Fat and fiber composition of nuts



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).

Flush-free niacin kills

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

CT coronary angiography is NOT a screening procedure

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.

The Wheat Deficiency Syndrome

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 Crap Shoot

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.

At what score should a heart catheterization be performed?

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.

"It's genetic"

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.

Tim Russert Revisited

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.

Water: Bottled vs. tap

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.

Can CRP be reduced?

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.

How old are you?

George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.

No high blood pressure

Primitive cultures that were, until recently, unexposed to the modern world, reveal some important insights into blood pressure.

The Yanomamo of South American, the Xingu Indians of Brazil, rural Kenyans, and the natives of Papua, New Guinea have average blood pressures of 103/63 mmHg. Even more incredibly, while 90% of modern Americans will develop high blood pressure as they age, the members of these primitive cultures do not develop age-related hypertension.

What's the secret? Perhaps the full "secret" of their remarkably low blood pressure has not been fully unraveled, but several observations have emerged:

--They are not exposed to modern processed foods like pretzels, crackers, and breakfast cereals.
--Low-carbohydrate foods. Carbohydrates are largely the product of the food industry, convenience foods bought in stores. No such thing in the jungle.
--Living outdoors, having to forage and hunt, walk to your destination, not drive or wait in line for food.
--Outdoor lives, wearing little more than a few strands of clothing, exposes you to plentiful vitamin D activation from sunlight exposure.
--Consuming wild game, rich in omega-3 fatty acids, enhances endothelial health and reduces blood pressure.
--Wild plants, roots, and berries, as well as wild game, along the coast, are richer in iodine.

The studies examining the habits of the Yanomamo and other primitive cultures focused principally on sodium intake. Indeed, the very low sodium intake of primitive cultures was associated with lower blood pressure--up to 6 mmHg reduction. But there's clearly more to learn than "cut your salt."

Name that food

What common food can:

• Cause destructive intestinal damage that, if unrecognized, can lead to disability and death?
• Increase blood sugar higher and faster than table sugar?
• Trigger an autoimmune inflammatory condition in the thyroid (Hashimoto’s thyroiditis)?
• Create intestinal bloating, cramps, and alternating diarrhea and constipation, often labeled irritable bowel syndrome?
• Trigger schizophrenia in susceptible individuals?
• Cause behavioral outbursts in children with autism?
• Cause various inflammatory diseases such as rheumatoid arthritis, ulcerative colitis, dermatitis herpetiformis, systemic lupus, pancreatic destruction, and increase measures of inflammation like c-reactive protein?
• Cause unexplained anemia, mood swings, fatigue, fibromyalgia, eczema, and osteoporosis?


The food is wheat. Yes, the ubiquitous grain we are urged to eat more and more of by the USDA (8-11 servings per day, according to the USDA food pyramid), American Heart Association, American Dietetic Association, and the American Diabetes Association. Wheat is among the most destructive ingredients in the modern diet, worse than sugar, worse than high-fructose corn syrup, worse than any fat.

What other common food can result in such an extensive list of diseases, even death?

Celiac disease alone, a severe intestinal inflammatory condition from wheat gluten, affects an estimated 3 million Americans (Celiac Disease Foundation). The medical literature is filled with case reports of deaths from this disease, often after many years of struggle with incapacitating intestinal dysfunction and the sufferer's last days plagued by encephalopathy (brain inflammation).

What happens when you remove wheat from the diet?

The majority of people quickly shed 20-30 lbs in the first few weeks, selectively lost from the abdomen (what I call “wheat belly”); blood sugar plummets; triglycerides drop up to several hundred milligrams, HDL increases, LDL drops (yes, wheat elimination is a means of achieving marked reduction in LDL cholesterol, especially the small, heart disease-causing variety); c-reactive protein plummets. In addition to this, intestinal complaints improve or disappear, rashes improve, inflammatory conditions like rheumatoid arthritis improve, diabetes can improve or be cured, and behavioral disorders and mood improve.

Along with the ill-fated low-fat dietary advice of the last 40 years, the advice to eat plenty of "healthy whole grains" is responsible for untold disease and suffering. Yes, if you start with a fast food and junk diet and replace some of the calories with whole grains, you will be better off. (That was the logic--the Nutritional Syllogism--of the studies that established the benefits of whole grains over processed, "white" grains.)

But eliminate wheat grains and health takes a huge leap forward. And, no, there is no such thing as wheat deficiency--B vitamins, insoluble fiber, some protein--can easily be replaced by other foods.

Heart Defects Simplified



For as long as I've known him, echocardiography technologist, Ken Heiden, has had a deep fascination with congenital heart disease. Ken has just written a wonderful book on congenital heart disease called Heart Defects Simplified.

While this is a bit off-topic for the Heart Scan Blog, I know that there is a serious lack of helpful information for people with congenital heart disease and parents of children with congenital heart defects. So I asked Ken to tell us something about his book.



