Let me float an idea

I'd like to float an idea.

The Track Your Plaque program is a fee-for-membership website. We chose this method of covering our costs--website development, graphics, software coding, etc.--since we do not accept advertising. I do believe that not having any advertising on our website has kept us impartial and unbiased--we mean what we say and not because we are selling something.

But there's a downside to assessing a membership fee: It limits the number of people who are willing or able to access the information. It also limits the dissemination of these concepts, due to such phenomena as limited content exposure to internet search engines.

Actos, Avandia, and vitamin D

Up until a few years ago, if a patient showed signs of the metabolic syndrome/pre-diabetes, or early diabetes, I would often prescribe one of the drugs, Actos (pioglitazone) or Avandia (rosiglitazone), known as the thiazolidinediones, or TZD's for short. Although I do not manage diabetes, I was witnessing a flood of patients with pre-diabetic patterns that inhibited correction of lipoprotein patterns. So I saw the TZD's as a means of potentially assisting with correction of these abnormalities.

My rationale back then was that many people with metabolic syndrome struggled to raise HDL cholesterol, reduce triglycerides, reduce small LDL, reduce the inflammatory measure c-reactive protein (CRP), as well as reduce blood sugars towards the normal range. The TZD's partially corrected these phenomena.

But over the last 2 1/2 years, I haven't written a single prescription for these agents since I've added vitamin D to the regimen.

Vitamin D in my experience in the Track Your Plaque approach:

--Raises HDL--far more than the TZD's ever did.

--Reduces small LDL

--Reduces triglycerides

--Reduces c-reactive protein

--Reduces blood pressure

--Reduces blood sugar

In other words, vitamin D appears to not only reproduce many of the effects of the TZD's, but exceeds the effects. The effects are often so wonderful that I've taken many people off their TZD's.

Vitamin D, of course, also provides numerous benefits for bone health, reduction of cancer risk, and other health benefits that the TZD's simply cannot compete with. Vitamin D also lacks the quite substantial side-effects of TZD's: water retention and weight gain (around 8 lbs in the first year of treatment), possible increase in risk for heart attack (Avandia), definite increased likelihood of congestive heart failure in those prone to it.

How about cost? Actos goes for about $2 per pill (30 mg tablet). Vitamin D in the gelcap form (the only form we use) costs around $0.05 per capsule--5 cents. That's a 40-fold difference in price for what I would regard as an inferior--substantially inferior--product.

Throw into the mix a dramatic reduction or elimination of wheat products and other high-glycemic index foods, and all the phenomena of the metabolic syndrome and its associated lipoprotein patterns show even more improvement or full reversal.

In fact, with this approach we are seeing record-setting magnitudes of correction of these parameters every day. Getting HDL, for instance, into the 60 mg/dl or 70 mg/dl range has never been so easy.

What if heart scans become obsolete?

What will we do if or when CT heart scans become outdated and something better comes along?

Heart scans are, after all, our principal tool for detection and precise quantification of coronary atherosclerotic plaque. They provide the basis for the Track Your Plaque program: serial heart scans to track progression or regression of coronary plaque.

So what the heck will we do if heart scans become obsolete, if some other technology proves superior for precise lengthwise quantification of coronary plaque?

Simple: Then we will convert to that measure.

Say, for instance, that in 5 years, MRI advances to the point where it is quick and precise, despite the rapid motion of the heart that has, in past, caused this technology to stumble for plaque quantification. Instead of obtaining a heart scan score of, say, 350, instead an MRI might yield information like:

Calcium volume: 350 cubic mm
Soft plaque elements: 200 cubic mm
Fibrous tissue: 700 cubic mm

In other words, while a CT heart scan provides a calcium score that serves as a surrogate measure of total plaque volume, perhaps the next wave of technology will directly measure total plaque volume.

Don't CT coronary angiograms already measure total plaque volume?

No, they definitely do not. At present, the best they can do is visualize the non-calcific elements and suggest the diameter reduction created by plaque at a specific point. Thus, results like "50% blockage in the mid-left anterior descending." What they do not provide is a lengthwise total volume of plaque and all its elements. Perhaps some software manipulation in future will yield such information (and I think it will, though I personally have been unable to accomplish it).

So neither the Track Your Plaque program nor the Heart Scan Blog are necessarily bound to heart scans. But heart scans, in 2008, remain the number one best tool for plaque quantification that is easy, precise, available, and inexpensive. For those reasons, CT heart scans continue to serve as the basis for these programs, and not CT angiograms, MRI, or other non-quantitative technology.

Scare tactics

Does the media engage in scare tactics?

Read the headlines in local newspapers, and you'd believe that your friends and neighbors are dropping like flies, all victims of heart attacks.

I occasionally peruse the headlines run in newspapers and magazines around the U.S. by subscribing to a feed service through Google. For the phrase, "heart attack," you can get a sample of what is being said around the country about people having heart attacks.

What continues to impress me is just how far off a truly constructive and helpful message the media provides every day. Not only are they guilty of delivering a flawed message, they also favor headlines and stories that scare the heck out of people. "This could happen to you!"

Is it just the quest for headlines that grab readers' attentions? Is there some complicity with the medical systems that pay significant advertising revenues for their heart disease programs and hospitals?

I doubt such complicity exists to any substantial degree. But the fact remains: Every day across the U.S., the media does an effective job of scaring the heck out of the public--enough for you to run to your doctor or hospital to find out if you, too, could fall victim to heart disease. A stress test, perhaps heart catheterization, three stents or bypass often results.

In effect, these headlines make great hospital PR, an inducement that flushes out the patient highly motivated to pursue further costly heart testing--whether or not it's needed.

A sampling:

Stress test could help prevent sudden heart attack

DAWN ZERA Times Leader Correspondent

Bob Schultz, 67, was feeling a persistent pain in his back, which he was pretty sure was caused by working on a deck for his son’s home.

But after the deck was finished, the pain was still there.

“It was nagging, but not enough to hurt,” Schultz said.

He visited his primary care physician, thinking maybe some muscle relaxants would be prescribed. The doctor sent him to a clinic in Tunkhannock to do a complete body CAT scan, and then had Schultz do a stress test. The on-site cardiac stress testing at a Geisinger Medical Group office in Tunkhannock showed that things did not look good: Schultz had a blockage. He was scheduled for a cardiac catheterization.

It was a surprise; a heart problem had not even crossed Schultz’s mind as a possible cause of his back pain.

“I had good cholesterol, have been the same weight for years, and had excellent blood pressure,” Schultz said.

He went for the catheterization at Geisinger Wyoming Valley, and there doctors discovered Schultz’s condition was even more serious. He had three blockages – 99 percent, 95 percent and between 80 and 90 percent.

“It shocked the living daylights out of everyone. It was surreal,” Schultz said.

The catheterization turned into open heart surgery that very same day.

The surgery was on a Tuesday, and he was home by Sunday. He never even had time to fully think about having the operation. And he had never experienced the typical warning signs of a heart problem, such as chest pain or shortness of breath.

“The doctors said I had the worst alarm system they’d ever seen,” Schultz said. “They probably saved my life, with me not knowing I had a problem.”

It also made him think about his brother, who had had been in good health but suddenly died in his 40s of a suspected heart attack.

“We never had any heart problems in our family, so we never believed it. But now I think, geez, it probably was true,” Schultz said.

His experience has served as a cautionary tale for friends and family. Just this past month, a friend specifically requested a stress test for himself.

“It sets off alarms in your circle. People think ‘if it can happen to him, it could happen to me,’ ” Schultz said. “It triggered people to think about what could happen to them.”



Firefighter Saves Heart-Attack Victim on D.C. Court

ABC News

A 30-year-old man suffered a heart attack while playing basketball on a D.C. court.

That's when a Brian Long's firefighter training kicked into action. The 25-year-old D.C. firefighter's team had just finished their pick-up league game Friday evening at Lafayette Elementary School's basketball court when the man stumble to the ground.

"He ran a few feet and collapsed again so I turned him over and I looked at him his eyes rolled back and he just stopped breathing," Long said.

Long began performing chest compressions and soon he was joined by Anthony Gadson, a pharmaceutical sales representative, who learned CPR years ago and starting assisting with mouth to mouth resuscitation.

"If that were me, somebody would've done the same thing for me, so I feel like I did what I was supposed to do," Gadson explained.

While Long and Gadson worked to keep the victim's heart going, all the players and spectators, including teammate and league commissioner Bob Johnson, gathered around the lifesaving effort.

"We gathered in a circle and one of the wives of one of the players just led us in this huge prayer," said Johnson.

"It makes me feel great," Long told ABC 7/NewsChannel 8. "I am just glad that I am a D.C. Firefighter."



Free Drugs After Heart Attack Would Save Money, Lengthen Lives
More patients would take recommended medications, study says


By Ed Edelson

MONDAY, Feb. 18 (HealthDay News) -- Eliminating the cost of medications for people who have heart attacks would lead to longer lives and lower overall medical costs, new research suggests.

"These are highly effective medications that are relatively inexpensive, and the events they are designed to prevent are extremely expensive," said study author Dr. Niteesh K. Choudhry, a researcher in the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women's Hospital in Boston and an assistant professor at Harvard Medical School. His report is published in the Feb. 19 issue of Circulation.

The study covered four drugs commonly prescribed after heart attacks -- aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers (ARBs), and statins. Use of those drugs is relatively low under the current system, in which people share the cost with Medicare or other health insurance plans, Choudhry said. For example, only 46 percent of people take beta blockers after heart attacks, and only 50 percent take cholesterol-lowering statins. Less than 20 percent of heart patients used all four of the medications, according to the study.

The model set up by Choudhry and his colleagues doesn't assume a major increase in compliance with prescriptions, because "cost is just one reason why patients do not take medications," he said, adding that relying on previous studies of drug cost and use, the model assumes an increase of about 14 percent, with perhaps 64 percent of people taking the medicines if they were free.

