More catheterizations would make me happy!

11. October 2006 William Davis (0)
I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

9. October 2006 William Davis (1)
I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

6. October 2006 William Davis (0)
A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!

6. October 2006 William Davis (0)


Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.

Fish oil in the news

3. October 2006 William Davis (2)


Hooray for the New York Times. They ran an article pointing out the miserable and inexcusable failure of American physicians to use fish oil after heart attack.

“It is clearly recommended in international guidelines,” said Dr. Massimo Santini, the hospital’s chief of cardiology, who added that it would be considered tantamount to malpractice in Italy to omit the drug.

...in the United States, heart attack victims are not generally given omega-3 fatty acids, even as they are routinely offered more expensive and invasive treatments, like pills to lower cholesterol or implantable defibrillators. Prescription fish oil, sold under the brand name Omacor, is not even approved by the Food and Drug Administration for use in heart patients."

The article focuses on the use of fish oil only after heart attack and doesn't tackle the larger issue of how fish oil is crucial for coronary disease in general. Of course, the article doesn't address the extraordinary effects of fish oil on lipoproteins, particularly triglyceride-containing varieties like VLDL and the postprandial (after-eating) intermediate-density lipoprotein (IDL).

It also talks about prescription fish oil and just glosses over fish oil as a nutritional supplement. I know of few reasons to use the prescription form. More than 90% of the time, nutritional sources of fish oil do the trick. (That is, fish oil capsule supplements, not just eating fish which doesn't provide enough for coronary plaque reduction or control.)

Occasionally, I'll meet someone who has a severe hypertriglyceridemia (very high triglycerides), or is a Apo E 2/2 homozygote (very rare). These special instances may, indeed, do better using prescription fish oil, since it is more concentrated--one prescription capsule providing the same omega-3 fatty acid content as three conventional capsules (1000 mg fish oil, 300 mg EPA+DHA).


But for most of us, the standard fish oil supplement you buy at the health food store or department store does just fine. If you read about the impurity of fish oil supplements (likely prompted by the manufacturer of Omacor, prescription fish oil), refer to the studies by Consumer Reports and Consumer Labs, both of which found no mercury or pesticide residues in dozens of fish oil preparations tested.

Look on the bright side. The conversation is growing. Fish oil, whether prescription or my favorite, Sam's Club Members' Mark brand, is a fabulously effective supplement with benefits that, in nearly all cases, exceeds the benefits of drugs.

Fish oil is an absolute requirement for your Track Your Plaque program and for you to hope to achieve control or reduction of your heart scan score.

Nutritional approaches to homocysteine reduction

3. October 2006 William Davis (0)

For an in-depth discussion of nutritional approaches to homocysteine reduction, see my new article, Nutritional Therapies for Managing Homocysteine , in the most recent issue of Life Extension magazine. You'll find it at:

http://www.lef.org/magazine/mag2006/oct2006_report_homocysteine_01.htm

The report contains a detailed discussion of how to use foods to control homocysteine levels. Though I'm not a homocysteine-crazed fanatic like Life Extension publisher, William Falloon, I still there's some interesting aspects of homocysteine metabolism that need to be explored. I also think there's some genuine benefit to reducing homocystine, preferably with foods, secondarily with supplements.

Also see our recent update on homocysteine on the www.cureality.com website at:
http://www.cureality.com/library/fl_01-006homocysteine.asp

In the update, we tried to make sense of what the new studies on homocysteine treatment, NORVIT and HOPE-2, tell us in light of all the other studies on homocysteine that preceded them.

The American Heart Association diet guarantees you get heart disease!

2. October 2006 William Davis (1)
Perhaps I stated that too strongly.

But the fact remains: the diet advocated by the American Heart Association is awful. The foods endorsed by their approach have no place on a list of healthy foods. Yes, you will find vegetables and fruits, etc.. But you will also find that the 2006 American Heart Association Diet and Lifestyle Recommendations dance around the issue of what foods to avoid. There's no explicit mention of how, for instance, common foods like Shredded Wheat cereal, ketchup, low-fat salad dressings, etc, among thousands of others, should be avoided.

No matter how you time your meals, mix them, combine proteins, fats, and carbohydrates, etc., you simply cannot squeeze health out of products like breakfast cereals, instant mashed potatoes, dried soup mixes, wheat crackers, etc. Yet these are the sorts of foods that are implicitly allowable in the Heart Association's diet program.

You can obtain a little insight into the motivations behind the diet design by looking at the Heart Association's Annual Report list of major supporters:

--ACH Food Companies--maker of Mazola margarine and corn oil. A contributor of between $500,000 and $999,000 to the Heart Association.

--ConAgra Foods--You know them as Chef BoyArdee, Peter Pan peanut butter, Kid Cuisine (pizza, macaroni and cheese). ConAgra contributed between $500,000 and $999,000 to the Heart Association.

--Archer Daniels Midland--Huge worldwide supplier of wheat flours, high-fructose corn syrup, and basic ingredients for manufacture of soft drinks, candies, and baked foods. ADM contributed between $1-4.9 million dollars to the American Heart Association.

Of course, the Heart Association provides many hugely positive services like funding research. But, on many official statements, you need to read between the lines. The Heart Association is funded by industry: medical device makers, drug makers, food manufacturers. Yes, some is contributed in the interest of health. But you can be sure that lots of money is also contributed in the hope of protecting specific commercial interests. Many of those decisions are made behind closed doors or on the golf course.

Be skeptical. Just because the Heart Association diet is a Casper Milquetoast version of a health program, it does not mean that you have to subscribe to their watered-down, politically correct, and downright useless nutrition recommendations.

I'm just right!