WD: I've reviewed your book and have been thoroughly impressed with the clarity and detail with which you handle a complicated topic. You somehow manage to make it easy to grasp, far more than any other resource I've used in past. Do you feel that your book serves a previously unmet need?

KH: This book serves an unmet need in that it presents the complex subject of congenital heart defects in a simplified manner. Most books on this subject are anywhere from 300-1700 pages in length and tend to be written for doctors. Further, most of these books have very few diagrams, and they rely upon their explanations to describe these defects.

Heart Defects Simplified is 104 pages in length, describes the most common defects, including surgical repairs, in a two-page format with full-color diagrams on the left and complete descriptions on the right of each chapter. The book is particularly written for sonographers, nurses and parents, but it is valuable for anyone interested in this subject. It is particularly useful in clinical situations because it is convenient to lay out at your side with a coil-bound format and durable pages. Further, there are appendixes which include "Surgical Procedures in Alphabetical Order," "Prevalence of Congenital Heart Disease," "Scanning Protocols for Echocardiographers," "Imaging Tips," a glossary and a worksheet for echocardiographers.


WD: I know that many people with loved ones who have congenital heart defects, particularly parents of children with such conditions, are often kept in the dark about the details of the condition. Is your book suitable for the non-technical reader, such as parents?

KH: This book is an excellent resource for parents. It is written in language that is understandable by parents as well as technologists and nurses. The full-color diagrams provide invaluable insight into this very complex world. Most importantly, this book attempts to make the subject of congenital heart defects accessible to anyone who wishes to comprehend this subject.


WD: I understand that people with congenital heart defects and parents are active participants in online discussion groups. Will your book serve as a resource for people who participate in these groups?

KH: This book is not only a resource for sonographers and parents, but the book is accompanied by a blog (HeartDefectsforEveryone.blogspot.com) that attempts to address many of the concerns commonly encountered with congenital heart defects. This blog is a work in progress, but I hope to provide a forum for parents, healthcare personnel, and others to share their questions and concerns about congenital heart disease.

My experience with the omega-3 index

I just got back my own results from the Gene Smart laboratory reporting my omega-3 index and omega-6:omega-3 ratio.

My results:

Omega-3 index: 8.2%

Omega-6:omega-3 index: 3.2 to 1

Not too bad, but not as good as I'd expected. Hmmm.

Although the omega-3 index of 8.2% puts me in the lower risk category for sudden cardiac death, I was hoping for a level of 10% or slightly greater, the level that I believe is more likely to be related to plaque inactivation or reversal. I obtained this level of omega-3 averaging an intake of EPA and DHA of about 2500 mg per day.

I was somewhat disappointed by the omega-6:omega-3 index. Although it's clearly better than the American average range of 20:1, it is short of the ideal of 2:1 or even 1:1. Since I purposely avoid omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils, I wonder if I've overdone the nuts. The two ways to improve the omega-6:omega-3 ratio are to 1) decrease omega-6, or 2) increase omega-3. I'm going to do both.

So I thought I was doing pretty well. But there's clearly room for improvement.

Remember: If just reduction of cardiovascular risk is your interest, then a lackadaisical attitude towards these issues might work. But if your interest is elimination of risk and reversal of atherosclerotic plaque, then it pays to go the extra mile. In this case, knowing your omega-3 index and omega-6:omega-3 ratio might tighten up your program.

The Omega-3 Index: The higher, the better?

So you take a few fish oil capsules every day and eat fish once or twice a week. What is the blood and tissue level of omega-3 fatty acids generated by your habits?

A number of variables enter into the equation. For instance, if you take fish oil capsules, what is the concentration of omega-3 fatty acids? How well are they absorbed? After absorption, how effectively are omega-3 fatty acids incorporated into cell membranes?

Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.


The Omega-3 index and sudden cardiac death

Two large studies have demonstrated that higher omega-3 blood (the level in red blood cells, or RBCs) levels were associated with reduced likelihood of sudden cardiac death. The risk for sudden cardiac death was 10-fold higher for the lowest omega-3 RBC levels compared to the highest.



Harris WS 2008; adapted from Siscovick DS et al 1995 and Albert CM et al 2002
(The omega-3 Index was derived from whole blood omega-3 levels, which correlate with RBC omega-3 levels, and are thus “estimated.”)



What’s the average omega-3 RBC level for Americans? Most Americans have omega-3 RBC levels in the 2.5-4.0% range, consistent with the tallest bars at the left and associated with greatest risk for sudden cardiac death. People with heart disease can have levels less than 1%. Some authorities propose that this new measure be called the omega-3 index.

Subsequent studies have shown that the omega-3 index has greater power to discriminate who will have a heart attack or die from sudden cardiac death better than any other common laboratory measure of coronary risk, including LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol to HDL ratio, homocysteine, and c-reactive protein.