The result would be an increase in average survival after a heart attack, from the present 8.21 quality-adjusted life years to 8.56 years. "That is small in an absolute sense, but in an aggregate sense, it is very large," Choudhry said.

And medical costs over a lifetime would go down, from the current $114,000 to $111,600, the study added.

"This study adds to a growing body of research showing how important it is to reduce or eliminate patient co-payment for drugs," said Robert M. Hayes, president of the Medicare Rights Center in New York. "Medicare should take the lead in forging the creation of drug coverage that allows patients to get the medications their doctors consider vital."

"It certainly makes sense from the medical point of view," said Dr. Richard A. Stein, a professor of medicine at New York University. "Studies have shown that giving even middle-income people free drugs improves outcome. The greatest benefit will go to people in the lower socioeconomic and immigrant population."

But the study is theoretical, Stein noted. "One would like to see some real-world trial to determine whether this works in fact, whether providing free drugs without co-payment would make a difference, he said.

Such a study has begun at Harvard, Choudhry noted. His group is working with a major health insurer, not Medicare, in a trial that assigns some people to get medications without cost, while others will get the standard co-payment.

"It will take several years for us to get answers," Choudhry said. But similar investigations are being started by other medical insurers and corporations, he added.

The idea is potentially applicable to some other chronic conditions, such as congestive heart failure and diabetes, Choudhry noted. And, if the use of recommended medications after a heart attack goes up more than predicted by the model, "the cost savings would be phenomenal," he said.

More information

To learn about how to stay on your statins, consult the National Heart, Lung, and Blood Institute.




Heart Attack Threatens Young, Old

BAKERSFIELD, Calif. -- Nearly 1.2 million men and women suffer a heart attack every year in the United States, according to the American Heart Association. However, not all of the victims are old.

Brian Connell considers himself a lucky guy. At the age of 39, he's physically active, he has a high-level job, and he is also a heart attack survivor. "I know I was overweight and obviously had some other risk factors against me," said Connell. "I wish I did more to prevent it, certainly."

Connell is doing plenty of things now. He met with a nutritionist and changed his diet. He gets regular exercise and takes medication to control his cholesterol. He also gets regular checkups.
Click here to find out more!

Cardiologist Jeffrey Popma said it's not unusual to see younger heart attack patients. "We have dozens of patients in our system every year who have been under 40 years old who have suffered a major heart attack," said Dr. Popma.

Popma said getting medical help quickly is the key to survival. Connell said that is what made all the difference for him. And when people ask him if that was his first heart attack, Connell said he is quick to tell them it was his last heart attack.

Copyright 2008 by TurnTo23.com. The Associated Press contributed to this report. All rights reserved.


The messages I take from such stories:

1) Get yourself to a hospital ASAP for any symptoms even vaguely suspicious of heart disease, because they will know what to do. You'll be doomed if you don't.

2) Hospitals and doctors are expert at saving you from the brink of disaster. The process, once you enter, is rapid and smooth and you will be eternally grateful.

3) Medicines save lives. You're going to die if you don't take medication.


As I've often said, one of the toughest battles of all in health and heart disease is sorting out fact from fiction. Unfortunately, the media continues to propagate the scare tactics that support the status quo of procedural heart care. Wittingly or unwittingly, they serve a $400 billion dollar a year gargantuan industry that remains hungry for growth.

Lost in the headlines are the messages that could have been included, like:

Heart disease detectable decades before disaster

Or:

"Heart disease preventable, reversible, and--curable?"



Copyright 2008 William Davis, MD

Which statin is best?

The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.


Copyright 2008 William Davis, MD

Lipoprotein(a)--neglected and unappreciated


Lipoprotein(a), or just Lp(a) to its close friends and neighbors, is among the most underappreciated and neglected of causes of coronary plaque. It's the Rodney Dangerfield of lipoproteins.

Lp(a) rarely gets diagnosed before people come to my office. They've often been through the ringer: doctors have thrown their hands up in frustration because of poor response to "standard" treatment (AKA statin drugs); the patient doesn't understand why they might be thin and active yet have the high blood pressure of someone 70 lbs heavier; they have heart disease despite wonderful cholesterol values.

One blood test and the answer becomes clear: They have Lp(a). It explains all these phenomena.

They why don't more physicians order this simple test? Why don't we hear more about this prevalent (1 in 5 people with coronary plaque have it) genetic pattern that accelerates risk for heart disease?

There are a number of reasons. But I believe the most powerful reason is simply that there is no big revenue-generating drug to treat it. Statins reduce LDL cholesterol to the tune of $27 billion dollars a year (2007 revenue). There's no such blockbuster for Lp(a). Of course, Niaspan represents the relatively anemic attempt to commercialize a pharmaceutical treatment for Lp(a), but side-effects and the lack of FDA trials for the Lp(a)-reducing indication have stalled its commercial success. (Efforts to block the flush with various products, by the way, may re-invigorate niacin as a pharmaceutical agent. The drug companies smell money here.)

Another reason for Lp(a)'s unpopularity: Though there are mounds of data that document--without question--that Lp(a) is an important risk for coronary disease and other forms of atherosclerotic disease, we lack treatment trials. For instance, niacin vs. placebo for 5 years, then count the number of heart attacks and deaths. We have numerous, repetitive, overlapping, redundant trials with statins adhering to this design. We have none for niacin and the treatment of Lp(a).

Niacin is also a pain in the neck for your doctor. He/she rapidly tires of the calls about the crazy and disconcerting flushing with niacin. Most are unaware that proper hydration reduces or eliminates the flush for the majority of people. It takes too much time and energy to educate people. (By the way, prescription Niaspan makes no mention of purposeful hydration. They only suggest the nonsensical "Take with a low-fat snack," i.e., snacks that actually counter the therpaeutic effects of niacin. What they should be saying is "take with a high-fat snack" like raw almonds, foods that facilatate the benefits of niacin.)

Should someone concoct a successful pharmaceutical treatment for Lp(a), it will make the news, headlines in health magazines and health sections of the newspaper will blare about how important Lp(a) is. Yet it has been there all along, frustrating people and their physicians.

In the Track Your Plaque experience, Lp(a) clearly 1) correlates with heart scan scores, 2) correlates with progression of heart scan scores without treatment, and 3) poses special challenges for treatment. Interestingly, some of our biggest failures have been with Lp(a), as well as some of our biggest successes. (Our current record holder for the largest percentage reduction in heart scan score has Lp(a).)

If you have coronary plaque, or if there is family risk of heart disease, then Lp(a), in my view, is an absolutely essential factor to test for. Yes, treatment poses challenges. But once you know who your enemy is, then you can focus your efforts on it. Not knowing whether or not you have it leaves your efforts unfocused and generally flawed.

Track Your Plaque Members, be sure to read our in-depth Special Report, Unique Treatments for Lipoprotein(a) Reduction.



Copyright 2008 William Davvis, MD

Wheat-free and still fat

Readers of The Heart Scan Blog know that I preach a diet that contains foods with low glycemic index to control weight, raise HDL, and reduce triglycerides, blood sugar, and small LDL.

A crucial aspect of a low glycemic index approach is to sharply reduce, preferably eliminate, wheat products.

I pick on wheat specifically because it has come to dominate the American diet. Look at the shelves in the supermarket: aisle after aisle of processed wheat products. The bread shelves alone in some of the grocery stores in my neighborhood are 40 feet long, six shelves high. There's also breakfast cereals, granola products, cookies, cakes, baking products, pretzels, crackers, pasta, and on and on.

Wheat products like these are tasty and they're addicting--literally. Test animals given processed wheat will eat more and gain more weight. Wheat fails to trigger satiety. So laboratory mice--and you and I--eat and eat, because eating wheat stimulates appetite, creates a hunger for more wheat, and a vicious cycle ensues. Eliminating wheat, on the other hand, results in dramatic drop in appetite, substantial weight loss, followed by correction of the metabolic disruptions it created.


A quick Google search for "gluten-free" turns up a startling array of wheat-free, gluten-free, yet high glycemic index products. The breakfast cereal pictured, for instance, can do as much damage as most wheat containing products--though it won't cause gluten enteropathy (also known as "celiac disease").




The product shown contains:

Brown rice flakes, rice bran, evaporated cane juice, brown rice syrup, raisins, cinnamon, gum arabic, vanilla, molasses, ground flaxseed, rosemary extract.

A 1/2-cup serving contains:
Total Carbohydrate 31g
Dietary Fiber 5g
Sugars 8g


And I'll bet that most people eat a lot more than a half-cup serving.

But you and I are not laboratory mice. If deprived of wheat, many people will then seek out processed rice products (rice cakes, Rice Krispies), processed cornstarch or cornmeal products (tacos, cornbread, many processed foods using these products for texture or thickness), or other products labeled "gluten-free."

Going wheat-free for our purposes is not about avoiding the gluten in wheat. It is about seizing control of appetite, eliminating a food that disrupts insulin responses, reduces HDL, raises triglycerides, and creates small LDL particles. But this applies to processed corn, rice, and other high glycemic index foods, as well.

So, occasionally, someone will declare, "I've eliminated wheat! Now I only eat rice, corn, and I've discovered all the gluten-free alternatives!"

Unfortunately, they've traded one evil for another. So it's not just about wheat. It's really about reducing or minimizing foods that mess up metabolic responses and lead to coronary plaque growth. Wheat is the biggest culprit and so I focus on it. However, you could easily transfer far less popular rice and corn products into center stage and allow them to wreak all the health damage of wheat.

Going wheat-free for our atherosclerotic plaque-control purposes is not the same as going gluten-free. So be careful of the distinction.


