Getting your dose of fish oil right

Confusion often stems from the simplest of calculations: dose of fish oil.

Actually, you and I don't take fish oil for fish oil. We take fish oil for its content of omega-3 fatty acids, the dominant ones being EPA and DHA. The contents of fish oil outside of its EPA + DHA content likely exert little or no benefit (beyond that of other dietary oils).

To determine what you are currently taking, simply examine the back of your fish oil bottle and look for the EPA + DHA composition. This should be clearly and prominently labeled. If not, don't buy that brand again. Add up the EPA + DHA content per capsule, then multiply by the number of capsules you take per day. That yields your daily EPA + DHA intake.

The only other substantial source of omega-3 fatty acids is fish. Other food sources, such as non-fish meats, eggs, etc., contribute little or none. Processed foods that bear health claims of "contains heart healthy omega-3" often contain linolenic acid or flaxseed oil, which contributes very little to total EPA + DHA, or contain relatively trivial quantities of DHA. What are you doing eating processed foods, anyway?

What should the total daily dose of EPA + DHA dose be? That depends on what your goals are.

If your goal is to modestly reduce the risk of dying from heart attack, then just eating fish a couple of times per month will begin to exert an effect, or just taking a dose of 300 mg EPA + DHA per day from a low-potency capsule will do it. However, that's an awfully unambitious goal.

Our starting omega-3 dose in the Track Your Plaque program has, over the years, increased and now stands at 1800 mg EPA + DHA per day. However, the dose for 1) full reduction of triglycerides and/or triglyceride-containing abnormal lipoproteins, 2) reduction of Lp(a), and 3) the ideal dose for coronary and carotid plaque control are substantially higher.

But once you know your desired daily target of total EPA + DHA, you can easily determine the quantity of capsules to take by doing the above arithemetic, totaling the EPA + DHA per capsule. For example, if you have been instructed to take 6000 mg per day EPA + DHA, and your capsule contains 750 mg EPA + DHA, then you will need to take 8 capsules per day (6000/750).

Flat tummy . . . or, Why your dietitian is fat

When I go to the hospital, I am continually amazed at some of the hospital staff: 5 ft 4 inch nurses weighing over 200 lbs, etc.

But what I find particularly bothersome are some (not all) hospital dietitans--presumably experts at the day-to-day of healthy eating--who waddle through the halls, easily 40, 50, or more pounds overweight. It is, to say the least, credibility-challenging for an obese dietitian to be providing nutritional advice to men or women recovering after bypass or stent while clearly not in command of nutritional health herself.

What's behind this perverse situation? How can a person charged to dispense "healthy" nutritional information clearly display such clear-cut evidence of poor nutrition?

How would you view a success coach dressed in rags? Or a reading coach who can barely read a sentence?

Easy: She follows her own advice.

Hospital dietitians are essentially forced to adhere to nutritional guidelines of "official" organizations, such as the American Heart Association and the USDA. There is some reason behind this. Imagine a rogue dietitian decides to advocate some crazy diet that yields dangerous effects, e.g., high-potassium diets in people with kidney disease. There is a role for oversite on the information any hospital staff member dispenses.

The problem, of course, doesn't lie with the dietitian, but with the organizations drafting the guidelines. For years, the mantra of hospital diets was "low-fat." More recently, this dated message has begun--only begun--to falter, but now replaced with the "healthy, whole grain" mantra. And that is the advice the hapless dietitian follows herself, unwittingly indulging in foods that make us fat.

Sadly, the "healthy, whole grain" message also contributes to heart disease via drop in HDL, increased triglycerides, a huge surge in small LDL, rise in blood sugar, increased resistance to insulin, tummy fat, and diabetes. Yes, the diet provided to survivors of heart attack increases risk.

The "healthy, whole grain" message also enjoys apparent "validation" through the enormous proliferation of commercial products cleverly disguised as healthy: Cheerios, Raisin Bran, whole grain bread, whole wheat pasta, etc. The "healthy, whole grain" message, while a health disaster, is undoubtedly a commercial success.

I'll bet that our fat dietitian friend enjoys a breakfast of healthy, whole grains in skim milk, followed by a lunch of low-fat chicken breast on two slices of whole grain bread, and ends her day with a healthy meal of whole wheat pasta. She then ascribes her continually climbing weight and size 16 figure to slow metabolism, lack of exercise, or the once-a-week piece of chocolate.

Wheat has no role in the Track Your Plaque program for coronary plaque control and reversal. In fact, my personal view is that wheat has no role in the human diet whatsoever.

More on this concept can be found at:

What's worse than sugar?

The Wheat-Deficiency Syndrome


Nutritional approaches: Large vs. Small LDL

Are you wheat-free?

Statin drug revolt

I sense a growing revolt against the intrusion of statin drugs into our lives.

No doubt, the statin drug industry is, at least from an economic perspective, a huge success: $27 billion annual revenues at last accounting. The latest big plug for more and more statins was the JUPITER trial that showed reduced cardiovascular events on Crestor in people with "normal" LDL cholesterol levels and increased c-reactive protein.

It seems that not one day passes that doesn't include some news story about the "benefits" of statin drugs: reduction in heart attack, stroke, colon cancer, osteoporosis, heart failure, etc.

Ironically, the overwhelming economic success of the statin drug industry also seems to be encouraging a grassroots revolt.





More and more people are coming to the office, more people commenting on the web over how they want to avoid statin drugs, stop a drug they are already taking, or at least reduce the dose of an ongoing drug.

My day-to-day experience with coronary plaque control and reversal is that, while statin drugs are helpful tools, they are not necessary tools for full benefit of a prevention program. "Need" for statin drugs can differ by the patterns measured, though not the usual patterns suggested by the drug industry. For instance, using C-reactive protein, a la JUPITER, as justification for statin prescription is, in my view, totally absurd and makes no sense whatsoever, since inflammatory responses can be effective reduced with plenty of other strategies besides statin drugs. Conventional LDL, likewise, is a fictitious number that often bear little or no resemblance to the true and genuine measured value (apoprotein B or LDL particle number).

So here are a number of strategies that can help reduce or eliminate the "need" for a statin drug:

--Elimination of wheat and cornstarch--This is no namby-pamby dietary strategy, as low-fat diets were. This is a powerful, enormously effective strategy, particularly if LDL is in the small category. Small LDL drops like a stone when these foods are eliminated. This means no breads, pasta, breakfast cereals, pretzels, crackers, chips, tacos, wraps, etc.
--Non-wheat fibers--Especially raw nuts, ground flaxseed, and oat bran.
--Vitamin D restoration
--Fish oil
--Weight loss
--Niacin

There are additional strategies that focus on specific subsets of LDL cholesterol (e.g., Lp(a) masquerading as LDL). But the above list can reduce LDL cholesterol substantially, reducing the apparent "need" for a statin drug.