Just as hemoglobin A1c offers a 3-month look into blood glucose levels, the omega-3 index reflects your long-term omega-3 intake. The quantity of RBC omega-3s also closely parallels the quantity of omega-3s in heart tissues.


What is an ideal omega-3 index?


The above studies relating RBC omega-3 levels and sudden cardiac death suggest that a level of 6.3-7.3% is associated with far fewer fatal events?but events are not eliminated at this level. Is there even greater benefit with levels higher than 6.3-7.3%?

A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks. This suggests that even higher levels are necessary to prevent non-fatal events.

Should we target 10%? 12%? Maybe higher? Any higher and we are toeing the level achieved by the Inuits, the “Eskimoes” of Greenland, northern Canada and Alaska who have been observed to have a low rate of heart disease.


What’s your omega-3 index?

The appreciation of the importance of omega-3 fatty acids marks one of the greatest health revelations of the last 50 years. We can now measure it.

The ability to measure the proportion of omega-3 fatty acids in red blood cells may provide yet another means for all of us to further reduce risk for cardiovascular events.

If you are interested in knowing your omega-3 index, we are now making the fingerstick test kits available by going here.

Vitamin D increased my cholesterol

A friend told me this story.

Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day.

However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl.

"It must have been the vitamin D! So I stopped it right away."

Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain.

Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:

Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5

This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol.

One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer.

Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL.

So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl.

So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program.

This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misinformation.

Nutrtional ignorance is not unique to the U.S.

Heart Scan Blog reader from Australia, Michaela, also a mother of a son with a complex congenital heart defect, wrote this series of e-mails to me. (Published with Michaela's permission.)


I've been reading the article, Valve disease and Vitamin D from April '07, by Dr William Davis. I'm hoping you may have some information on the topic. I'm hoping someone will have time to help me.

I have been supplementing my 15 year old son with Vit D for 4 months but only 1000 (U) per day. I would like to increase the dosage but am not sure if I would do him more harm than good.

I have been researching vitamins and supplements on the net for a few months and have been amazed at what I have found. I only wish I had done it years ago. My son has been let down by the Australian Medical Profession and it's a race against time now to keep him well and avoid a heart transplant.

My son was born with aortic stenosis and had a valvotomy at 4 weeks of age. This damaged the aortic valve and he had a Ross Repair procedure at aged 3. This left him with a damaged heart muscle and leaking aortic & pulmonary valves. In May '08, his heart grew more enlarged, causing the mitral & tricuspid valves to also leak.

I took him to Bangkok in Feb this year where he had 70 million of his own Adult Stem Cells directly injected into his heart muscle with the hope of strengthening the muscle and eventually valve replacement.

My son has recovered from the surgery and is once again symptom-free, thanks to the wonderful advice followed by the Author & Cardiologist, Stephen T. Sinatra. I have followed his supplement regime and what a difference! Of course, this won't last while my son's valves continue to leak.

My son has also developed secondary hyperparathyroidism, bone thinning and hypothyrodism. Vit D & Calcium have something to do with this I believe.

My Australian Doctors have never made mention of any vitamins or supplements .... EVER! Transplant is all they will consider and we are not having it.

If you have any info or links to any sites which may be useful to me, could you email them to me? I would be grateful for any help I could get.

Sincerely
Michaela



I responded to Michaela's e-mail:

Hi, Michaela--

Vitamin D is extremely important. Sometimes, hyperparathyroidism and calcium derangements are caused by vitamin D deficiency. You might be able to get help with this from an endocrinologist, since they are the ones who deal with hyperparathyroidism. An endocrinologist might even be familiar with several recent studies that document this phenomenon:

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Vitamin D deficiency and primary hyperparathyroidism

Also, see the discussions at www.vitamindcouncil.org from Dr. John Cannell.

Because of the complexity of your son's health, it might be hazardous to stray too far away from conventional care though you and I know that there are limitations to that perspective. For that reason, I would urge you to press for answers from a knowledgeable endocrinologist.

I hope you find the answers you need.

William Davis, MD



Several months later, Michaela provided this update:

Hi Dr Davis,

I wrote to you back in July regarding my 15 year old son's need for a Heart Transplant through a failed Ross Repair and the possible Vitamin D connection. You sent me some valuable links and I thank you again for that.

I just wanted to let you know, I think you have given me the answers. I increased Lee's Vitamin D supplement to 6000U a day and, along with the recommended nutritional supplements of US Cardiologist Dr Stephen T Sinatra, there have been remarkable improvements! Lee also had 70 million of his own Adult Stem Cells injected into his heart in February. As we know, Stem Cell Therapy takes time and Lee was looking like time was quickly running out.