Wheat-free gummi bears:


Contents:
Organic dehydrated cane juice, organic corn malt syrup, organic juice concentrates (may contain organic apple, organic apricot, organic aronia, organic carrot, organic cranberry, organic elderberry, organic lemon or organic red beet), organic spinach powder, organic apple pectin, citric acid, natural fruit flavors.

Virtually pure sugar--yet wheat-free.



Wheat-free rice bread


Ingredients:
White rice flour, water, honey, soy oil, natural gum, salt, yeast, natural gum














Copyright 2008 William Davis, MD

Heart disease is reversible

In a previous post, Take this survey: I double-dare you, I posed a challenge:

Ask your doctor: Is heart disease reversible? Their answer:

1) No. Heart disease is definitely not reversible.

2) Yes, in rare instances, like lightning striking twice.

3) Yes, of course it is! Let's talk about how to do it!

I predicted that few readers of this blog would respond. I also predicted that the few who did would respond with the first answer, Heart disease is definitely not reversible. After all, in nearly all medical practices, the only parameters routinely followed to track risk for heart disease are LDL cholesterol and blood pressure. A measure of the disease itself (i.e., coronary atherosclerotic plaque) is not followed. So how can your doctor actually tell whether heart disease is reversed or not? When I engage in this conversation with colleagues, it goes no farther than rolled eyes or a snort. In my experience, talking about reversal of heart disease is a wasted effort.

To my great surprise, this simple survey received a total of 177 responses. Even more surprising, 122 (69%) of respondents chose number 3, claiming that their doctor said that heart disease is reversible.

Overall results:

1--31 responses (17.5%)

2--24 responses (13.5%)

3--122 responses (69%)


Now wait a minute: Where is the disconnect? Why are doctors saying that heart disease is reversible, yet not following this concept in practice? Contrary to the survey results, I have yet to meet a patient who said their doctor was trying to reverse their heart disease. Of course, this may be a skewed population, but I find it hard to believe that the prevailing view is that heart disease is reversible.

Anyway, this simple survey cannot settle the why or how, nor can it suggest just how prevalent this opinion is.

I am encouraged by these results. If true, it means that the message that heart disease is a reversible process is spreading. It may be make-believe heart disease reversal as preached by Dr. Dean Ornish or claimed by statin drug manufacturers. It may be the hocus-pocus of practices like chelation, or scams like nattokinase. But perhaps the seed of this notion has been planted in the minds of the medical community.

I'd be interested in hearing from the respondents who reported that their doctor said heart disease is reversible. How exactly are they going about achieving reversal?

Looking for health in all the wrong places

The American public now has unprecedented freedom to explore new directions in health.

Never before have we had the enormous resources now available to add to our health experience: nutritional supplements, endless books on health and diet, the internet, online discussion groups, insurance products to permit spending on self-directed health services like medical savings accounts and flex-spending. The Track Your Plaque program is just one facet of this emerging and exciting area of self-empowerment in health. Compare what you can achieve with such a program with the situation of just 25 years ago, when the most you might get to reduce your risk for heart disease was to take the (largely ineffective) drug cholestyramine, probucol, and a low-cholesterol, low-fat diet.

Unfortunately, it also means that people have unrestrained potential to be tripped up, to be misled down some dead end of health that fails to accomplish desired goals, maybe even dangerous. The more freedom we have, the greater the choices, the more room we have to screw up.

Among the unproductive strategies I've witnessed recently:

--Nattokinase--The staying power of this scam continues to shock me. There is no rational basis for its use. A woman today declared that she would like to stop the warfarin that she was taking to prevent stroke from atrial fibrillation by taking nattokinase. This would be a mistake that could cost her a major and disabling, even fatal, stroke. Though warfarin is far from perfect, it at least achieves its goal of reducing stroke risk. Nattokinase does not. Nattokinase does nothing but make money for the people who sell it.

--Poly-nutritional supplements. You've heard of polypharmacy, the phenomenon of taking numerous medications with overlapping effects and side-effects, usually because of multiple doctors, each prescribing drugs without knowledge or interest in what colleagues are prescribing. I'm seeing the same phenomenon with supplements: 20,30, or more supplements per day, all in the hopes of heightening health. A focused few supplements is, in my view, superior to a shotgun approach of trying to improve health by taking hawthorne, silymarin, chrysin, calcium, Chinese herbs, and 25 other supplements.

--Chelation--Based on the notion that heavy metal toxicity causes heart disease; removal of heavy metals cures it. I've read some of the books on chelation, in addition to the slim scientific data, to decide whether there was anything to it. In my view, it is a complete and utter scam. It does make money for its practitioners, however. That's not to say that heavy-metal chelation doesn't have a role in health--it does. But it serves no purpose in coronary disease prevention and control.

--Colonic purges--Achieved by a number of routes, some oral, others via enema. Promotions for purging are often accompanied by a pile of scum that apparently lined somebody's intestinal tract. Purges purportedly, well, purge it from the intestine. This is also plain nonsense. There is no such toxic scum lining anybody's intestinal tract. However, if calorie restriction or a fast results inadvertently from the effort, perhaps some good comes from it.

--Statin drug alternatives--The unprecedented $27 billion dollar a year success of the statin drug industry, accompanied by the enormous marketing push by their manufacturers, has spawned an entire industry of statin alternatives. They range from red yeast rice, to guggulipid, to various concoctions of sterol esters, Chinese herbs, chitosan, and a variety of others. Some actually do reduce cholesterol a few points. Preparations like red yeast rice even pose a side-effect profile not too different from the prescription statin agents. Unfortunately, even among those agents that work, the effects tend to be small to trivial. While I am no lover of statin drugs nor the statin drug industry, I find these preparations to be anemic imitators. You'd be better off with raw nuts and ground flaxseed than wasting your money on these cheap imitations.

--Worries about liver toxicity--A day doesn't go by that I don't have at least several questions about suffering toxic liver effects from niacin, vitamin D, statin drugs, etc. I have treated thousands of patients for heart disease in its various stages and forms and have used many different strategies. How many times have I seen serious liver toxicity? A handful of times and usually from either mis-use of the agent or drug, or in a person with several other coexisting diseases. (Other serious health conditions, like kidney failure, raise the toxicity of drugs and supplements.) Liver toxicity in the vast majority of otherwise healthy people is close to being a non-concern.


Readers of The Heart Scan Blog and of the Track Your Plaque website know that I celebrate expansion of knowledge and information access to the public. However, I am concerned that the flip side of this growing self-empowerment is expanding potential for mistakes. It reminds me of an attorney friend, who, when diagnosed with prostate cancer, explored all manner of alternative treatments, from laetrile to heavy metal chelation to high-dose lycopene tablets. At the initial stage of diagnosis, his cancer was readily treatable. He now has widely metastatic cancer.

Maintain an open mind, but think before you commit to some crazed claim of cure, some "secret" to health, somebody's brazen but concealed attempt at steering profits in their direction.

With freedom comes responsibility. Otherwise, you might be looking for love . . .oops, I mean health . . . in all the wrong places.

Track Your Plaque APB

I'm posting this intriguing comment from the Track Your Plaque Member Forum because I would like to speak to the Member who posted it.

The Member said:

I tested at 965 last year, and while I have followed the TYP diet and nutraceutical recommendations, I was totally unprepared for my first repeat scan (at the same lab/machine) on January 29, 2008. My result was 4.0, and at first I assumed the rating scale had been changed.

I then noted that 3 of the big four arteries received scores of 0, which means the same in any scale, and that four nodules had disappeared from the scan field.



Wow!!

If this is true, it would represent the biggest success in the Track Your Plaque program--ever! It would be an incredible story to tell, to convince the public and medical community that it is indeed possible, and a cause for popping a bottle of champagne! It would also represent what I would regard as essentially a cure for coronary atherosclerosis, a virtual elimination.

While we have plenty of success in stopping the progression or reducing heart scan scores, we do not have 100% success. I wish we did. The Track Your Plaque program is, to some degree, a work in progress. We learn from experiences, continually adjust to obtain the results we desire. Even as it stands today, the Track Your Plaque program is superior to any program of heart disease prevention known--by a long stretch. But it's not infallible, it's not foolproof.

That's all the more reason I would like to communicate with the Track Your Plaque Member who posted this comment. I would also like permission to view the heart scans themselves. (I can't obtain them nor view them without the individual's permission.) While we often have difficulty judging reversal just by looking at heart scans, presumed reversal to this profound degree should be obvious, even to the naked eye.

I would like to know--in detail--precisely what steps were taken and whether there was anything unique about this person's medical history or in the program they followed. This is all in an effort to learn and help others do the same.

If you are the Member who posted this comment, I would like to hear more. Please post your further thoughts on the Track Your Plaque Member Forum, or privately through our Contact page . Or e-mail us at contact@cureality.com.

Biscuits and Gravy



Biscuits and gravy: the ultimate comfort food . . . one you thought you’d never have again!

The familiar dish of breakfast and holiday meals is recreated here with a delicious gravy that you can pour over piping hot biscuits. Because it contains no wheat or other unhealthy thickeners like cornstarch made with “junk” carbohydrates, there should be no blood sugar or insulin problems with this dish, nor joint pain, edema, acid reflux, mind “fog,” or dandruff—life is good without wheat!

While the gravy is also dairy-free for those with dairy intolerances, the biscuits are not, as there are cheese and butter in the biscuits, both of which are optional, e.g., leave out the cheese and replace butter with coconut or other oil.