You will notice that there are few money makers in the above list, compared to the billions of dollars reaped by the statin drug industry. There is therefore little incentive to allow a pretty sales rep to go to your doctor and pitch the use of over-the-counter vitamin D or make changes in diet.

Statin drugs in my view need to be shoved back into their more limited role as drugs to be used on occasion when necessary (e.g., heterozygous familial hypercholesterolemia with LDL cholesterol values of 250 mg/dl in a person with measurable coronary plaque). These should never have achieved the "celebrity" status they enjoy, complete with gushing endorsements by TV personalities, daily news stories, and back-to-back TV commercials.

Join the revolt!

Lovaza Rip-off

Lovaza is GlaxoSmithKline's prescription fish oil, an ethyl ester modification to allow higher concentration of omega-3 fatty acids, EPA + DHA, per capsule. Each capsule contains 840 mg EPA + DHA.

It is FDA-approved for treatment of high triglycerides (>500 mg/dl). In their marketing, they claim "Unlike LOVAZA, dietary supplements are not FDA approved to treat any disease." They also highlight the "patented five-step" purification process that eliminates any concerns over mercury or pesticide residues.

What does Lovaza cost? In Milwaukee, it costs about $70 per capsule per month (PCPM). Most people are taking four capsules per day: $280 per month, or $3360 per year to obtain 3360 mg of EPA + DHA per day. (Funny coincidence with the numbers.)

Did you catch that? $3360 per year, just for one person to take Lovaza.

What if I instead went to Costco and bought their high-potency fish oil. This is also an ethyl ester form. It costs $14.99 for 180 capsules, or $2.50 PCPM; each capsule contains 684 mg EPA + DHA. I would therefore have to take five capsules per day to obtain the same 3360 mg EPA + DHA per day. This would cost me 5 x $2.50 = $12.50 per month, or $150 per year.

$3360 per year vs. $150 per year to obtain the same dose of omega-3 fatty acids, or a 22.4-fold difference.

Lovaza is FDA-approved for treatment of high triglycerides. But I am seeing more and more people take it for other reasons at this four-capsule-per-day dose. Regardless, this "drug" is adding $3360 per year costs to our healthcare. A school teacher, for instance, recently commented to me that she didn't care about the costs, since her insurance (in Milwaukee county, teachers have unbelievably generous healthcare coverage) covers Lovaza. I've heard this from others: insurance covers it, so they don't care how much it costs.

Guess who eventually has to pay the $3360 per year per person costs? Yup, you and me. We all bitch and moan about the costs of healthcare and health insurance, but many of us are more than willing to shift the costs to our friends and neighbors to save a few bucks. You think Lipitor makes a bundle of money for Pfizer at about $120 per month? Lovaza is making a bundle of money for GlaxoSmithKline, and all because people are cheap and willing to selfishly shift costs to other people.

Keep in mind that $3360 per year is just for fish oil. It's not for surgery, it's not for hospital care, it's just for stinking fish oil.

Santa Claus is alive . . . and works for the drug industry



Maybe your teenagers no longer believe in Santa Claus, but I assure you: Not only is he alive, I believe that we have evidence that he works for the drug industry!

Psshaww! you say. Yet another rant from that kook, Davis. Who can he pick on next? What other imagined "conspiracies" can he uncover?

Let me recount the evidence and I'll let you decide how damning it all is:

--Christmas is a culture of excess, overeating, celebration: Cookies, candy canes, pie, chocolate, egg nog, more cookies . . . A virtual wheat and sugar frenzy!

--Wheat and sugars make us diabetic!

--What does a diabetic look like? How about big protuberant abdomen, florid cheeks, baggy eyes (from sleep apnea)? The red outfit and beard is optional, of course. Could you think of a better representation of what happens to a person when they eat goodies all the time?


I therefore submit that Santa Claus is at the root of a campaign to cultivate diabetes! Diabetes: a growth industry that is raking in billions of dollars for the drug companies!

I'd bet that Mr. Claus would agree with the dietary advice dispensed by the folks at the American Diabetes Association website:

A place to start is at about 45-60 grams of carbohydrate at a meal. You may need more or less carbohydrate at meals depending on how you manage your diabetes.


Eat more carbohydrates, get fatter in the abdomen, require more medication to keep sugar low. Then start over: eat more carbohydrates, get fatter, more medicines. Kaching!

"You may need more?" Personally, I'd be rendered comatose and helpless if I indulged in such carbohydrate gluttony.

If Mr. Claus were, instead, interested in our health and keeping us non-diabetic, Christmas would be a time for pistachios, almonds, dark chocolates, and tea.

You want health advice? Don't ask Santa Claus!

Another case of aortic valve disease reduced with vitamin D

I watched Seth's aortic valve deteriorate over a two year period.

I was first consulted in 2004 to offer an opinion on Seth's heart scan score of 779 and flagrantly abnormal cholesterol patterns, including triglycerides in the 400 mg/dl range. But I heard a murmur, as well, a murmur of a leaky aortic valve, "aortic valve insufficiency."

Over the next two years, I watched Seth's aortic valve worsen, going from mild leakiness to severe.

In 2006-2007, I tiptoed into vitamin D replacement and asked Seth to add some vitamin D. Time passed and Seth's aortic valve got progressively worse.

Over the past year, However, he's maintained a truly healthy level of vitamin D, with blood levels consistently in the 60-70 ng/ml range.

While Seth's last echocardiogram showed a severely leaky aortic valve, the most recent echo showed mild leakiness ("mild aortic insufficiency")--a dramatic reduction.

I continue to see this in many, though not all, patients with aortic valve disease. Though I've more frequently witnessed either stalled progression or reversal of aortic valve stenosis (stiffness), I've now seen a handful of people with aortic valve leakiness (insufficiency) also reverse.

I've posted about this peculiar phenomenon previously:

Aortic valve disease and vitamin D
More on aortic valve disease and vitamin D

Prior to vitamin D, I had NEVER witnessed any aortic valve disease stop or reverse.

A formal trial at some point would be invaluable.

Track Your Plaque Program Data Tracking Tools

At last: After talking about the new Track Your Plaque community tools for the last year, our data tracking software is now available!



Track Your Plaque is, admittedly, somewhat data-intensive. The basic concept relies on the fact that we track heart scan scores, cholesterol values, lipoprotein values like percent small LDL and Lp(a), vitamin D blood levels, intake of omega-3 fatty acids, etc. Our new data tracking tools will help Members track their data over time.