I have removed him from the transplant list. He is now reading normal Kidney function, the BNP (Brain Natriuretic Peptide, a measure of heart failure] has dropped by 7000 and his liver size has reduced to where it no longer causes him discomfort. The liver tests show it's still affected but it's function is improving each month. His last Echo was in early July and there had been a reduction in the size of his heart, which is so important.

To the Doc's, Lee can't get better, there is only transplant or death so you can imagine the surprise on their faces to see him looking and feeling so well with their tests to back it up. Still, even though it's staring them in the face, they don't want to know about it. They have no interest in what supplements he is on or Stem Cell therapy. God help their other patients. I view them in the waiting room and think of them as lambs to the slaughter.

We are not spoiled for choice with Doc's here in Western Australia. I have to take what I can get and there is not many who would take on Lee's case. He was number 1 on the transplant list and a most urgent case. Not many were willing to even look at him with his cardiac history and all I had to help was the arrogant Doc's at the Advanced Heart Failure Unit. They were not at all interested in his secondary hyperparathyroidism. I suppose it didn't matter what else he had compared to his heart problems.

Anyway, I'm writing to thank you. Lee would be transplanted or dead now if it wasn't for Dr's like you sharing their knowledge online. I wish I had researched things years ago, Lee might not have sunk so low if I had. I don't know if the transplant can be held off indefinitely, but like I tell Lee, "Stay well. There are amazing people out there doing amazing things, if you can just hang on. The miracle is around the corner." He's so well, you'd have to see him to believe it. But I have 7 kids and Lee is as physically active and as well as the other 6! For how long he can stay like this, I don't know but if his ejection fraction [a measure of left ventricular strength] can keep climbing and his body gets stronger, I have hope for another attempt at valve replacement.

I'm still shocked and angry that nutritional supplements have never been mentioned in the 15 years I've been dealing with cardiologists. Surely they know about them. I have read through dozens of reports online of the benefits of them--Why haven't they?! Thank God for the online Doc's such as yourself, the valuable info would never make it out of a Doctor's office in Western Australia! I've had to leave my country for Stem Cell therapy and then implore overseas Doc's for advice and information. What does that say for the Australian Medical Profession? Not a lot! They put him in the position he is in yet don't want to help get him out.

I'm so very grateful to you, thank you and God bless.

Michaela



Note: The above is not meant to be an implicit endorsement of stem cell therapy. This was just part of Michaela's story about her son.

Eat cranberries

Most people already know that cranberries are useful for preventing urinary tract infections. Cranberries can also be useful for preventing other sorts of infections, such as dental cavities and stomach ulcers because of cranberry's ability to block bacterial adhesion.

Cranberries can also be a useful component of a heart healthy program.

Several unique properties of cranberries contribute to various aspects of heart health:

• Cranberries are a rich source of pectin--Pectin is a soluble fiber, the sort that binds bile acids in the intestinal tract and naturally reduces LDL cholesterol.
• Cranberries are a rich source of polyphenols and flavonoids--Including the wonderfully fascinating anthocyanins, the flavonoids that confer the beautiful red color. Surprisingly, cranberries are richer in polyphenols and flavonoids than blueberries, strawberries, and grapes. Cranberry juice is also rich in these compounds. However, beware of cranberry juice "cocktail," which is diluted with other liquids such as high-fructose corn syrup. Like grapes, cranberries are a source of resveratrol, the polyphenol also found in red wines that some believe is responsible for reduced risk for heart disease and extending life.
• Cranberries have high antioxidant activity--Cranberries are among the highest in antioxidant capacity against superoxide radicals, hydrogen peroxide, and hydroxyl radicals, oxidizing factors believed to underlie heart disease, cancer, and aging. Cranberries also reduce the oxidation of LDL cholesterol particles.
• Cranberries block uric acid production--Cranberries have the unique ability to block the activity of an enzyme, xanthine oxidase, that converts xanthine to uric acid. Uric acid is believed to add to heart disease risk and is the factor responsible for gout.
• Cranberries increase HDL cholesterol--Cranberry juice increases HDL by 3-4 mg/dl.

Cranberries are only modest sources of sugars, with 7.19 grams “net” carbohydrates (total carbohydrates minus fiber content) per cup of whole raw cranberries.

The best way to eat cranberries is to consume the real thing: eat the whole berry, as in sugar-free cranberry sauce or added to baked dishes like chicken. Second best are dried cranberries. However, be careful of the overly-sweetened dried cranberries that contain added sugar (for a total of 78 grams sugar per cup--far too much). Unsweetened dried cranberries can be purchased, or you can dry them yourself.

Cranberry juice is another way to obtain the health benefits of cranberries; the unsweetened juice, while quite tart, is the best with 30.5 grams sugar per 8 oz--so don't drink more than 4 oz at a time. The more common cranberry juice “cocktails” are generally too sugary and/or too dilute for full health benefit.