Makes 10 biscuits

Gravy:
2 tablespoons extra-virgin olive oil
1 pound loose sausage meat
2½ cups beef broth
¼ cup coconut flour
½ cup coconut milk (canned variety)
1 tablespoon onion powder
1 teaspoon garlic powder
½ teaspoon sea salt
Dash ground black pepper

Biscuits:
1 cup shredded cheddar (or other) cheese
2 cups almond meal/flour
¼ cup coconut flour
¾ teaspoon baking soda
½ teaspoon sea salt
2 large eggs
4 ounces butter, melted (or other oil, e.g., extra-light olive, coconut, walnut)

To make gravy:
In large skillet, heat oil over medium heat. Sauté sausage, breaking up as it browns. Cook until thoroughly cooked and no longer pink.

Turn heat up to medium to high and pour in beef broth. Heat just short of boiling, then turn down to low heat. Stir in coconut flour, little by little, over 3-5 minutes; stop adding when gravy obtains desired thickness. Pour in coconut milk and stir in well. Add onion powder, garlic powder, salt, and pepper and simmer over low heat for 5 minutes. Add additional salt and pepper to taste. Remove from heat and set aside.

To make biscuits:
Preheat oven to 325° F.

In food chopper or processor, pulse shredded cheese to finer, granular consistency.

Pour cheese into large bowl, then add almond meal, coconut flour, baking soda, and salt and mix thoroughly. Add the eggs and butter or oil and mix thoroughly to yield thick dough.

Spoon out dough into 10 or so ¾-inch thick mounds onto a parchment paper-lined baking pan. Bake for 20 minutes or until lightly browned and toothpick withdraws dry.

Ladle gravy onto biscuits just before serving.

The Perfect Carnivore

People who carry the gene for lipoprotein(a), Lp(a), tend to be:

--Intelligent--The bell curve of IQ is shifted rightward by a substantial margin.
--Athletic--With unusual capacity for long-endurance effort, thus the many marathoners, triathletes, and long-distance bikers with Lp(a).
--Tolerant to dehydration
--Tolerant to starvation
--Resistant to tropical infections

In other words, people with Lp(a) have an evolutionary survival advantage. More than other people, they make clever, capable hunters who can run for hours to chase down prey, not requiring food or water, and less likely to succumb to the infections of the wild. In a primitive setting, people with Lp(a) are survivors. Evolution has likely served to select Lp(a) people for their superior survival characteristics.

But wait a minute: Isn't Lp(a) a risk for heart attack and stroke? Don't we call Lp(a) "the most aggressive known cause for heart disease and stroke that nobody gives a damn about"?

Yes. So what allows this evolutionary advantage for survival to become a survival disadvantage?

Carbohydrates, especially those from grains and sugars. Let me explain.

More so than other people, Lp(a) people express the small LDL pattern readily when they consume carbohydrates such as those from "healthy whole grains." Recall that the gene for Lp(a) is really the gene for apoprotein(a), the protein that, once produced by the liver and released into the bloodstream, binds to an available LDL particle to create the combination Lp(a) molecule. If the LDL particle component of Lp(a) is small, it confers greater atherogenicity (greater plaque-causing potential). Thus, carbohydrate consumption makes Lp(a) a more aggressive cause for atherosclerotic plaque. The situation can be made worse by exposure to vegetable oils, such as those from sunflower or corn, which increases production of apo(a).

Also, more than other people, Lp(a) people tend to show diabetic tendencies with consumption of carbohydrates. Eat "healthy whole grains," for instance, or if a marathoner carb-loads, he/she will show diabetic-range blood sugars. I have seen long-distance runners or triathletes, for instance, have a 6 ounce container of sugary yogurt and have blood sugars of 200 mg/dl or higher. The extreme exercise provides no protection from the diabetic potential.

Because carbohydrates are so destructive to the Lp(a) type, it means that people with this pattern do best by 1) absolutely minimizing exposure to carbohydrates and vegetable oils, ideally grain-free and sugar-free, and 2) rely on a diet rich in fats and proteins.

The perfect diet for the Lp(a) type? It would be a diet of feasting on the spoils of the hunt, devouring the wild boar captured and slaughtered and eating the snout, hindquarters, spleen, kidneys, heart, and bone marrow, then eating mushrooms, leaves, nuts, coconut, berries, small rodents, reptiles, fish, birds, and insects when the hunt is unproductive.

Capable hunter, survivor, consumer of muscle and organ meats: I call people with Lp(a) "The Perfect Carnivores."

Track Your Plaque in the news

The NPR Health Blog contacted me, as they were interested in learning more about health strategies and tools that are being used by individuals without their doctors. The Track Your Plaque website and program came up in their quest, as it is the only program available for self-empowerment in heart disease.

Several Track Your Plaque Members spoke up to add their insights. The full text of the article can be viewed here.

How's Your Cholesterol? The Crowd Wants To Know
Mainstream medicine isn't in favor of self-analysis, or seeking advice from non-professionals, of course. And anyone who does so is running a risk.

But there are folks who want to change the course of their heart health with a combination of professional and peer support. Some are bent on tackling the plaque that forms in arteries that can lead to heart disease. They gather online at Track Your Plaque, or "TYP" to the initiates.

"We test, test, test ... and basically experiment on ourselves and have through trial and error came up with the TYP program, which is tailored to the individual," Patrick Theut, a veteran of the site who tells Shots he has watched his plaque slow, stop and regress.

The site was created in 2004 by Bill Davis, a preventive cardiologist in Milwaukee, Wisc. Davis is also the author of Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health, which argues that wheat is addictive and bad for most people's health. Davis recommends eliminating wheat from the diet to most new members of Track Your Plaque.

"The heart is one of the hardest things to self-manage but when you let people take the reins of control, you get far better results and far fewer catastrophes like heart attacks," Davis tells Shots.

Doctors typically give patients diagnosed with heart disease two options: take cholesterol-lowering statin drugs, or make lifestyle changes, like diet. It's usually far easier for both parties — the doctor and the patient — to go with the drugs than manage the much more difficult lifestyle changes, Davis says.

"Doctors say take the Lipitor, cut the fat and call me if you have chest pain," he explains. "But that's an awful way to manage care."

TYP has members submit their scores from heart CT scans, cholesterol values, lipoproteins and other heart health factors to a panel of doctors, nutritionists and exercise specialists. Then they receive advice in the form of an individualized plaque-control program. But the online forum, where users share their results with other members and exchange tips, is where most of the TYP action happens.

The community currently has about 2,400 members who pay $39.95 for a quarterly membership, or $89.75 for a yearly membership. Davis says all proceeds go towards maintaining the website.

Ilaine Upton is a 60-year-old bankruptcy lawyer from Fairfax, Va., and a TYP member. At a friend's suggestion, Upton decided to get a heart CT scan in July. Her score was higher than it should have been (22 instead of 0), so she decided to get her blood lipids and cholesterol tested, too, and sent a sample off to MyMedLabs.com.

She learned that her LDL particle count was over 2,000 ("crazy high," she says), and she posted her results on TYP. Davis advised her that a low-carb diet would reduce it, so she decided to try it.

Since July, she says she has had "excellent results" with the program, and her LDL counts are coming down.

"It would be nice to have a [personal] physician involved in this, but [my insurer] Blue Cross won't pay if you are not symptomatic, and I am trying to prevent becoming symptomatic," says Upton. "I feel very empowered by this knowledge and the ability to take better control of my health by getting feedback on the decisions I make."

Pecan Streusel Coffee Cake


This is about as decadent as it gets around here!

Here’s a recreation of an old-fashioned coffee cake, a version with a delicious chewy-crunchy streusel topping.

I’ve specified xylitol as the sweetener in the topping, as it is the most compatible sweetener for the streusel “crumb” effect and browning.

Variations are easy. For example, for an apple pecan coffee cake, add a layer of finely-chopped or sliced apples to the cake batter and topping.

Additional potential carbohydrate exposure comes from the garbanzo bean flour and molasses. However, distributed into 10 slices, each slice provides 7.2 grams “net” carbs (total carbs minus fiber), a perfectly tolerable amount. Be careful not to exceed two slices!

Yield 10 slices

Cake:
2½ cups almond flour
½ cup garbanzo bean flour
1 tablespoon ground cinnamon
1 teaspoon baking soda
Sweetener equivalent to ¾ cup sugar
Dash sea salt

3 eggs separated
3/8 teaspoon cream of tartar
1 tablespoon vanilla extract
4 ounces butter, melted
Juice of ½ lemon

Topping:
½ cup almond flour
¼ cup pecans, finely chopped
1 tablespoon ground cinnamon
½ cup xylitol
1 tablespoon molasses
6 ounces butter, cut into ½-inch widths, at room temperature

Preheat oven to 325º F. Grease bread pan.

In bowl, combine almond flour, garbanzo flour, cinnamon, baking soda, sweetener, salt, and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low speed, blend in egg yolks, vanilla, melted butter, and lemon juice.

Pour liquid mixture into almond mixture and mix thoroughly. Pour into microwave-safe bread pan and microwave on high for 3 minutes. Remove and set aside.

To make topping, combine almond flour, pecans, cinnamon, xylitol, and molasses in small bowl and mix. Mix in butter

Spread topping on cake. Bake for 20 minutes or until toothpick withdraws dry.

Recipe: Peanut Butter and Jelly Macaroons



If you miss peanut butter and jelly sandwiches, you’re going to absolutely love these peanut butter and jelly macaroons!

Not everybody loves the taste or texture of coconut. This issue is solved by the first step: toasting shredded coconut, then reducing them down to a granular consistency. This yields a macaroon consistency without the dominant coconut taste, replaced instead with the flavors of PB & J.

I’ve specified liquid stevia as the sweetener, but this is easily replaced by your choice of sweetener. Note that, regardless of which sweetener used, they vary in sweetness from brand to brand and the quantity required to equal the ½ cup of sugar equivalent can vary. It always helps to taste your batter and adjust sweetness.

Also, I used Swerve in this recipe, the erythritol-inulin mix that enhances texture, but its use is optional.