Even more interesting, you can allow other Members (not required) to view your data for comments and feedback. You can also view the program data of other Members (if they choose to make their data "public") to learn how they are going about stopping and reversing their coronary plaque.

In other words, our graphic data tracking tools are yet another way we are using to acquire a collective wisdom on how to put a stop to coronary heart disease, heart attack, and perverse "let's make money with heart procedures" hospital solutions.

One of the aspects that helps make this work is the sharing of data. So far, the people who have begun to enter their data have all made their information "public." It's not truly "public," but viewable only by other Track Your Plaque Members. Also, Members can, in effect, anonymize their data simply by using a nickname, e.g., heartprotection or hearthawk.

The data tracking tools are in beta-test version, so there are bound to be a few glitches. But we're eager to hear from our Members' experiences on how to improve these tools. Report any problems or make your suggestions on the Track Your Plaque Member Forum--Technical Support.

Yet another reason to avoid fructose

Have you seen the Corn Refiners Association commercial campaigns to educate the American public on the safety of fructose? If you haven't, you can view these interesting specimens on You Tube:

"Get the facts--You're in for a sweet surprise: Fructose is safe in moderation!"

Two Moms

Two lovers


Beyond the fact that fructose stimulates liver production of glycerol, which thereby increases liver VLDL production and raises blood levels of triglycerides; likely stimulates appetite; increases cholesterol levels; fructose has also been clearly implicated in increasing blood levels of uric acid.

Uric acid is the substance that, in some people, precipitates in joints and causes gout, the painful inflammatory arthritis that has been increasing in prevalence over the last four decades since the introduction of fructose in 1967. While blood levels of uric acid in the early part of the 20th century averaged 3.5 mg/dl, more recent population assessments have averaged 6.0 mg/dl or higher. (Non-human mammals who don't eat processed foods, drink fruit drinks or beer, and don't eat candy have uric acid levels of <2.0 mg/dl.)

Uric acid is looking like it may prove to be an important risk factor for coronary disease and atherosclerotic plaque. It is no news that people with higher blood levels of uric acid are more likely to experience adverse cardiovascular events like heart attack. People with features of the metabolic syndrome also have higher uric acid blood levels; the more characteristics they have, the higher the uric acid level. However, the prevailing view has been that uric acid is simply an accompaniment of these processes, but not causal.

However, more recent observations suggest that increased levels of uric acid may instead be a cause of metabolic syndrome and high blood pressure.

Increased blood levels of uric acid have been shown to:

--Increase blood pressure
--Induce kidney damage (even in the absence of uric acid kidney stones)
--Antagonize insulin responses

A diagnosis of gout is not required to experience all of the adverse phenomena associated with uric acid. (For not entirely clear reasons, some people, perhaps based on pH or other factors, are more prone to trigger crystallization of uric acid in joints, similar to the phenomena of sugar crystallization when making rock candy.)

Which brings us back to fructose, a sweetener that clearly substantially increases uric acid levels. I suppose that the mothers and lovers in the Corn Refiners' commercials are right to a degree: Our kids will survive, as will you and I, despite increases in triglycerides, enhanced diabetic tendencies, amplified appetites, and increased uric acid due to fructose in our diet. We will also likely survive despite being 100 lbs overweight, partly due to the effects of fructose.

But if long-term health is your desire for you and your family, fructose has no role whatsoever to play.

Interestingly, the obviously expensive and slick ad campaigns from the Corn Refiners' videos have triggered some helpful video counterarguments:

High-fructose corn syrup
Conspiracy for Fat America
High-fructose corn syrup truth


A full discussion of uric acid, the scientific data behind uric acid as a coronary risk factor, and the nutritional means to reduce uric acid will be the topic of a thorough discussion in an upcoming Special Report on the Track Your Plaque website.

Free the Animal

Richard Nikoley from the Free the Animal Blog contributes this informative comment:



'Bout 18 months ago, I was at 230 (5'10) and looked awful. I was on Omeprezole for years for gastric reflux, a variety of prescription meds since early 20s for seasonal sinus allergies, culminating finally in the daily, year round squirts of Flonase-esque sprays (the best for control without noticeable side-effects), and finally, Levothroid for about the last 7 years or so, as I had elevated TSH (around 9ish).

My BP was regularly 145-160 / 95-110.

I decided to get busy. I modified diet somewhat, cutting lots of junk carbs, and began working out -- brief, intense, heavy twice per week. BP began coming down immediately, such that within only a couple of weeks I was borderline rather than full blown high. Then after about six months, a year ago, I went to full blown low-carb, high fat, cutting out all grains, sugar, veg oils, etc, and replacing with animal fats, coconut, olive oil. You know the drill. Then, first of the year I felt great and simply stopped all meds, including the thyroid. I also began intermittent fasting, twice per week, and for a twist, I always do my weight lifting in some degree of fast, even as much as 30 hours.

That's when the weight really started pouring off. Take a look:

http://www.freetheanimal.com/root/2008/09/periodic-photo-progress-update.html

http://www.freetheanimal.com/root/2008/08/faceoff.html

In July I figured it's about time for a physical. Here's the lipid panel, demonstrating am HDL of 106 and Try of 47, great ratios all around:

http://www.freetheanimal.com/root/2008/07/lipid-pannel.html

However, my TSH was even higher -- 16ish. It seems odd that I was able to lose 40-50 pounds of fat (10-15 pounds of lean gain for a 30 pound net loss at that time -- now an additional 10 pounds net loss).

One disclosure is that I was drinking too much, almost daily, and quite a bit (gotta save some vices...). Anyway, I'm at the point now where I want to drill down. I know I need to see an endocrinologist and have T3 and T4 looked at, but in advance, I wanted to see if the recent changes I've made could make a difference:

1. Stopped all alcohol.
2. Stopped most dairy, except ghee and heavy cream, and cheese is now used as a "spice," i.e., tiny quantities -- no more milk.
3. 6,000 IU Vit D per day.
4. 3 grams salmon oil, 2 grams cod liver oil.
5. Vit K2 Menatetrenone (MK-4) -- side story: getting off grains reversed gum disease for which I have had two surgeries, then supplementing the K2 DISSOLVED calculus on my teeth within days -- hygienist and dentist are dumbfounded. Stephan (Whole Health Source), who comments here, has an amazing series on K2.



If you view his photos, you'll appreciate just how far he has come.

Overall, Richard's program is wonderful and his pictures clearly display his success. However, Richard, thyroid function is indeed a problem, a problem that needs to be fixed ASAP. Remember, low thyroid function used to be diagnosed at autopsy at which time the coronary arteries and other arteries of the body were found to be packed solid with atherosclerotic plaque, even in young people.