The cranberry harvest season in Wisconsin, Michigan, Oregon, Massachusetts, and New Jersey is just getting underway, so we should be seeing fresh cranberries on store shelves or farmers' markets any day now.

Procedures 'R Us

Kay came to the office for an opinion.

Over the past 8 months, she'd received a stent to the left anterior descending coronary artery and, during a separate procedure, a stent to the left subclavian artery.

"My cardiologist was very capable doing procedures. But when I asked, 'What do I do now?' he barely said a word and handed me a presciption for Crestor."

This kind of incredible neglect is the norm: Write a prescription for statin drug, delegate dietary advice to the hospital dietitian who advocates a heart disease-causing low-fat diet, followed by hospital discharge. You are expected to report any recurrent symptoms (which are inevitable), at which point you might "qualify" for another procedure.

It would be malpractice if it were not the prevailing standard in the community. Yes, the prevailing standard is neglect--neglect to identify, quantify, and correct all the identifiable causes of heart disease; neglect to discuss the nutritional methods that actually correct the abnormal patterns that cause heart disease; neglect to discuss nutritional supplements or medications beyond statins that further reduce heart disease risk and "need" for more procedures. In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures.

I see consultation after consultation involving stories just like Kay's. People are frightened and they sense intuitively that nobody raised the question of why they have a potentially fatal disease.

Don't allow yourself to fall victim to this incredibly neglectful mode of practice, the one that has enriched hospitals, the drug industry, many cardiologists, but does little to address the actual disease.

Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

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? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

D2 and D3 are two different things

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!



Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Weight loss: Different causes, different solutions

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

Calling all losers!

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

Weight loss and vitamin D

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
All posts by william-davis

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 
All posts by william-davis

Estrogens and CT heart scan scores

A recent study from the Women's Health Initiative (WHI), the large study that originally showed no reduction in heart attack with use of estrogens in postmenopausal females, has just published a new study.

In this new effort, women who took Premarin (horse estogens) had up to 61% lower CT heart scan scores. This new study was confined to the women from the original WHI study who had entered the study between the ages of 50-59 years (average 55 years old), since this was the significant subgroup of women who actually showed a reduction in heart attack risk, whereas other groups showed no benefit or a slightly increased risk.

For a full discussion of this fascinating result, see the Track Your Plaque report, Can estrogen reduce CT heart scan scores? at http://cureality.com/library/fl_06-017estrogen.asp. (This report is open to both Track Your Plaque Members and non-Members.)

I truly wish that the issues surrounding female hormone replacement were clearer. This new perspective adds just another interesting twist on a strategy that too many people, in my view, dismissed too readily with the initial WHI results.

To add to an already confusing situation, the WHI study was sponsored by Wyeth Pharmaceuticals, the maker of Premarin, and many of the investigators participating in the study obtained financial compensation from Wyeth. On the one hand, we have to give credit to the company and the investigators for publishing the initial study that panned the effects of Premarin. On the other hand, it makes any positive data somewhat suspect, particularly since there is a far less costly and probably superior preparation called human estrogens.

Incidentally, Wyeth is also behind the maddening FDA petition to prevent "compounding" pharmacies from dispensing human hormones like estrogen unless made by a drug manufacturer. They hide behind claims of concerns over safety. Nonsense. This is pure profiteering and protection of their enormously profitable franchise and has nothing to do with public safety. If there were genuine concerns that the compounding pharmacies, around for decades with an excellent reputation, pose safety issues, why not just lobby for improved oversite?

If only we had data like WHI that used human estrogens and human progesterone. I suspect that we'd see bigger, better effects with less of the ill effects peculiar to the cross-species use of Premarin and the synethetic progestin, Provera.

The wheat-free life

"There's nothing else I can do with my diet," declared Whitney, a 53-year old university faculty member.

"I don't eat meat. I never eat fried foods. I can't remember the last time I used butter. My idea of having a treat is a handful of blueberries. What else can I do?"

Whitney was clearly frustrated. With a CT heart scan score of 264, she was worried that trouble was just around the corner. Her lipoprotein panel had demonstrated a severe small LDL pattern, with 70% of all LDL particles in the small category. HDL was also low at 41 mg/dl.

"What did you eat for breakfast?" I asked.

"Same as always: Either Fiber One cereal or Shredded Wheat. No sugar, just skim milk. Sometimes I have some orange juice, fresh-squeezed of course."

"How about lunch?"

"If I brown-bag it, I'll usually have a reduced-fat turkey breast sandwich on whole grain bread. About once a week, I'll have a whole wheat bagel--no cream cheese, of course."

"Dinner?"

"Sometimes I have chicken--skinless--with a vegetable, corn, or salad. I love pasta, but I always use whole wheat."

"How about snacks?"

"I try not to snack. But, when I'm desperate, I usually grab some Triscuits or pretzels."