As written, each macaroon contains just over 3 grams “net” carbohydrates (total carbs minus fiber), meaning you can have several before doing any damage!

Makes 24 macaroons

3 cups shredded unsweetened coconut
2 tablespoons vanilla extract
1 teaspoon almond extract
¼ cup coconut flour
¼ cup dried unsweetened cherries (or other unsweetened berries)
2 tablespoons coconut oil
¼ cup natural peanut butter, room temperature
2 egg whites
½ teaspoon liquid stevia or sweetener equivalent to ½ cup sugar
2 tablespoons Swerve


Preheat oven to 300° F.

In large bowl, combine coconut, vanilla and almond extracts, and mix.

Spread mixture on baking sheet and bake for 10 minutes, stirring occasionally, until very lightly browned. Be careful not to burn. Remove and cool. (Leave oven at 300° F.)

When cooled, using food chopper, food processor, or coffee grinder, pulse coconut mixture until coconut reduced to consistency of coffee grounds. Pour back into bowl. Stir in coconut flour.

Place cherries or other berries in food chopper, food processor, or coffee grinder and pulse until reduced to small granules or paste. Remove with spatula and add to coconut mixture. Set aside.

Place egg whites in bowl and whip until frothy and stiff peaks form.

In small microwave-safe bowl, combine coconut oil and peanut butter and microwave in 10-second increments until warm (not hot) liquid. Stir in egg whites, followed by stevia and Swerve, and blend thoroughly.

Dispense dough onto a parchment paper-lined baking sheet using a 1 ½-inch cookie scooper or spoons.

Bake for 15 minutes or until lightly browned.

I Wish I Had Lipoprotein(a)!

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.

What WERE they thinking

When the Dietary Guidelines for Americans were drafted and the USDA and U.S. Department of Health and Human Services charged with disseminating this information to us . . .

When the American Heart Association created its Total Lifestyle Change (TLC) diet to reduce cardiovascular risk and reduce cholesterol . . .

When the American Diabetes Association developed its diet to help diabetics manage their blood sugars and prevent hypoglycemia . . .


How did conditions like Familial Hypertriglyceridemia fit into this scheme?

Green Tea Ginger Orange Bread

How about all the health benefits of green tea in wheat-free bread form, spiced up with the magical combined flavors of ginger and orange?

Frequent consumption of green tea accelerates loss of visceral (“wheat belly”) fat, increases HDL and reduces triglycerides, reduces blood pressure, and may provide cardiovascular benefits that go beyond these markers such as reduction of oxidative stress. In this Green Tea Ginger Orange Bread, we don’t just drink the tea—we eat it! This provides an even more powerful dose of the green tea catechins believed to be responsible for the health benefits of green tea.

You can grind your own green tea from dried bulk leaves or it can be purchased pre-ground. I’ve used sencha and matcha green tea varieties with good results. The Teavana tea store sells a Sencha preground green tea that works well. If starting with bulk tea leaves, pulse in your food chopper, food processor, or coffee grinder (cleaned thoroughly first!) to generate green tea powder. You will need only a bit, as a little goes a long way.

The entire loaf contains 26 grams “net” carbohydrates; if cut into 10 slices, each slice therefore yields 2.6 grams net carbs, a perfectly tolerable amount.


Bread:
1¼ cup almond meal/flour
½ cup coconut flour
2 tablespoons ground golden flaxseed
1 teaspoon baking powder
Sweetener equivalent to 1 cup sugar
1 tablespoon ground green tea
1½ teaspoons ground ginger
1½ teaspoons ground allspice
1½ ground cinnamon
2 large eggs, separated
¼ teaspoon cream of tartar
1 tablespoon vanilla extract
1 teaspoon almond extract
Grated zest from 1 orange + 2 tablespoons squeezed juice
1/2 cup coconut milk

Frosting:
4 ounces cream cheese, room temperature
1 teaspoon fresh lemon juice
Sweetener equivalent to 1 tablespoon sugar

Preheat oven to 350° F. Grease a 9” x 5” bread pan.

In large bowl, combine almond meal/flour, coconut flour, flaxseed, baking powder, sweetener, green tea, ginger, allspice, and cinnamon and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low mixer speed, blend in egg yolks, vanilla extract, almond extract, orange zest and juice, and coconut milk.

Pour egg mixture into almond meal/flour mixture and mix by hand thoroughly.

Pour dough into bread pan and place in oven. Bake for 40 minutes or until toothpick withdraws dry. Remove and cool.

For frosting, combine cream cheese, lemon juice, and sweetener and mix. When cooled, spread frosting over top of bread.

Chocolate Bomb Bars

These healthy bars will blast you with chocolate from several directions!

Look for cacao nibs in health food stores, Whole Foods Market, or at nuts.com. If unavailable, the bars are still delicious without them.



These bars contain around 4-5 grams "net" carbs per bar, well within the tolerance for most people.

Yields approximately 10 bars

1 cup ground almonds
2 tablespoons coconut flour
1 tablespoon unsweetened cocoa powder
1/2 cup cacao nibs
1/2 cup unsweetened shredded coconut
2 ounces 85-90% cocoa chocolate, finely chopped
3/4 cup raw pumpkin or sunflower seeds
Sweetener equivalent to 3/4 cup sugar
2 tablespoons almond butter
1/4 cup coconut milk
2 tablespoons coconut oil or cocoa butter (food grade)

Preheat oven to 200 degrees F. Lay sheet of parchment paper on large baking pan.

In large bowl, combine ground almonds, coconut flour, cocoa powder, cacao nibs, coconut, chocolate bits, pumpkin seeds, and sweetener (if dry) and mix.

In microwave-safe bowl or in small sauce pan, add almond butter, coconut milk, and coconut oil and sweetener (if liquid) and heat for 15 second increments in microwave until liquid, but not hot. If using stove, heat at low-heat enough to make liquid easily mixed, but not hot.

Pour liquid into dry almond mixture and mix together thoroughly. If too stiff, add water one tablespoon at at time until the consistency of thick dough.

Spoon out approximately 1 1/2-inch balls, shaping with the spoon and/or your hands into bar shapes.

Bake for 35 minutes. Remove and cool.

An iodine primer

What if your diet is perfect--no wheat, no junk carbohydrates like that from corn or sugars, you are physically active--yet you fail to lose weight? Or you hit a plateau after an initial loss?

First think iodine.

Iodine is an essential nutrient. It is no more optional than, say, celebrating your wedding anniversary or obtaining vitamin C. If you forget to do something nice for your wife on your wedding anniversary, I would fear for your life. If you develop open sores all over your body and your joints fall apart, you could undergo extensive plastic surgery reconstruction and joint replacement . . . or you could just treat the scurvy causing it from lack of vitamin C.

Likewise iodine: If you have an iodine deficiency, you experience lower thyroid hormone production, since T3 and T4 thyroid hormones require iodine (the "3" and "4" refer to the number of iodine atoms per thyroid hormone molecule). This leads to lower energy (since the thyroid controls metabolic rate), cold hands and feet (since the thyroid is thermoregulatory, i.e., temperature regulating), and failed weight loss. So iodine deficiency is one of the items on the list of issues to consider if you eliminate wheat with its appetite-stimulating opiate, gliadin, and high-glycemic carbohydrate, amylopectin A, and limit other carbohydrates, yet still fail to lose weight. A perfect diet will not fully overcome the metabolism-limiting effects of an underactive thyroid.

Given sufficient time, an enlarged thyroid gland, or goiter, develops, signaling longstanding iodine deficiency. (The treatment? Iodine, of course, not thyroid removal, as many endocrinologists advocate.) Your risk for heart attack, by the way, in the presence of a goiter is increased several-fold. Goiters are becoming increasingly common and I see several each week in my office.

Iodine is found in the ocean and thereby anything that comes from the ocean, such as seafood and seaweed. Iodine also leaches into the soil but only does so coastally. It means that crops and livestock grown along the coasts have some quantity of iodine. Humans hunting and foraging along the coast will be sufficient in iodine, while populations migrating inland will not.

It also means that foods grown inland do not have iodine. This odd distribution for us land dwelling primates means that goiters are exceptionally common unless iodine is supplemented. Up to 25% of the population can develop goiters without iodine supplementation, a larger percentage experiencing lesser degrees of iodine deficiency without goiter.

In 1924, the FDA became aware of the studies that linked goiters to lack of iodine, reversed with iodine supplementation. That's why they passed a regulation encouraging salt manufacturers to add iodine, thought to be an easy and effective means for an uneducated, rural populace to obtain this essential nutrient. Their message: "Use more iodized salt. Keep your family goiter free!" That was actually the slogan on the Morton's iodized salt label, too.

It worked. The rampant goiters of the first half of the 20th century disappeared. Iodized salt was declared an incredible public health success story. Use more salt, use more salt.

You know the rest. Overuse of salt led to other issues, such as hypertension in genetically susceptible people, water retention, and other conditions of sodium overexposure. The FDA then advises Americans to slash their intake of sodium and salt . . . but make no mention of iodine.

So what recurs? Iodine deficiency and goiters. Sure, you eat seafood once or twice per week, maybe even have the nori (sheet seaweed) on your sushi once in a while . . . but that won't do it for most. Maybe you even sneak some iodized salt into your diet, but occasional use is insufficient, especially since the canister of iodized salt only contains iodine for around 4 weeks, given iodine's volatile nature. (Iodized salt did work when everybody in the house salted their food liberally and Mom had to buy a new canister every few weeks.)

Iodine deficiency is common and increasing in prevalence, given the widespread avoidance of iodized salt. So what happens when you become iodine deficient? Here's a partial list:

--Weight loss is stalled or you gain weight despite your efforts.
--Heart disease risk is escalated
--Total and LDL cholesterol and triglyceride values increase
--Risk of fibrocystic breast disease and possibly breast cancer increase (breast tissue concentrates iodine)
--Gingivitis and poor oral health increase (salivary glands concentrate iodine)

(Naturopathic doctor Lyn Patrick, ND, has written a very nice summary available here.)

