both small LDL particles and lipoprotein(a) are being knocked down to zero values.

Incidentally, the combination of lipoprotein(a) with small LDL is among the most atherogenic (atherosclerotic plaque-causing) patterns known. Despite his athletic, slender build and avoidance of unhealthy habits, Ted's heart scan score was 922--very high.

So Ted followed the diet I advocate, i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted's case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose.

The result:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L

Not everybody, of course, is achieving these incredible--and previously impossible--results. But the numbers are growing. Ted is the third person to achieve zeroes all around, in fact, over the past 10 days.

Heart disease prevention is getting better and more powerful every day. And it ain't all about Lipitor and low-fat.

Chocolate almond biscotti

22. July 2011 William Davis (8)

Biscotti are twice-baked biscuits or cookies that are perfect for dipping into coffee, latté, or espresso. These wheat-free, low-carb biscotti are rich with the taste of chocolate and almonds.

Yield: approximately 15 biscotti

Ingredients:

2 cups almond meal
½ cup chopped walnuts
1/4 cup cocoa powder (undutched)
½ cup dark chocolate chips
Sweetener equivalent to ½ cup sugar (e.g., liquid stevia, Truvia)
½ cup ricotta cheese, room temperature (replace with coconut milk if lactose intolerant)
4 tablespoons butter, melted (replace with coconut oil if lactose intolerant)
2 large eggs
¼ cup milk, unsweetened almond milk, or soy milk
¼ cup almond, peanut, or sunflower seed butter, room temperature

Preheat oven to 350º F.

Mix almond meal, walnuts, sweetener, cocoa powder, and chocolate chips in bowl. Mix in ricotta, butter, eggs, milk, and nut butter and blend by hand thoroughly.

Pour mix onto baking pan lined with parchment paper or greased with coconut oil or other oil. Shape into loaf approximately 1 inch deep and 3½ to 4 inches in width. Place in oven and bake for 40 minutes.

Remove loaf and allow to cool 15 minutes. Slice into approximately ¾-inch widths and lay each biscotto on its side on baking pan. Put back in oven for 10 minutes.

Remove pan and flip biscotti over. Place back in oven and bake an additional 5 minutes. Remove and cool.

Optional: For a little dark chocolate "icing":
Melt 3-4 oz semisweet or dark chocolate in microwave (in 15 second increments until melted) or in metal bowl placed in heated water. Stir in 1-2 teaspoons butter.
Dip each biscotti into melted chocolate mix or drizzle chocolate mixture over top of each biscotto.

Sun green tea

21. July 2011 William Davis (11)

Here's a great way to enjoy the health benefits of green tea during the summer: sun green tea.

I dropped two green tea bags into approximately one-half gallon of cold water in a clear glass jar. I placed the jar in the sun (with top on) for four hours, then brought it into the kitchen. I served it as iced tea with a slice of lemon and mint leaf.

The sun green tea was a smoother than standard green tea brewed with hot water. Ordinarily, if you brew hot green tea for more than 3-5 minutes, it becomes more bitter or tannic. This sun green tea, despite steeping for four hours, was not the least bit bitter or tannic.

The green tea lasted well for about 48 hours, more than enough to enjoy several glasses per day.

Calling all super-duper weight losers!

9. July 2011 William Davis (12)

Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

8. July 2011 William Davis (35)

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year. Some have required two years. Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is. But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

1. July 2011 William Davis (35)

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

22. June 2011 William Davis (36)

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

18. June 2011 William Davis (14)

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

16. June 2011 William Davis (18)

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.

All posts by william-davis

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.