The problem with Whitney's diet was clear: Too many sugar-equivalents, otherwise known as wheat. I suggested that her diet was far too heavily laden with wheat products. She seemed skeptical. "But this is as low-fat as I can get! Now you're going to take away wheat?"



What happens when you eliminate wheat from your diet?

Several predictable, consistent changes can be observed:


--HDL cholesterol goes up.

--Triglycerides go down.

--Small LDL particles are reduced.

--LDL cholesterol drops (the amount dropped depends on the proportion of small LDL pattern)

--Blood sugar drops.

--Blood pressure drops.

--C-reactive protein (an index of imperceptible inflammation) drops.


In addition to these measurable changes, several perceptible improvements often develop: more energy, less afternoon "slump," better sleep, sometimes less rashes.

Since Whitney was skeptical, I suggested a simple 4 week "experiment": Eliminate wheat products entirely for 4 weeks and see for herself what happens. I also warned her that, while I believe that elimination of wheat is a great strategy, she could negate the benefits by indulging in candy, soft drinks, and other junk products. It would therefore be necessary to maintain an otherwise healthy diet.

So Whitney gave it a try for 4 weeks. To make up for the dropped calories, she increased her reliance on vegetables, fruits, lean proteins, nuts, seeds, and healthy oils.

After losing 6 lbs over the 4 weeks without otherwise trying, she was convinced. She was further convinced when we reassessed her laboratory work: HDL went up 10 mg/dl; triglycerides down 120 mg/dl; blood sugar dropped from 112 mg/dl (pre-diabetic) to 95 mg/dl (normal). Several months later, we checked her lipoproteins. Small LDL had dropped to around 30% of total LDL--a big improvement.

It's contrary to conventional wisdom. It's counter to the USDA Food Pyramid. It's certainly not what the American Heart Association says. It could potentially disrupt the economics and politics of the enormously powerful food industry.

But, more often than not, the results are impressive to phenomenal.

Death of a $7 billion industry

Vitamin D has taken its place as a crucial ingredient for coronary plaque control and control of CT heart scan scores.

Vitamin D replacement is also crucial for bone health, particularly the prevention of osteoporosis. But conversations about vitamin D replacement to true healthy levels is notably absent from the conversation on treatment and prevention of osteoporosis. Yes, you will find a small dose of vitamin D in calcium tablets and in multivitamins. Those of us who check blood levels of 25-OH-vitamin D3 in patients will tell you: They don't work. These are unabsorbable forms of vitamin D and at trivial doses. There was an attempt to give this issue a little cursory attention when a small dose of vitamin D was added to Fosamax (Fosamax D).

There are an estimated 50 million Americans with various degrees of osteoporosis. It's numbers like this that make the drug manufacturers salivate. Osteoporosis treatment is also chronic. This is among the holy grails of the drug industry: developing agents for widespread ailments that require long-term treatment that extends over years. That's a lot more profitable than 10 days of antibiotics that are over and done with in one treament course.

The osteoporosis market now stands at $7 billion per year and is expected to grow 6-7% per year, according to industry analysts. Drugs like Fosamax, Evista, and Actonel will eventually be replaced by Boniva, Eclasta, and bazedoxifene, and later by AMG-172 and balicatib. Monthly costs for these drugs can be $70 or more per month, sometimes several hundred dollars. (Experience has shown that the introduction of new drugs does not necessarily mean that other drugs will drop in price.)

Here's a clinical trial I'd like to see performed: Vitamin D restored to healthy levels of 50-100 ng/ml over an extended period and compared to a group treated with placebo. My prediction is that there will be dramatic differences in bone density. (Small studies have been performed, but no large, long-term trials of the sort that would yield real firepower.) Or, how about vitamin D to true therapeutic levels over 5 years compared head-to-head with one of the drugs. My prediction: little difference.

Vitamin D also provides an enormous panel of health benefits beyond restoration of bone density, like rise in HDL, drop in triglycerides, facilitation of control over CT heart scan scores, drop in fracture risk, drop in blood pressure and C-reactive protein, reduction in risk for colon, prostate, and breast cancer. None of the drugs can hope to provide any of these effects, except a drop in fracture risk.

Vitamin D usually costs around $2 per month. I doubt that such trials will be performed. If I were a manufacturer of osteoporosis drugs and my career success was dependent on the increasing revenues of these drugs, I would be quaking in my shoes, hoping that the public does not learn what a powerful tool good old vitamin D is. But if you are an individual just looking for health tools, vitamin D is, in my view, amongst the most powerful natural, nutritional tools you have available with outsized health benefits.

Lose weight and HDL goes . . . down

Steve started with a miserable HDL cholesterol of 27 mg/dl. As expected, the low HDL was associated with all its evil friends: small LDL, deficiency of healthy, large HDL, high triglycerides, VLDL, and a pre-diabetic blood sugar.