So how do you ensure that you obtain sufficient iodine every day? You could, of course, eat something from the ocean every day, such as coastal populations such as the Japanese do. Or you could take an inexpensive iodine supplement. You can get iodine in a multivitamin, multimineral, or iodine drops, tablets, or capsules.

What is the dose? Here's where we get very iffy. We know that the Recommended Daily Allowance (RDA), the intake to not have a goiter, is 150 mcg per day for adults (220 mcg for pregnant females, 290 mcg for lactating females). Most supplements therefore contain this quantity.

But what if our question is what is the quantity of iodine required for ideal thyroid function and overall health? Ah, that's where the data are sketchy. We know, for instance, that the Japanese obtain somewhere between 3,500 and 13,000 mcg per day (varying widely due to different habits and locations). Are they healthier than us? Yes, quite a bit healthier, though there may be other effects to account for this, such as a culture of less sweet foods and more salty, less wheat consumption, etc. There are advocates in the U.S., such as Dr. David Brownstein in Michigan, who argues that some people benefit by taking doses in the 30,000 to 50,000 mcg per day range (monitored with urinary iodine levels).

As is often the case with nutrients, we lack data to help us decide where the truly ideal level of intake lies. So I have been using and advocating intakes of 500 to 1000 mcg per day from iodine capsules, tablets, or drops. A very easy way to get this dose of iodine is in the form of kelp tablets, i.e., dried seaweed, essentially mimicking the natural means of intake that also provides iodine in all its varied forms (iodide, sodium iodate, potassium iodide, potassium iodate, iodinated proteins, etc.) This has worked out well with no ill effects.

The only concern with iodine is in people with Hashimoto's thyroiditis or (rarely) an overactive thyroid nodule. Anyone with these conditions should only undertake iodine replacement carefully and under supervision (monitoring thyroid hormone levels).

Iodine is inexpensive, safe, and essential to health and weight management. If it were a drug, it would enjoy repeated expensive marketing and a price tag around $150 per month. But it is an essential nutrient that enjoys none of the attention-getting advantages of drugs, and therefore is unlikely to be mentioned by your doctor, yet carries great advantage for helping to maintain overall health.

Kitchen sink approach for Lp(a)


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

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

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

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

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

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

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

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

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

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

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

Making Dr. Friedewald an honest man

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

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

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

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

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

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

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

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

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

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

Some basic vitamin D issues

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

Anne said:

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

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


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

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


Twinb asked:

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

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


Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

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


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

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


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

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

“How much vitamin D should I take?”

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

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

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

Utter nonsense.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

You probably don't take enough fish oil

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:


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

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

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

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

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

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



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

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

But what dose is sufficient? What dose is ideal?

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

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

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

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

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

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

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

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

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

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

Vitamin D and HDL

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

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

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies


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

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

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

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

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

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

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

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

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

Why? How?

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

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

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

Weight loss and blood pressure

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.

(Lack of ) Quality of nutritional supplements

In my last post, I blogged about how we must not confuse marketing with truth. They are often two different things.

A patient I saw today was absolutely convinced that his fish oil was the best available in the world: purer, uncontaminated by mercury or pesticides--"not like that other crap on the shelves." I asked him how he knew this. "They say so," he proudly declared.

Do you recognize this? He fell for the marketing. While there may be some truth in the manufacturer's claims, you can't believe it from the mouth of the manufacturer. True judgements about quality and purity have to come from an independent source like Consumer Reports, Consumer Lab, or the FDA.

But the FDA doesn't regulate the quality and purity of nutritional supplements. On the positive side, this has allowed supplement manufacturers to keep costs down, not having to navigate arcane and complex regulatory restrictions.

On the negative side, a fair number of supplement manufacturers get away with 1) producing supplements that fail to contain the stated amounts of ingredients, occasionally containing none of the essential ingredient(s), 2) contain contaminants like lead, and 3) make extravagant and often unfounded claims like "superior", "more effective", and "purer". (DHEA, for instance, is a particular landmine of poor quality. I recently suggested that a patient take DHEA; despite consistently taking 50 mg of a specific brand for several months, the blood level of DHEA-S didn't budge one bit--there was likely little or none in the capsule.)

The Fanatic Cook at http://fanaticcook.blogspot.com has posted some very insightful discussions on this issue and the proposed FDA regulations of supplements. They're worth perusing.

I really wish regulation weren't necessary and that the industry could have policed itself. But it clearly has failed and perhaps federal oversight is not such a bad thing, as long as the FDA regulations restrict themselves to oversight over quality and purity and not to efficacy. It's the efficacy regulation that could hogtie innovation in supplement development.

Marketing and truth are not the same

I often remind people: Don't confuse marketing with the truth.

Today, I spent a total of probably an hour and a half dissuading patients that some crazed piece of marketing trying to sell them something was not the same as truth.

I spent approximately 40 minutes alone with a woman who was absolutely convinced that:

--Nattokinase would cure her of all heart disease. It does not. Despite the promising health benefits of natto and vitamin K2 supplementation, nattokinase is a scam with no basis in science nor logic.

--Niacin destroys your liver and homeopathic remedies are superior. Quite simply, homeopathy = quackery. No rational thinking scientist endorses the utter nonsense practiced in this strange and outrageous set of practices that requires you to suspend all reason.

--Sufficient vitamin D is obtainable through a "potent" multivitamin. I know of no multivitamin preparation that even begins to provide the dose of vitamin D that is actually required by adults, nor is it absorbed since these D preparations are powder based.

--Fish oil will poison you with mercury. Accordingly, one brand of fish oil claims to be the only safe form. Those of you following these posts, or the reports of the USDA and FDA, as well as the reports of Consumer Reports and Consumer Lab (www.consumerlab.com) know that, unlike fish itself, there is no mercury in fish oil capsules.

--All coronary atherosclerotic heart disease is caused by heavy metal poisoning. Thus chelation with EDTA represents a cure for heart disease.


People are inundated with marketing that promise extravagant cures, remove need for any medication, make you smarter, sexier, thinner, and on and on.

If you see a TV ad for Ford that says they make the best cars in the U.S., do you immediately run out and put a For Sale sign on your GM car and buy a Ford? No, of course not. You recognize the ad for what it is: marketing. It may be true, but a TV commercial is not enough to convince you.

Then why would an ad promising extraordinary cures for cancer or heart disease convince you that this is true? It should not. Marketing ads should only serve to alert you to the possibility of value or benefit, but should never-- never--stand alone as proof. Take marketing for what it is: marketing of a product or service, not a scientific report, not a factual report, not news.

Marketing is advertising. Period.

More on erectile dysfunction

Several facts on erectile dysfunction and coronary plaque:


If you have erectile dysfunction, there's at least a 50% chance you also have coronary plaque.

If you have coronary plaque by a CT heart scan, there's a 50% chance you have erectile dysfunction.

If you have symptomatic coronary disease (chest pains, breathlessness, prior heart attack), there's a 90% chance you also have erectile dysfunction.


Coronary disease is characterized by a dysfunctional state of the "endothelium", or inner lining of the coronary arteries. Erectile dysfunction is characterized by dysfunction of the endothelium of the penile circulation. Same phenomenon, different territories. (There are other differences, of course, but the two conditions share this fundamental phenomenon.)


If you have any doubts about the physiologic effects of the supplement, l-arginine, just give it a try if you have erectile dysfunction. The erection enhancing effects alone should convince you that a genuine artery-dilating effect is exerted by this very powerful nutritional supplement.

If l-arginine fails by itself to restore full erectile capacity, there are additional strategies, both nutritional and medical, that you can consider.

Our newest Track Your Plaque Special Report on erectile dysfunction is coming out any day now.

High LDL cholesterol--only

As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?

In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.

Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation.

Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque.

Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits.

In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life.

Heart disease = statin deficiency

Judging from the conversations I hear from colleagues, what I hear from the media, and drug company advertising, you'd think that heart disease has one cause--a deficiency of statin drugs.

As their thinking goes, if you have coronary disease, you need a statin drug (Lipitor, Zocor, Crestor, pravachol, etc.). If you have progressive coronary disease, you need more statin drug. If you have a heart attack while on a statin drug, you need even more statin drug.

Some "experts" have even proposed that we do away with LDL cholesterol and we just give everybody a statin drug at high doses.

Does this make any sense to you?

Doesn't it make better sense that if someone has progressive heart disease or heart attack while on a statin drug, then target the other causes largely unaffected by a statin drug? Perhaps if LDL cholesterol remains high on the statin drug, then a higher dose is justified. But more often than not, it's not a high LDL on statin drugs that responsible, it's other causes. And there's many of them: low HDL, VLDL, IDL, Lp(a), deficiency of omega-3 fatty acids, inflammatory processes, vitamin D deficiency, among others. (An important exception to this is when the conventional calculated LDL substantially underestimates true LDL as measured by LDL particle number by NMR, apoprotein B, or 'direct' LDL.)

Imagine someone has pneumonia. After 2 weeks of antibiotics, they are only partly better. The solution: a higher dose of the same antibiotic--but never question if it was the right antibiotic in the first place. That's what is going on in heart disease.

The doctors have been brainwashed into believing this $22 billion dollar per year bit of propaganda. The drug companies actively try to recruit the public into believing the same. Don't fall for it.

The statin drugs do indeed have a role. But they are not the complete answer. More of the same when disease progresses makes no sense at all.

Fish oil and mercury

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, 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.

How much omega-3s are enough?

The basic dose we advocate for the Track Your Plaque program is 1200 mg per day of EPA + DHA, the essential omega-3 fatty acids.