I'd recommend:

1) Consider 200 mcg Iodine per day from kelp if you do not use iodized salt.

2) Seeing your doctor right away for thyroid replacement, hopefully with consideration of your T3 status.

3) A heart scan--Not to lead to procedures, but something for you to track over time as your program improves and thyroid function is restored.

Beyond this, keep up the great work. Great blog, too!

Low Thyroid and Plaque

Having now tested the thyroid status of several hundred patients over the last few months, I have come to appreciate:

1) That thyroid dysfunction is rampant, affecting at least 25% of everyone I see.
2) It is an enormously effective means to reduce cardiovascular risk.


I'm not talking about flagrant low thyroid dysfunction, the sort that triggers weight gain of 30 lbs, gallons of water retention, baggy eyes, sleeping 14 hours a day. I'm talking about the opposite extreme: the earliest, subtle, and often asymptomatic degrees of thyroid dysfunction that raises LDL cholesterol, lipoprotein(a) (Lp(a), a huge effect!), and adds to coronary plaque growth.

Correcting the subtle levels of low thyroid:

1) Makes LDL reduction much easier

2) Facilitates weight loss

3) Reduces Lp(a)--best with inclusion of the T3 fraction of thyroid hormone.

Recall that, 100 years ago, the heart implications of low thyroid weren't appreciated until autopsy, when the unfortunate victim would be found to have coronary arteries packed solid with atherosclerotic plaque. It takes years of low thyroid function to do this. I advise you to not wait until you get to this point or anywhere near it.

I find it fascinating that many of the most potent strategies we are now employing in the Track Your Plaque process are hormonal: thyroid hormones, T3 and T4; vitamin D (the hormone cholecalciferol); testosterone; progesterone; DHEA, pregnenolone. Omega-3 fatty acids, while not hormones themselves, exert many of their beneficial effects via the eicosanoid hormone pathway. Elimination of wheat and cornstarch exert their benefits via a reduction in the hormone insulin's wide fluctuations.

We haven't yet had sufficient time to gauge an effect on coronary plaque and heart scan scores. In other words, will perfect thyroid function increase our success rate in stopping or reversing coronary plaque? I don't know for sure, but I predict that it will. In fact, I believe that we are filling a large "hole" in the program by adding this new aspect.
All posts by william-davis

Drive-by angioplasty

Don had an angioplasty 6 months ago. When asked about the symptoms that prompted him to go to the hospital, he explained:

"I remember feeling really tired for about a week before I went. I'd read that fatigue can sometimes be a sign of heart disease. But then I had some trouble breathing. You know, like not being able to get a deep breath."

"My wife and I were planning on going on vacation. So I wanted to be certain something wasn't going on in my heart. That's when my wife insisted that she take me to the hospital.

"I kind of remember going there and arriving in the emergency room, but then I don't remember anything. Next thing I know, I'm waking up in a hospital bed. My wife and kids were there, looking all concerned. They said that I just got two stents and that the doctor just barely saved my life."

Happy story, happy ending? Not quite.

I reviewed the angiograms made during Don's hospital stay. They did, indeed, show some plaque, but not anywhere close to the amount necessary to account for symptoms like fatigue or breathlessness. For symptoms like this to occur without physical exertion, say, at your desk or relaxing at home, a critical >90% blockage would be required.

The worst "blockage" Don had was 50% at most. The leap was made to connect his relatively vague symptoms with these "blockages," leading to the implantation of two stents.

This is not as uncommon as you think. Yes, the practice of cardiology can be a life of acute procedures, urgent situations, and crises. Unfortunately, some people with questionable need for these procedures also get swept up in the wave. Sometimes it's due simply to the doctor's need to do "something," nervous family waiting in the wings. Sometiems it's intellectual laziness: putting in two stents seems to satisfy many patients' needs to have something "fixed," even when symptoms like fatigue could be due to anemia, sleep deprivation, a thyroid disorder, or any other myriad conditions that require a diagnostic effort (otherwise known as thinking). And sometimes it's simply done with financial motives, since angiplasty and related procedures pay well.

I call this "drive-by angioplasty," the impulsive, poorly considered coronary procedure that really should never have happened. How often does this happen? What percentage of heart procedures fall into this category? There are no clear-cut estimates. There are crude attempts by independent agencies that have put the number of unnecessary heart catheterizations up to 20% of the total number performed. The proportion of angioplasty procedures, stents, etc. that are not necessary is a tougher number to pinpoint, given the uncertainties surrounding the indications for these procedures, physician judgment that factors into the decision-making process, and the fact that many decisions are made on a qualitative basis, not precise quantification.

In real life, I would put the proportion of flagrant drive-by procedures at no more than 10%. However, that is 10% of an enormous number. The annual cardiovascular healthcare bill is $400 billion. 10% of that is $40 billion--an unimaginable sum. It also adds up to tens of thousands of people per year needlessly subjected to procedures. Consider that 10,000 heart procedures were performed today alone.

Should we push for legislation to control how and when heart procedures are performed? I don't think so. Despite my criticisms of the status quo in heart care, I still favor the freedom and rapid development of a free-market approach. However, you as a healthcare consumer need to be armed with information. You don't go to the car dealer unarmed with information on prices and comparative performance of the car you want. You should do the same with health. Information is your weapon, your defense against becoming the victim of the next drive-by heart procedure.

"Heart Healthy" and other lies

"Bankers believe liquidation has run its course and advise purchases."

New York Times headline, Oct 30, 1929, at the start of the Great Depression.






"I did not have sexual relations with that woman, Ms Lewinsky."

Former President Bill Clinton at a Washington Press Conference, 1998.






"The third quarter is going to be great."

Enron CEO, Ken Lay, just before the company reported a $638 million third-quarter loss, triggering the company's collapse.




Should we add the following to the list?


Heart Healthy Bisquick





















Heart Healthy snacks according to the National Heart, Lung, and Blood Institute:

Animal crackers, devil's food cookies, fig and other fruit bars, ginger snaps, graham crackers, vanilla or lemon wafers

Angel food cake or other lowfat cakes

Low fat frozen yogurt, ice milk, fruit ices, sorbet, sherbet

Pudding (make it with fat free or 1% milk), gelatin desserts

Popcorn without butter or oil; pretzels, baked tortilla chips






67% digestible carbohydrates/sugars from corn syrup, sugar, raisins, and honey. Oh, yes . . . and it contains plant sterols.





"Heartzels are a healthy snack alternative for anyone wanting to control fat intake and add fiber to their diet," said Tracy LaRosiliere, a Frito-Lay vice president of marketing. "What better time for Frito-Lay to launch its first heart-healthy snack than during American Heart Month and just in time for Valentine's Day."