Steve committed to a strict diet of reduced processed carbohydrates like wheat products, reduced meat and saturated fats. He relied on vegetables, fruit, lean proteins, and healthy oils. Over a 6 month period, he lost an impressive 39 lbs. He proclaimed that he hadn't felt this good in 30 years.

We rechecked his HDL: 25 mg/dl.

"I don't get it!" Steve declared, understandably.

There's a curious phenomenon with HDL. If you lose weight, HDL goes up--but not right away. Steve had lost a substantial quantity of weight and was continuing to lose weight when the blood work was obtained. While HDL does indeed rise with weight loss, it doesn't do so immediately. In fact, in the first two or so months after significant weight lost, HDL goes down.

Why? I don't really have an explanation, but it is a very consistent effect.

Losing weight towards ideal weight is truly an effective strategy for raising HDL. But we need to be patient. If you've lost many pounds like Steve did, then waiting at least two months after weight has stabilized may be necessary to fully gauge the effect on raising HDL.

Addictive Foods

Kraft Foods, Inc. is manufacturer of Kool Aid, Oscar Mayer, Kraft Macaroni and Cheese, Velveeta, Honey Maid Grahams, and hundreds of other processed food products. Post cereals also falls under the umbrella of Kraft with products like Raisin Bran, Post Toasties, and Fruity Pebbles. Annual revenues in 2006 for Kraft: $34.4 billion. A big operation with enormous influence over our eating habits.

Nabisco is manufacturer of Oreos, Ritz Crackers, Chips Ahoy and many others. Like Kraft/Post, it is also a big player.

While Nabisco was owned for several years by tobacco giant RJ Reynolds, in 2000 it was acquired by Philip Morris, another big tobacco manufacturer.

More recently in Spring, 2007, Philip Morris (now called Altria--you'd change your name, too, if it was synonymous with dirt) spun off its Kraft subsidiary for a big profit. However, the management structures remain intertwined.

In other words, despite the shuffling of shares, the two industries, big tobacco and big food, are in many respects one and the same.

Is it any surprise that the same industry that made billions of dollars pushing addictive nicotine products responsible for the deaths of hundreds of thousands of people is now intimately involved with addictive products produced and marketed by the processed food industry?

If you believe that food manufacturers are innocently and honestly conducting their businesses, simply think back to the testimony provided in front of Congress during the tobacco industry hearings. Broad deception, concealed truths, and outright lies were commonplace. There was no conscience involved. This was about money--and lots of it.

Why should the processed food industry, intimate with the tobacco industry, be any different?

If you want control over heart disease and your heart scan score, buy produce and buy local. Spend your time in the produce aisle, not the cereal or chip aisle. Unprocessed food, unadorned by bright labels, cartoon animals, American Heart Association endorsements, that's what we should seek.

Heart Scan Curiosities #7




Here's a situation that crops up once in a while, occurring in perhaps 2% of heart scans.

The white within the circled area represents calcium, and thereby atherosclerotic plaque, situated immediately at the "mouth", or opening, of the the right coronary artery. What is somewhat unusual is that this plaque is not principally coronary, but aortic. That is, the plaque is mostly situated in the large vessel called the aorta. The three coronary arteries arise from the aorta.

In this instance, the aortic plaque involves the mouth of the right coronary artery. (In views not shown, the plaque also extends into the artery as well.) I call this a "double whammy" because the same plaque can post risk for heart attack and stroke.

Generally, aortic plaques pose risk for stroke. When aortic plaque fragments, little bits and pieces can travel upward to the brain and block an artery, thus a stroke.

In the coronaries, disrupted ("ruptured") plaques don't generally shower debris, but permit blood clot formation, resulting in heart attack.

This plaque, however, poses the theoretical risk of both heart attack and stroke because of its strategic location.

Should a plaque like this be handled any differently? I don't think so. But it does provide another reason to take atherosclerotic plaque in any artery seriously.

The nutrition counterculture

When we look back over our American nutritional history over the last 50 years, it's hard not to come to the conclusion that much of the innovation in nutrition did not come from official agencies like the Food and Nutrition Board of the Institute of Medicine, the National Academy of Sciences, the FDA, the USDA, or the AMA.

Instead, it came from the popular culture. It came from bold, extravagant claims made by maverick figures like Ancel Keys, Nathan Pritikin, Dean Ornish, and Robert Atkins. Of course, some ideas have now fallen by the wayside, dismissed in a broad American "experiment" as ineffective, impractical, or kooky. But it permitted experimentation on an extraordinary scale with millions of people following a particular strategy at a time.

The advice of the official agencies tended to be reactionary. When nutritional deficiencies (remember those?) of the early 1900s were prevalent, they issued advice on food choices to help alleviate deficiencies. When deficiency transformed into excess after World War II, "smart" food choices from food groups and "sensible eating" became the theme.