1200 mg EPA+DHA is generally obtainable by taking 4 capsules of 1000 mg of fish oil, since the majority of preparations contain 180 mg EPA and 120 mg DHA per capsule.

But how will you know if a higher dose wouldn't be even better?

The principal parameter to look at is triglycerides. If triglycerides remain above 60 mg/dl, we usually consider increasing fish oil.

Another measure that's very important is intermediate-density lipoprotein, or IDL, also called "remnant lipoproteins" on a VAP panel. Persistence of any IDL or remnant lipoproteins is reason to consider more fish oil. Most commonly, if there is some persistence of either, we increase fish oil to 6000 mg per day of a standard preparation, or 1800 mg/day of EPA+DHA.

The only time we see persistence of IDL or remnant lipoproteins with this higher dose is when triglycerides are really high. If starting triglycerides are, for instance, 500 mg/dl, then even this higher dose may be insufficient. This is when more highly concentrated preparations of fish oil may be necessary, occasionally even the prescription form, Omacor. (We currently use Omacor only when high doses of EPA+DHA are required, most because of its outrageous cost. Two capsules per day costs around $120 per month; three capsules per day to provide 1800 mg/day of EPA+DHA costs $180 per month. I think this is outrageous and so we use it only when absolutely necessary.)

You might even argue that a higher dose of 1800 mg EPA+DHA, or 6000 mg of a standard capsule, might be preferable for more assured reduction of heart attack risk--even when triglycerides and IDL are perfectly under control. I wouldn't argue with you. But you won't observe any measurable feedback that tells you that a heightened effect is being obtained. I take that dose myself, in fact, despite the fact that elimination of wheat products and weight loss was sufficient to drop my triglycerides to the target level. I figure it's a small additional effort for added peace of mind.

Repentance for past sins

If you are new to the Track Your Plaque program and would like to jump start your effort, or if you are struggling with losing weight and excess weight is a part of the situation that created your CT heart scan score, then don't forget about fasting.

Fasting is the cessation of eating. However, recall from the Track Your Plaque Special Report, Fasting: Fast Track to Control Plaque at http://www.cureality.com/library/fl_04-012fasting.asp, there are many variations on fasting that permit some intake of healthy foods. (Thus, they are not, in the strict sense, "fasting". Accurate or no, there are variations that may be more palatable or do-able in the real world by real people.)

My personal favorite method to fast is to use a low-sugar, low-fat soy milk such as Light Silk, available at most major grocery stores. This high-protein, low-fat, low-sugar soy milk takes the edge off hunger and provides a minimal quantity of calories. A minimum of 72 hours is required for substantial results. (My one reservation about this brand of soy milk is that the Fanatic Cook claims that the manufacturer, Dean Foods, is a factory farm operation that abuses livestock--a discussion for another day.)

Fasting yields more than weight loss. It refreshes your appreciation for food. It reawakens you to the amount and quality of food you've been putting in your body. Fasting also allows you to recognize just how bad you might feel from the diet you were eating.

You also emerge from a fast with a reduced appetite and a renewed sense of appreciation for food. It makes the discipline of healthy eating a lot easier when you break your fast.

I tell people that fasting is not punishment. It is a form of enlightenment, of re-experiencing food and life. Fasting allows you to "catch up" on all the indiscretions you've been guilty of over the years.

It also provides enormous advantage in gaining control over coronary plaque.

A fanatic for Fanatic Cook

If you haven't already done so, I'd urge you to peruse the wonderfully insightful, sophisticated, and biting commentary provided by the Fanatic Cook Blog at http://fanaticcook.blogspot.com.

She (I assume it's a she) has been discussing the proposed Safe Food Act recently, an effort to address all the dangers in foods that have come to attention lately, like melamine in pet food and E. coli in bagged spinach. Her most recent post is:

Nebraska Farm Bureau Thinks Food Safety Act Bad Idea, the latest in a series of posts exploring this issue.

I'd like to know who the Fanatic Cook is, or "Bix" as she calls herself. (I assume it's a "she" but I don't really know that for a fact.) I've corresponded with her and she prefers to remain anonymous for unspecified reasons. I'd like to know who this person is both for a more secure sense of credibility, as well as I'd simply like to know who can write so intelligently and why. I suspect that she's a professional nutrition scientist or something along those lines, since the level of insight into many scientific issues is quite impressive. Her Blogs will make great material for a book, if compiled and organized. Watch out for this one.

Erectile dysfunction and coronary plaque

Erectile dysfunction (ED), previously known as "impotence," and coronary atherosclerotic plaque go hand in hand.

A recent study in men with advanced coronary disease showed that 93% experienced ED. The participants in the Track Your Plaque program, for the most part, do not have advanced coronary atherosclerosis, but have an earlier form detected by a CT heart scan.

What proportion of men with asymptomatic coronary plaque as measured by a CT heart scan have ED? Around 50%. In other words, it's not a rare occurrence.

The conversation about ED (and even its renaming from impotence) really gained momentum with the development of ED-drugs like Viagra and Cialis. The drugs are reasonably effective and safe. However, you will hear little about all the strategies that can either precede your need for these drugs and/or enhance your response to these drugs if the response is partial. That part of the conversation, of course, doesn't yield loads of drug company revenues.

One of the most helpful and specific nutritional supplements available that can partially restore the nitric oxide-deficiency of ED is l-arginine. L-arginine is the body's source of nitric oxide (NO), the master dilator (relaxing agent) for all arteries of the body. NO dilates penile arteries, it dilates coronary arteries. Lack of NO disables the penile capacity for erection and encourages growth of coronary atherosclerotic plaque. Track Your Plaque Members are already familiar with l-arginine as a facilitator of coronary plaque regression.

We will detail the supplements that you can use safely in your Track Your Plaque program to both enhance erectile function if you suffer ED, as well as impact positively on coronary health, in an upcoming and detailed Special Report on the www.cureality.com website.

The Big Squeeze

Some colleagues of mine brought this scary phenomenon to my attention last evening.

As insurance and Medicare reimbursement to doctors and hospitals fall (Medicare is enacting a series of substantial cuts, which will be followed by the private health insurers), you would expect the use of hospital procedures to drop. Makes sense, right? Less money paid per procedure, less incentive to do them.

Unfortunately, that's not how it's playing out in the real world. Your neighborhood interventional cardiologist or cardiothoracic surgeon is accustomed to a level of income and lifestyle. That lifestyle is now threatened by shrinking reimbursement. True to the Law of Unintended Consequences, rather than reducing use of procedures, diminishing procedural fees are prompting a good number of practitioners to do more.

In other words, if each heart catheterization pays less, why not do more of them, along with more stents, pacemakers, defibrillators, and the like? If four heart catheterizations per day pays less, why not do five to make up the difference?

Voila! Income protected. Of course, it comes at the cost of more work. But I will give one thing to my colleageus: They are a generally hard-working bunch who rarely balk at 12-16 hours days in the hospital.

How do you do more procedures? Easy. Just lower the bar on who to do a procedure on. Use more aggressive criteria for pacemaker implantation. Interpret the always-fuzzy nuclear stress tests weighed more towards abnormal. Use scare tactics: "You never know--that chest pain could be the last warning you're going to have!" Because the criteria for performing procedures is "soft" in the real world, it is easy to bend the criteria any way you want.

It's too early to measure the full impact of this unintended consequence of reduced reimbursement. But don't allow yourself to become a casualty in the reimbursement war. Remain vigilant. Recognize that, despite the fuzziness at the edges, there are still rational reasons for performing heart procedures. Always be armed with information and the right questions. Never submit unquestioningly or without satisfactory answers to your questions.

Tim Russert's heart scan score 210. . .in 1998

Despite the media blathering over how Mr. Russert's tragic death from heart attack could not have been predicted, it turns out that he had undergone a heart scan several years ago.

A New York Times article, A Search for Answers in Russert’s Death, reported:

Given the great strides that have been made in preventing and treating heart disease, what explains Tim Russert’s sudden death last week at 58 from a heart attack?

The answer, at least in part, is that although doctors knew that Mr. Russert, the longtime moderator of “Meet the Press” on NBC, had coronary artery disease and were treating him for it, they did not realize how severe the disease was because he did not have chest pain or other telltale symptoms that would have justified the kind of invasive tests needed to make a definitive diagnosis. In that sense, his case was sadly typical: more than 50 percent of all men who die of coronary heart disease have no previous symptoms, the American Heart Association says.

It is not clear whether Mr. Russert’s death could have been prevented. He was doing nearly all he could to lower his risk. He took blood pressure pills and a statin drug to control his cholesterol, he worked out every day on an exercise bike, and he was trying to lose weight, his doctors said on Monday. And still it was not enough.

“What is surprising,” Dr. Newman said, “is that the severity of the anatomical findings would not be predicted from his clinical situation, the absence of symptoms and his performing at a very high level of exercise.”


Buried deeper in this article, the fact that Mr. Russert had a heart scan score of 210 in 1998 is revealed.

That bit of information is damning. Readers of The Heart Scan Blog know that heart scan scores are expected to grow at a rate of 30% per year. This would put Mr. Russert's heart scan score at 2895 in 2008. But the two doctors providing care for Mr. Russert were advising the conventional treatments: prescribing cholesterol drugs, blood pressure medication, managing blood sugar, and doing periodic stress tests.

Conventional efforts usually slow the progression of heart scan scores to 14-24% per year. Let's assume the rate of increase was only 14% per year. That would put Mr. Russert's 2008 score at 779.

A simple calculation from known information in 1998 clearly, obviously, and inarguably predicted his death. Recall that heart scan scores of 1000 or greater are associated with annual--ANNUAL--risk for heart attack and death of 20-25% if no preventive action is taken. The meager prevention efforts taken by Mr. Russert's doctors did indeed reduce risk modestly, but it did not eliminate risk.