The relationship with the American Heart Association and the launch of Rold Gold Heartzels Pretzels is the latest move by Frito-Lay to continue its commitment to offering a wide variety of low-fat and better-for-you snacks nationally, which like the company's assortment of regular chips can be enjoyed as part of a healthy diet and lifestyle.

Calcium chaos


Imagine that I'm planning to build a wall of bricks. I start by throwing cement at a pile of bricks, hoping that it forms a nice, orderly brick wall.

Fat chance, you say.

I believe that is what appears to be emerging as the situation with calcium supplementation.

A recent study from New Zealand reported an experience with 1,471 postmenopausal women, mean age of 74 years, who were randomized to treatment with either calcium supplements or placebo. Calcium was supplied as calcium citrate (Citrical) to provide 1000 mg of (elemental) calcium per day (400 mg morning, 600 mg evening).

(Bolland MJ, Barber PA, Doughty RN et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. Brit Med J BMJ, doi:10.1136/bmj.39440.525752.BE; published 15 January 2008)

Over 5 years, women taking calcium had twice the risk of having a heart attack compared with women taking the placebo; women taking calcium had a 47 percent higher risk of having any one of three "events" (heart attack, stroke or sudden death) than women in the placebo group.

The findings of this study run counter to what we've been telling people all these years: Calcium supplementation, usually taken to halt deteriorating bone health and osteoporosis, modestly reduces blood pressure, reduces LDL and raises HDL cholesterol. At first blush, we might thereby presume that it also reduces cardiovascular events.

This study suggests that calcium supplementation does not result in reduction of cardiovascular events, perhaps even increases risk.

Certainly, this new finding will serve to confuse the public even more than it is already, particularly when it comes to strategies that modify risk for heart attack. However, this may make more sense once we stop and think for a moment.

Calcium supplementation inarguably slows, occasionally halts, calcium resorption from bone (through suppression of parathyroid hormone). Calcium also accumulates as part of atherosclerotic plaque in coronary and other arteries.

How does oral calcium know where to go--bones, not arteries or kidneys, in addition to serving all its other crucial functions?

Keep in mind that, in many roles, calcium is passive, something that responds to control exerted by some other factor. Vitamin D is that factor. Vitamin D controls the absorption of calcium in the intestinal tract (calcium aborption quadruples when vitamin D is restored to normal), it controls whether calcium is deposited in bone or extracted from arteries. It is the master control over the fate of calcium. Calcium just goes along for the ride.

Bone and arterial health do indeed intersect via calcium, but not through calcium supplementation. Instead, the control exerted by vitamin D (and vitamin K2, another conversation) connects the seemingly unrelated processes.

At what calcium dose threshold do the benefits stop and the adverse effects begin? That remains unanswered, particularly in light of this new study. However, this study calls into serious question the wisdom of supplementing calcium at a dose of 1000 mg, particularly when taken without normalization of vitamin D.

Calcium is therefore emerging as an important player in artery health. But just taking calcium makes no more sense than our brick wall and cement analogy. You might regard vitamin D as the mason that skillfully lays down both brick and cement in a neat, orderly way.

Another big Track Your Plaque success story

Lorenzo is an 81-year old retired manufacturing engineer whose intial heart scan score in late 2006 was an alarming 1102.

Recall that, despite feeling well and having a normal stress test, Lorenzo was facing a heart attack and death risk that was as high as 25% per year without preventive action.

Lorenzo was moderately interested in the Track Your Plaque concepts. While not exactly the most highly motivated, he did see the rationale in our approach. But he came to us mostly because his primary care doctor told him to.

Nonetheless, one year later, he underwent another heart scan. His score: 588--a 46.6% drop in score, nearly cutting his plaque in half. While Lorenzo didn't set any new records in terms of percentage drop in score, he has reduced his score in real numbers more than anybody else before: a 514 point drop in score.

Lorenzo joins the ranks of our current record holders, Amy, with a 63% drop in heart scan score, and Neal with a 51% drop in score. Both of these Track Your Plaque record holders, while achieving larger percentage reductions in score, achieved less when viewed on an absolute number basis.

Now, breaking records is not necessary to succeed in the Track Your Plaque program or at heart disease reversal. Even 1% reversal is still a big success, certainly more than is achieved in conventional practice.

No special commitment was necessary in Lorenzo's case. All he required was a little of the right kind of information. I can tell what he didn't do: Lorenzo did not follow a low-fat American Heart Association diet, he did not take high-dose statin drug, he did not deprive himself of food, he did not exercise to extremes. He just applied some simple strategies from the Track Your Plaque program.

I play these sorts of games just to make a point and to show just what is possible. While the world of hospital procedures and emergency management of coronary disease marches on, we are quietly reversing the disease. Sometimes, we achieve results that even surprise ourselves.

Lorenzo's full story will be detailed in the February 2008 Track Your Plaque newsletter. If you are not yet a subscriber, you can sign up (without cost)here.


Copyright 2008 William Davis, MD

The myth of mild coronary disease

I hear this comment from patients all the time:

"They told me that I had only mild blockages and so I had nothing to worry about."

That's one big lie.

I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?

"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild."

The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result.

So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture.

One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage.


Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up.

The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions.


Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)



Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.

Vytorin study explodes--But what's the real story?

The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Dr. Arthur Agatston in the news



The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:
The South Beach Diet doctor takes on cardio care

Agatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III).

The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:


• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

• Do aerobic exercise, along with stretching and strengthening workouts.

• Ask your doctor about taking statins and other cholesterol-lowering drugs.


We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others.

But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this.

As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)

Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program.

That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.

Take this survey: I DOUBLE-DARE YOU

In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed.

Here's what I said:

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.


I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.

But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible.

What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?

No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease.

But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries.

Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially.

I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am.



Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism



The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book.

The new book is In Defense of Food: An eater's manifesto.

As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store.

In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."

In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:

"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters."


Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.

With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"
All posts by william-davis

Weight loss and blood pressure

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

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

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

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

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

Why the age-dependent difference?

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

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

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

Brad needed to lose weight.

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

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

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

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

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

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

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

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

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

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

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

I call these changes "transitional" changes in lipids.

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

Divorce court for the doctor-patient relationship?

The doctor-patient relationship has gone sour.

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

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

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

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



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

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

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


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

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

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

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

But a caveat: The patient MUST be informed.

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

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

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

It will be a startling change.

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


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

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

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

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

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

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

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

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

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


Wow. A woman after my own heart.

How much fish oil is enough?


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

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

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

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




Several observations jump out:

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

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

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




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

Taken at face value, this study would argue that:

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

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


We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.