2. October 2006 William Davis (1)
Ben is an energetic 45-year old entrepreneur. He started his own security alarm company and has, with tremendous hard work and long hours, built it into a successful local business. Despite his long hours, he found time to coach his son's football team and help with raising his 3 kids.

Ben's life took a detour when he had urgent bypass surgery at age 39. Just three years later, the chest pains and fatigue he'd experienced before bypass returned. Another heart catheterization revealed that all of his bypass grafts except one had closed. Three stents were implanted to salvage his original coronary arteries.

That's when I met Ben. Shockingly (perhaps I should know by now!), Ben was taking Lipitor and had been advised to follow a low-fat diet. That was the full extent of his heart disease prevention program. The burning question that I wanted answered was "Why did a 39-year old man have heart disease?".

Our analysis uncovered a smorgasbord of hidden patterns. You name it, Ben had it: postprandial (after-eating) patterns like IDL, low HDL, and, most notably, small LDL and lipoprotein(a). That's why Ben had heart disease as a 39-year old man--plain and simple.

We proceeded to correct all of his patterns. But the one aspect of his program that he struggled with: weight. At 5 ft 9 inches, Ben started at 285 lbs before bypass. He did manage to get to 270 after his surgery. I told him that, if he was going to get full control of his small LDL pattern, he needed to get to <210 lbs, perhaps even lower. Without substantial weight loss, he would never seize full control over coronary plaque.

Ben was satisfied that we had identified the hidden causes of his heart disease. But he remained skeptical that that magnitude of weight loss was necessary. Built like a football player, he looked stocky but not outright fat. He got down to 240 lbs but then he decided that he looked too skinny and just went right back up to 250-260 in weight.

At a weight of 250, this puts Ben's BMI (body mass index) at around 37, way over the cut-off of 30 for obesity. Now, the BMI can be misleading in people with larger frames and more muscle. But Ben undeniably had a generous abdomen, encasing the visceral fat that drives small LDL.

Unfortunately, Ben remained skeptical until I put three more stents into his right coronary artery last evening.

Small LDL is a powerful activator of lipoprotein(a). In other words, there's something peculiarly evil about the combination of small LDL and lipoprotein(a) that brings out the worst in both. You can't correct just one or the other. You've got to correct both. Don't learn this lesson the hard way.

I think (hope) that Ben is on track to get to around 200 lbs.

Prevention: Bad news in bits and pieces

30. September 2006 William Davis (1)
Jan clearly did not want to talk about her heart scan. Her score of 502 came as a shock to her. After all, she'd survived breast cancer just a year earlier, having been through dozens of radiation treatments, chemotherapy, not the mention the emotional upheaval.

Now I was telling Jan that she had a very high heart scan score with a heart attack risk of 5% per year. Then we got to her lipoprotein patterns: Jan had several striking abnormalities, including a misleading LDL cholesterol that underestimated her true LDL by nearly 100% (LDL particle number), small LDL, and the dreaded lipoprotein(a).

"I can't handle this! Why did I get the stupid scan in the first place?!"

Giving her a chance to collect her emotions, I discussed how, even though this business can be frightening, it's far--FAR--better than the alternative: heart attack at 3 am, rush to the hospital, stents, bypass surgery, etc. Or, death for the >30% of people who don't make it to the hospital in time.

That's why I often tell people that prevention of disease is bad news in bits and pieces. But it's a lot more manageable this way. Coronary plaque is a controllable process. You don't have much control in the midst of a heart attack.

A second chance

29. September 2006 William Davis (1)
Stewart had a CT heart scan in 2004. Score: 475.

As always in the Track Your Plaque program, Stewart had his lipoproteins assessed. Among his patterns were LDL 157 mg/dl, severe small LDL, and the (post-prandial, or after-eating) IDL. Stewart was also "pre-diabetic" with a blood sugar of 123 mg/dl. Blood pressure was also a major issue. Although initially concerned, life and distractions got in the way, and Stewart's attentions drifted away.

Two years of a lackadaisical effort and Stewart's heart scan score was 600, a 26% increase. Not as bad as it could have been doing nothing (i.e., 30% per year), but still far from great. But, even with the increase in score, we still really didn't get Stewart's attention. He went about his business with a very lax dietary program, overindulging in breads, crackers, goodies, hot dogs, etc., and following a virtually non-existent exercise program except for playing golf once or twice a week.

Unfortunately, Stewart started having pains in his chest with very minimal efforts like climbing a single flight of stairs. His stress test proved abnormal. Stewart then received a stent in his left anterior descending coronary and another in his circumflex. His right coronary artery had a 40-50% blockage, close to requiring a stent.

I stressed to Stewart that this had been preventable. Should motivation remain unchanged, the next step would be bypass surgery.

I think I finally succeeded in getting Stewart's attention. He found the prospect of a bypass operation a lot more concrete than the idea of progression or regression of coronary plaque. So Stewart is being given a second chance. Unfortunately, we will no longer be able to track Stewart's plaque very effectively, since two of three arteries now contain stents, and only the right coronary remains scorable.

I hope Stewart succeeds. But I sure wish he had done this earlier. He had realistic hopes of never requiring stents or bypass surgery.

Learn from Stewart's mistakes. Attention to your program requires vigilance. You can't ignore the causes of your coronary plaque for any length of time without it catching up to you. But seize your first and best chance.
All posts by william-davis

Fat and fiber composition of nuts

30. November 2008 William Davis (16)


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

29. November 2008 William Davis (12)
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

28. November 2008 William Davis (3)
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

26. November 2008 William Davis (21)
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

22. November 2008 William Davis (2)
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?

21. November 2008 William Davis (2)
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"

17. November 2008 William Davis (17)
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

16. November 2008 William Davis (7)
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

16. November 2008 William Davis (4)
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?

13. November 2008 William Davis (17)
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.