Unfortunately, the advice was always adulterated by the enormous influence of various special interests, anxious to protect their national franchise. Powerful groups like the meat industry, wheat producers, and the dairy industry all made sure they had a big hand in crafting and influencing what was told to the American people.

The result: the advice offered by official groups has always represented the compromise of what some agency wished to convey to the people and the very powerful input of industry. What if the government decided to advise us what automobile to buy? Imagine the uproar in the auto industry when Washington tells us to buy Toyota for fuel economy and reliability. How long would that advice last?

That's why almost no knowledgeable adult follows the advice of the USDA, the National Academy of Sciences, or the Food Pyramid. I believe that we all intuitively recognize that the advice is watered-down, sometimes silly, sometimes downright unhealthy.

Nonetheless, the national experiment in diet that has taken place since 1950 has led to a collective wisdom of what is good and what is bad. The most productive conversations on nutrition therefore take place outside of the USDA and Washington. It occurs, instead, in places like bookstores, websites, and the media. Of course, there's lots of misinformation and profiteering in these sectors, as well. But like the enormous force unleashed by the collective wisdom of those contributing to the Wikipedia phemonenon, we've zig-zagged to something closer to the truth than ever uttered by an official agency.

Prescription vitamin D

Niacin:

Over-the-counter: $2-5 per month
Prescription: $120 per month


Fish oil:


Over-the-counter: $3-6 per month
Prescription: $120 per month


Vitamin D:


Over-the-counter: $2 per month
Prescription: $70 per month



With vitamin D in particular, the prescription form is vastly inferior to the over-the-counter preparation. This is because the prescription form is ergocalciferol, or vitamin D2, not the effective human form, vitamin D3 or cholecalciferol.

When you're exposed to sun, what form of vitamin D is activated in the skin? It's all vitamin D3, no vitamin D2 whatsoever. Vitamin D3 is also far more effective than D2. People taking D3 (as long as it's oil-based) easily obtain healthy levels of vitamin D in the blood. People taking 50,000 units per day of D2 (the recommended quantity) remain miserably deficient, with minor increases in vitamin D blood levels. In short, D2 barely works at all. D3 works easily and effectively.

Moreover, D2 is the plant-based form. It is a form not found naturally in humans. D3 is the mammalian form, the same found in humans that exerts all its biologic benefits.

Then why is the prescription form of vitamin D2 (brand names Driscol and Calciferol) more expensive?

It's the same old pharmaceutical industry scam: Look for something patent protectable, regardless of whether it's superior to the non-patent protectable product, then sell it for exagerated profits. Though it is inferior and the science and clinical experience prove that it's inferior, you can still fool lots of people, including prescribing physicians. So what if you only make $50 or $100 million?

Don't fall for it. Prescription doesn't necessarily mean superior. In fact, the prescription form may be significantly inferior, as with vitamin D2. But the pharmaceutical industry carries such power and persuasion, who's going to know?

Nutrition activist Mike Adams













I borrowed the above comic from the website of nutritionist, more properly nutrition activist and author, Mike Adams. His website, www.newstarget.com, was a pleasant surprise.

I was actually looking for some thoughts on pharmaceutical advertising and its pervasive and destructive effects and came across one of Adam's reports, Pharmaceutical television advertising is a grand hoax at http://www.newstarget.com/021526.html. The piece is a rant against the pharmaceutical industry's constant bombardment of the media, who have also been co-opted into their service, enticed by the enormous advertising revenues the drug industry brings.

But I was surprised to find an insightful, informative website on health issues, particularly healthy eating that rejects the manufactured food industry's intensive effort to persuade us to eat their products. While I don't agree with everything Adams has to say, his website provides some great food for thought. He also provides lots of downloadable information.

There's also some great laughs at his poke at the pharmaceutical industry with his Disease Mongering Engine at http://www.newstarget.com/disease-mongering-engine.asp, in which you get to create your own diseases. I got a real kick out of this.

CT scans and radiation exposure



The NY Times ran an article called

With Rise in Radiation Exposure, Experts Urge Caution on Tests at

http://www.nytimes.com/2007/06/19/health/19cons.html?_r=1&adxnnl=1&oref=slogin&adxnnlx=1182254102-vQpytpx6W/Z9gvAaNPDZvA



“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”


Where do CT heart scans fall?

Let's first take a look at exposure measured for different sorts of tests:



Typical effective radiation dose values

Computed tomography Milliseverts (mSv)

Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv

Non-CT Milliseverts (mSv)

Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv

Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN


If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

A heart scan on a 16- or 64-slice multidetector device, your exposure is around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 chest x-rays or 20 mammograms. Now that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legimate medical questions. They are not screening tests to be applied broadly and used year after year.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.



Detail on radiation exposure with CT coronary angiograms on multidetector devices can be found at Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305-1310, one of several studies on this issue.