Omega-6 / omega-3 ratio

Most of us already know that the intake of omega-6 fatty acids in the American diet has gone overboard, much at the expense of the omega-3 fraction. This occurred as a result of the misguided advice of the 1970s and 1980s to eat polyunsaturated oils like corn, sunflower, and safflower, because of their presumed cholesterol-reducing properties compared to saturated fats. However, more recent examinations of this advice have suggested that the omega-6 fraction of oils present in polyunsaturated oils may amplify arachidonic acid and other inflammatory patterns despite the reduction in cholesterol (total and LDL).

Dr. Artemis Simopoulos of the Center for Genetics, Nutrition and Health in Washington, D.C. has written extensively on the role of omega-6 and omega-3 fatty acids in diet.

In a review entitled The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cadiovacular Disease and Other Chronic Disease , Dr. Simopoulos collects the following comparison of omega-6 to omega-3 ratios from various populations:


Paleolithic humans 0.79
Greece (prior to 1960) 1.00-2.00
Current Japan 4.00
Current India, rural 5-6.1
Current United Kindom and northern Europe 15.00
Current United States 16.74
Current India, urban 38-50

(The numbers refer to the ratio of omega-6 to omega-3 intake.)


If we believe the observations of Dr. Loren Cordain and others, while paleolithic man died of trauma and infectious diseases, they did not die of heart disease. Paleolithic human intake of omega-3 exceeded that of omega-6.

Likewise, the traditionally low cardiac event regions of the world like Japan and Greece have less omega-3 intake than Paleolithic man, but still many times more than the U.S. and U.K.

Worst of all with an enormous preponderance of omega-6 over omega-3 are urban Indians, who experience among the highest rates of heart disease in the world.

Just for perspective, let's assume you eat an 1800 calorie per day diet, of which 30% of calories come from fat. This would amount to 540 calories per day from fat. With 9 calories per gram of fat, this means that there are 60 grams, or 60,000 mg, of fat in your diet per day.

Paleolithic man has been found to have existed on a diet consisting of 21% of calories from fats. Again assuming an 1800 calorie per day diet, that comes to 42 grams of fat per day (42,000 mg).

If we were to try to recreate the Paleolithic fat composition of diet, we would ingest 21,000 mg of omega-3 fatty acids (EPA, DHA, linolenic acid) per day. Even recreating a Japanese experience with a 4:1 ratio, it would mean 8400 mg of omega-3 per day. (Curiously, this does not agree with all estimates of Japanese intake of omega-3s.)

No matter how you look at it, cultures with lower rates of cardiovascular disease take in greater--much greater--quantities of omega-3 fatty acids.

So don't complain about your six fish oil capsules (usually containing 6000 mg of total oil, 1800 mg omega-3s)!

Dr. Bernadine Healy on heart scans


A Heart Scan Blog reader brought the following tidbit to my attention.

Cardiologist and now writer for U.S. News and World Report, Dr. Bernadine Healy, wrote this editorial, a glowing endorsement of heart scans:

The approach is beautifully simple. Calcium accumulates in advanced plaques, so calcium visible in the heart's arteries indicates atherosclerosis. An exploding number of studies in the past few years have unequivocally shown that the calcium score predicts both heart attack and sudden death. As a generalization, patients with scores between 100 and 400 face three to four times the risk of a heart attack or death compared with others at the same age with a zero score. Over 400, that elevated risk more than doubles.

Most doctors rely instead on the Framingham calculator, which estimates a symptom-free person's risk of a heart attack in the next 10 years based on smoking history, blood pressure, cholesterol levels, sex, and age. It's available free online from the National Institutes of Health. Most people taking the test will have minimal or no coronary disease, though risk estimates over 9 percent should inspire vigorous preventive efforts. For some, however, coronary heart disease is sneaky, and Framingham will underestimate what lies ahead. Roughly half of those who suffer a major heart attack or sudden coronary death are symptom free. Calcium scores are additive to Framingham; they pick up the individual surprises by using X-ray vision to look inside the heart. No wonder insurance companies are scrambling to use coronary calcium scores—life insurers, that is.



Dr. Bernadine Healy is no small-time player. In addition to her academic credentials, she is former chief of the National Institutes of Health (the first woman to hold the influential post), former head of the American Red Cross, and former deputy director of the White House Office of Science and Technology Policy under the Reagan administration. An endorsement of CT heart scans, though written under the guise of a probing editorial, will do an enormous amount of good to overcome the hurdles in gaining wider acceptance of heart scans.

Those of us applying heart scans in everyday practice have long appreciated their enormous power to detect and track coronary plaque. Framingham scoring can't even touch the certainty and quantification provided by heart scans in day-to-day life. Hundreds of studies have validated their use, but they still suffer from lying in the shadows of the procedural bullies aiming to boost the number of heart catheterizations, angioplasties, stents, bypass surgeries.

Dr. Healy, a voice with great weight, not just a political figure but also a cardiologist and scientist, has done a great service to broadcast the message of heart scanning.

Mercury and fish oil

As time passes, the dose of fish oil advocated in the Track Your Plaque program is going upward.

While epidemiologic studies, like the Chicago Western Electric Study and the Nurses' Health Study suggest that decreases in mortality from heart disease begin by just eating fish a couple times per month, there are newer data that suggest greater quantities confer greater benefits.

In the last Heart Scan Blog post, I discussed the recently-released ERA JUMP Study that demonstrated a relationship between higher omega-3 fatty acid blood content and reduced quantities of carotid and coronary plaque. The JELIS Study demonstrated a 19% reduction in cardiovascular events when fish-consuming Japanese added 1800 mg of EPA (only).

However, the suggestion that increased quantities of fish oil potentially yield greater protection from heart attack and facilitate coronary plaque regression is also stirring up worries about mercury exposure. So I dug up a Heart Scan Blog post from a year ago that discussed this issue and reprint it here.


I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor [now Lovaza], or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.



I am not advocating ad libitum eating of fish. Sadly, this may be related to excessive accumulation of contaminants. I am suggesting that greater quantities of omega-3 fatty acids from relatively contaminant- and mercury-free fish oil capsules.

More on this in an upcoming webinar on the Track Your Plaque website: Fish Oil and the Track Your Plaque Program - Is More Better?

ERA JUMP: Omega-3 fatty acids and plaque


The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Mediterranean diet and blood sugar


Data such as that from the Lyon Heart Study have demonstrated that a so-called Mediterranean diet substantially reduces risk for heart attack.

But there are aspects of the Mediterranean diet and lifestyle that are not entirely sorted out.

For instance, what specific component(s) of the diet provide the benefit? Is it olive oil and linolenic acid? Is it red wine? Is it the reduced exposure to processed snack foods that Americans are indundated with? Is it their more slender builds and greater tendency to walk? How about exposure to the Mediterranean sun? What about the inclusion of breads, since in the Track Your Plaque program I advocate elimination of wheat products for many abnormalities?

Anyway, here's a wonderfully thoughtful set of observations from Anna about her experiences traveling Italy, trying to understand the details of the Mediterranean diet while also trying to keep blood sugar under control.


I just returned from a two week stay in Italy, doing a bit of my own "Mediterranean Diet" experiments. When practical, we sought out food sources and places to eat that were typical for the local area, and tried as much as possible/practical to stay away from establishments that mostly catered to tourist tastes. I was really curious to see how the mythical "Mediterranean Diet" we Americans are urged to follow compared to the foods really consumed in Italy.

The first week, we stayed in a rural Tuscan farmhouse apartment (agriturismo), so many, if not most of our meals were prepared by me with ingredients I bought at the local grocery store (Coop) or the outdoor market in Siena. In addition, I purchased really fantastic free-range eggs from the farm where we were staying. (Between some language issues and seasonality, eggs and wine were what we could buy from them - though I was tantalized by the not-quite-ripe figs heavy on many trees). Mostly, our meals consisted of simple and easily prepared fresh fruits and vegetables, rustic cured meats (salami, proscuitto, pancetta, etc.) hand-sliced at the deli down the road, fresh sausages, various Italian cheeses, plus plenty of espresso. It was a bit disappointing to find underripe fruit & tomatoes as well as old green beans in the grocery stores, not to mention too many low fat and highly processed foods, but all over Europe the food supply is becoming more industrialized, more centralized, and homogenous, so I'm not too surprised that it happens even in Italy. But even with the smaller grocery store size, the amount of in-season produce was abundant, yet one still was better off shipping from the perimeter of the store, venturing into the aisles only for spices, olive oil, vinegar, coffee, etc. Without the knowledge of where to go and the language to really talk in depth about food with people, I wasn't able to find truly direct and local sources for as many foods as I would have liked, but still, we ate well enough!

The first week I maintained blood sugar levels very similar to those I get at home, because except for the Italian specialties, we ate much like we always do. A few rare exceptions to my normal BG tests were after indulging in locally made gelato or a evening limoncello cordial, but even then, the BG rise was relatively modest and to me, acceptable under the circumstance. Even with the gelato indulgences, it felt like I might have even lost a few pounds by the end of the first week and my FBG didn't rise much over 100.

The second week we stayed in two cities (Florence & Rome), and I didn't prepare any of my own food because I didn't have a kitchen/fridge. I found it impossible to get eggs anywhere for breakfast, and the tickets our hotels provided for a "continental" breakfast at a nearby café/bar was always for a coffee or hot chocolate drink and some sort of bread or roll (croissant, brioche, danish, etc.). At first I just paid extra for a plate of salami and cheese if that was available - or went to a small grocery store for some plain yogurt, but then I decided to go off low-carb and conduct a short term experiment, though I didn't consume nearly as many carbs as a typical Italian or tourist would.

So I breakfasted with a brioche roll or plain croissant for breakfast with my cappuccino, but unfortunately no additional butter was available. I didn't feel "full" enough with such a breakfast and I was usually starving an hour or two later. Additionally, when I ate the "continental" breakfast, I noticed immediate water retention - my ankles, lower legs, and knees looked like someone else's at the end of a day walking and sightseeing, swollen heavy. Exercising my feet and lower legs while waiting in lines or sitting didn't seem to help.

Food is much more expensive in Europe than in the US, and the declining US$ made everything especially expensive (not to mention the higher cost of dining out rather than cooking at home), so we tried to manage food costs by eating simple lunches at local take-away places, avoiding the corporate fast food chains. I was getting tired of salami/proscuitto & cheese plates, but the typical "quick" option was usually a panini (sandwich). At first I tried to find alternatives to paninis, but the available salads were designed for side dishes, not main meals and rarely had any protein, and the fillings of the expensive sandwiches were too skimpy to just eat without the bread. So I started to eat panini, although I sometimes removed as much as half of the bread (though it was nearly always very excellent quality pan toasted flatbreads or crusty baguette rolls, not sliced America bread). So of course, my post-prandial BGs rose, as did my FBG. I also found my hunger tended to come back much too soon and I think overall I ate more than usual in terms of volume.

Then we deviated from the "Italian" lunch foods and found a better midday meal option (quick, cheaper, and easier to customize for LC) - stopping at one of the numerous kebab shops and ordering a kebab plate with salad, hold the bread (not Italian, but still Mediterranean, I guess). I felt much better fueled on kebab plates (more filling and enough protein) than paninis, though I must say I still appreciated the taste of caprese paninis (slices of fresh mozzerella and tomato, basil leaves, mustard dressing on crusty, pan-toasted flat bread). If I followed my appetite, I could have eaten two caprese paninis.

We had some great evening dinners, at places also frequented by locals. This often was a fixed price dinner of several courses ("we feed you what we want you to eat"). Multi-course meals included house wine, and invariably consisted of antipasta (usually LC, such as a cold meat and cheese plate), pasta course (much smaller servings than typical US pasta dishes), main course plus some side vegetables, and dessert/coffee. These were often the best meals we experienced, full of local flavor and tradition (sometimes with a grandmotherly type doing the cooking), and definitely of very good quality, though we noticed the saltiness overall tended to be on the high side. I ate from every course, including some of the excellent bread (dipped in plenty of olive oil) and usually about half of the pasta served (2 oz dry?), plus about half of the dessert. After these meals I always ran BGs higher than usual, varying from moderately high (120-160 - at home I would consider this very high for me) to very high (over 180). By late in the week, my FBG was into the 115 range every morning (usually I can keep it 90-100 on LC food). Nearly everything that week was delicious, well-prepared food, but the high carb items definitely were not good for my BG control in the long run.

And most days I was doing plenty of walking, sprinting for the Metro subway trains, stair climbing (4th and 5/6th floor hotel rooms!), etc. but since I didn't have my usual housework to do, it probably wasn't too different from my usual exertion level.

So it was very interesting to experience the "Mediterranean Diet" first hand. Meats and cheeses were plentiful, fruits and vegetables played a much more minor role (main courses didn't come with vegetables other than what was in the sauce, but had to be ordered as additional items), but the overall carbs were decidedly too many. As I expected, it wasn't nearly as pasta-heavy as is portrayed in the US media/health press, but it is still full of too much grain and sugar, IMO. Low fat has become the norm in many dairy products, sadly, and if the grocery stores are any indication, modern families are gravitating towards highly processed, industrial foods. Sugar seems to be in everything (I quickly learned to order my caffe freddo con panno or latte sensa zuccero - iced coffee with cream or milk without sugar) after realizing that adding lots of sugar was the norm).

And, after several days of breakfasting at the café near our Rome hotel (where carbs were the only option in the morning), I learned that our very buff, muscular, very flat-stomached, café owner doesn't eat pasta (said as he proudly patted his 6 pack abs). I probably could have stuck closer to the carb intake I know works better for my BG control, but I figured if I was going to go off my LC way of eating and experiment, this was the time and place.

And yes, there were far fewer really obese people than in the US and lots of very slender people, but I could still see there were *plenty* of overweight, probably pre-diabetic and diabetic Italians (very visible problems with lower extremities, ranging from what looked like diabetic skin issues, walking problems, acanthosis nigricans, etc.). Older people do seem to be generally more fit than in the US (fit from everyday life, not exercise regimes), but there were plenty of "wheat bellies" on men old and young, even more young women with "muffin tops", and simply too many overweight children (very worrisome trend). So it may well be more the relaxed Italian way of living life (or a combination of other factors such as less air conditioning, strong family bonds, lots of sun, etc?) that keeps Italian CVD rates lower than the American rates, more than the mythical "Mediterranean diet".

Who is your doctor?


Primary care physicians are the initial entry point for healthcare for the majority of Americans.

Develop pneumonia; go to your family or internal medicine physician (internist) to be prescribed an antibiotic. Need your blood pressure or cholesterol checked? Develop a sore knee or swelling in your leg? Once again, go to your primary care physician.

Image courtesy Dedde'


Primary care physicians are a patient’s guide to a bewildering array of technology and specialists. If you require a specific diagnostic test or consultation with a specialist, your primary care physician will help you navigate through the maze, choosing the path that is best for you. He or she will order a chest x-ray for a cough and fever, provide vaccines to prevent flu or pneumococcal pneumonia, perform an annual physical. If you require hospitalization, your primary care physician will admit you. He or she will order diagnostic tests like MRI’s, ultrasounds, x-rays, and blood testing, usually performed in the hospital or a hospital-owned facility. If you require the services of a gastroenterologist, orthopedist, general surgeon, or neurologist, your primary care physician will refer you to the appropriate specialist.

That’s how it’s supposed to work, at least in principle. In fact, during the first eight decades of the 20th century, it did work that work way for the most part. Your primary care physician acted not just as a provider of healthcare, but as your advocate, someone who knew you and worked to protect your welfare. Your family doctor often knew your parents, maybe even delivered you at birth, and cared for your children. His children often went to the same schools as your children. He and his family lived in the same town and sometimes went to the same church.

That hardly happens any more. It’s more likely you got the name of your primary care physician from a doctor referral service provided by a hospital. Or you picked a name off a list provided by your health insurer. It’s also common to see one doctor, only to see another a year later. Two, three, or more different primary care physicians over a five-year period are common. Doctors come and go, since physician turnover in clinics and practices has been on the increase for years. Insurance companies frequently force policyholders to change doctors, requiring you to choose from a list.

The end result of this shuffling of primary care is increasing impersonality of the relationship. You probably don’t know your primary care physician outside of the 10-minute interaction you had six months ago. She probably never met your mother and will likely not care for your children. Two years from now, she will likely not be your doctor any more, replaced by someone else who obtains the details of your health from a chart. Your chart is more likely to be electronic, with the details of your health history listed in a checklist. There’s little room to detail the idiosyncrasies and quirks of your unique personality or health profile. Throw into this impersonal equation the fact that many doctors have become scared of patients because of potential for lawsuits, often over the most trivial of issues, or because of an error of oversight or misdiagnosis.

This flawed and impersonal system, though emotionally unsatisfying, can still work if each doctor who assumes a patient’s care maintains the ethic of putting health and welfare above all.

But what if your primary care physician is not just an advocate for your welfare, but is a representative of the hospital? What if there are hidden, unspoken financial incentives paid to your doctor to direct you to the hospital for diagnostic testing, hospitalization, and referral to specialists? If a headache becomes a $4800 MRI, or chest pain becomes a $4200 nuclear stress test, then a $14,000 heart catheterization, your primary care physician becomes the purveyor of far greater financial opportunity for the hospital. The entire interaction, founded on the proposition that your doctor actually cares about you, collapses in a heap of financially motivated testing and procedures. It appears to work, and you and your family can still obtain access to healthcare. The problem is that you’re likely to get too much of it.

This message has not been lost on the shrewd administrators at hospitals. Take a look at the ranks of primary care physicians who refer patients to some of your local hospitals. It is typical that a hospital system maintains several hundred primary care physicians on their payroll, all of whom are expected to refer patients to the hospital, cardiologists, and other proceduralists. Why so many?

Most primary care physicians today have signed contracts with a hospital. In other words, they are employees of the hospital. This practice is not unusual: the American Medical Association reported that 4 of 5 primary care physicians are now bound by such employment arrangements across the U.S. In effect, 80% of primary care physicians are legally bound by contract to direct patients to cardiologists who work at hospitals.

On top of contractual obligations, there are financial incentives for the volume of procedures that are generated as a result of referrals. The more procedures generated from an internist’s or family practitioner’s practice, the greater the end-of-year productivity bonus will be, not uncommonly totaling tens of thousands of dollars. Dr. Ted Phillips (not his real name, since he declined to allow me to use it) received a bonus check of $9,437 this year for his “productivity,” defined murkily as the return on specialist referrals. While the bonus may have helped him pay for his son’s college tuition, it clearly was a situation that made him acutely uncomfortable when asked.

Several primary care physicians are also quietly dismissed every year from the ranks of employed physicians for not maintaining a minimum flow of patients into the system.

Another hazardous point of entry: Many patients enter the hospital through the emergency room (ER). A patient in the emergency room is at his or her most vulnerable, seeking help for an urgent complaint and usually willing to accept whatever the ER physician advises. Hospitals know this. That’s why many systems insist that the ER physicians be employees of the hospital, with their practice habits subject to control. A patient goes to the ER with chest pain or breathlessness. The worst thing that can happen from a financial standpoint is for the patient to be evaluated and discharged. For this reason, a growing number of hospitals employ ER physicians, then proceed to legislate practice patterns. Consulting a cardiologist is strongly encouraged, since they generally provide access to the downstream revenue-producing procedures offered in the hospital. That way, what might have been a four hour, $2500 ER visit is converted into a $10,000 to $40,000 hospital stay, even when nothing was wrong in the first place. There are millions of people nationwide who have the hospital bills to prove it after being discharged with a diagnosis of indigestion.

Caveat emptor: Buyer beware.