We know that growing plaque is active plaque. Active plaque means rupture-prone plaque. Rupture prone plaque means continuing risk for heart attack and death. Heart attack and death means the approach used in Mr. Russert was a miserable failure.

While the press blathers on about how heart disease is a tragedy, as Mr. Russert's doctors squirm under the fear of criticism, the answers have been right here all alone. It sometimes takes a reminder like Mr. Russert's tragic passing to remind us that tracking plaque is a enormously useful, potentially lifesaving approach to coronary heart disease.

Who needs to go next? Matt Lauer, Oprah, Jay Leno, some other media personality? Someone close to you? Can this all happen right beneath the nose of your doctor, even your cardiologist?

I don't need to remind readers of The Heart Scan Blog that heart disease is 1) measurable, 2) trackable, 3) predictable. Mr. Russert's future was clear as long ago as 1998. Every year that passed, his future became clearer and clearer, yet his doctors fumbled miserably.



Copyright 2008 William Davis, MD

Another failure of conventional cardiac care


Though Tim Russert was widely known and respected for his political commentary, he will likely be better remembered as an example of the gross shortcomings of the conventional approach to heart disease.

Let's face it:

Standard heart disease prevention efforts are a miserable failure.

A Track Your Plaque member brought this interview of Mr. Russert's doctor to my attention.

It appears that his doctor did all the correct conventional things. You know what became of it. In the eyes of the public and of any attorney, or even of my colleagues, no wrong was committed. The blame does not lie with Mr. Russert's hapless doctor. The blame lies on the system that endorses procedures, prescription medications, the blind adherence to dogma dictated by the pharmaceutical industry and FDA, along with a prevailing philosophy of preferring the management of catastrophes to preventing them. Dr. Newman's idea of a solution: Making an automatic defibrillator (AED) more widely available (!!!).

How long does this sort of idiocy have to go on? How many people have to die before the system uses the tools that are already available, tools that could have prevented this tragedy and many more like it?

If you and your doctor subscribe to the program that the unfortunate Mr. Russert was prescribed and the brainwashing, unthinking nonsense that his doctor follows, you are a fool. Shame on you. You therefore likely subscribe to the same variety of marketing BS that issues from food manufacturers about Cheerios, whole grains, and low-fat diets.

Get with the program. Sadly, Mr. Russert is not the first, he's not the last. The tragedies of conventional advice that line the pockets of drug and food manufacturers number in the millions. We're not talking about some obscure, rare disease. We're talking about the number one cause of death in both males and females nationwide.

I deeply wish this message could have reached Mr. Russert before his untimely death. We could all look forward to another Sunday morning with his usual incisive, unforgiving probing of the day's political figures.

Tribute to Tim Russert

The sudden passing of news giant, Tim Russert, yesterday of sudden cardiac death struck a blow to American consciousness.

Perhaps his hard-hitting interviewing style, while making guests squirm, made him seem invincible. But, of course, none of us is invincible. We are all vulnerable to this disease.

We should not allow Mr. Russert's tragic death to occur without taking some lessons. The media have already resorted to interviewing prominent doctors for their opinion.


Douglas Zipes, M.D., former President of the American College of Cardiology,was quoted in the media:

"An automated external defibrillator (AED) could have been a life-saver. AEDs should be as common as fire extinguishers."

This is typical sleight-of-hand, medicine-is-too-complex-for-the-public-to-understand sort of rhetoric that is surely to issue from the conventionally-thinking medical people and the press. Instead, let's cut the BS and learn the real lessons from Mr. Russert's needless death.

It is virtually certain that:

--Mr. Russert ruptured an existing coronary atherosclerotic plaque, prompting rhythm instability, or ventricular fibrillation.

--Making automatic external defibrillators (AED) available might have Band-Aided the ventricular fibrillation, but it would not have stopped the heart attack that triggered it.

--Though full details of Mr. Russert's health program have not been made available, it is quite likely that he was prescribed the usual half-witted and barely effective panoply of "prevention": aspirin, statin drug, anti-hypertensive medication. Readers of The Heart Scan Blog and members of Track Your Plaque know that this conventional approach is as effective as aspirin for a fractured hip.

--It is highly unlikely that all causes of Mr. Russert's heart disease had been identified--did he have small LDL (it's certain he did, given his body habitus of generous tummy), Lp(a), low HDL, pre-diabetic patterns, inflammatory abnormalities, vitamin D deficiency, etc.? You can be sure little or none of this had been addressed. Was he even taking simple fish oil that reduces the likelihood of sudden cardiac death by 45%?

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

Far more can be done to prevent future similar deaths among all of us.

Our jobs are to use the tragic death of Mr. Russert to help those around us learn that heart disease is identifiable and preventable. Though Mr. Russert did not stand for BS in his political commentary, he sadly probably received it in his health advice. Don't let this happen to you or those around you.

Why do skinny people get heart disease?

There's no doubt about it: The majority of people with heart disease are overweight. They may not be grotesquely overweight, just a few pounds over. But weight plays a crucial role in activating numerous factors that heighten risk for heart disease.

Excess weight reduces HDL cholesterol, raises triglycerides, increases small LDL (enormously), fans the fires of inflammatory responses (CRP, IL-6, TNF-alpha, etc.) raises blood pressure, increases resistance to insulin and raises blood sugar. Overweight people tend to be less physically active, may develop diseases of obesity like sleep apnea, and on and on. You've heard this all before.

But why do slender people develop heart disease? If we can't blame weight, what is to blame? By slender, I mean body mass index (BMI) of <25. (Yes, I know there are other ways, better ways, to gauge healthy weight. But, for simplicity, I'll use BMI.) Let's put aside the two obvious causes of heart disease, cigarette smoking and Type I diabetes. (I'd be shocked if any cigarette smokers read this blog.)

Slender people develop heart disease because:

1) They have lipoprotein(a)--The big, big neglected risk factor. In fact, the Lp(a) genotype is, in my casual observation, associated with a slender phenotype (genotypic expression). The prototypical example that makes headlines is the marathon runner--slender and superbly fit, but develops heart disease anyway. People wax on about the uncertainties of exercise and fitness when they hear about Jim Fixx and Alberto Salazar. But one factor would explain it all: Lp(a).

2) The murky category of the normal weight obesity. These people are generally recognizable by their flaccid tummies despite falling into a favorable BMI <25. Small LDL is the standout red flag in these people.

3) They were previously overweight but lost it.

4) They were former smokers.

5) Vitamin D deficiency--Deficiency of vitamin D is important for everyone's health. But there appears to be some people for whom it is the dominant risk. I believe that one of our great Track Your Plaque success stories, Neal, falls into this group. Some people who are vitamin D deficient develop colon cancer, others develop diabetes, others develop osteoporosis or multiple sclerosis, while others develop coronary heart disease and plaque. The likely reason for the varied expression is variation in vitamin D receptor genotypes (VDR genotypes).

6) The murkiest of all: Hypertension genotypic variants. This is a poorly sorted-out category, and one principally based on my observations along with scattered observations in such things as variations in the angiotensin converting enzyme genotypes. But I am convinced that there is a small percentage of slender people who show variation in some genetic type that predisposes to hypertension and heart disease. They also show a propensity towards enlargement of the thoracic aorta. This group is also among the most difficult to control in the Track Your Plaque approach, i.e., they have difficulty slowing or stopping the growth of heart scan scores. While blood pressure control in this group is important, it does not seem to remove the excess source of risk.

So, yes, being slender does put you into a lower risk for heart disease category. But it does not mean you are immune.

You can also be an overweight person who still harbors some of the features of the slender--you're an overweight slender person. The above list can still therefore apply.

Cardiology Confidential


Okay, so it's a shameless knockoff of chef Anthony Bourdain's titillating Kitchen Confidential.

But the confidences that I've heard whispered in the corridors of health involve something more provocative than how your food was prepared. Any service for humans performed by other humans is subject to the idiosyncrasies and weaknesses of human behavior. That's just life.

In healthcare for your heart, the consequences can be more profound than eating three day old fish on Monday's dinner menu.

Over my 15 years practicing cardiology in a variety of settings in three different cities, I've witnessed just about everything from shocking to sublime. Some of it speaks to the extraordinary commitment of people in healthcare, the unexpected courage people show in the midst of illness, the devotion of family in difficult times. It can also speak of mewling, sobbing carryings-on over the most minor conditions, the meanness that emerges when people are frightened, the vultures circling just waiting for Grandpa to kick the bucket and leave his will declaring the spoils.

For the most part, my cardiology colleagues are a hard-working bunch committed to . . . Uh oh. I was going to say "Saving lives, preserving health." But that's not true. Once upon a time, it was true for many of my colleagues, often revealed over $2-a-pitcher beer-softened, "we're going to save people" conversations in medical school. Ahhh, medical school. I remember walking along the street alongside my medical school in St. Louis, bursting with pride and a sense of purpose.

But, for many of us, something sours our purpose through the years. Maybe it's the smell of money, maybe it's the series of distasteful experiences that show that healthcare providers are, in the midst of health crises, the innocent recipients of anger, frustration, disappointment.

Whatever the genesis, the stage is set for an imperfect scenario that pits healthcare provider against patient in a less-than-perfect system.

This would read as a mindless rant if it wasn't based on such pervasive and pravalent truths, tales of the flawed deliverers of healthcare driven by motives less lofty than "saving people."

Take Dr. S, a doctor who performs a large number of procedures on patients. I'm told he is very capable. He manages an extraordinary amount of heart work--in between jail time for wife beating and Medicare fraud.

Or Dr. C, well-known in the region for his procedural talents, also. Usually acerbic and freely-swearing, he opens up engagingly when drinking--which is most of the time. Paradoxically, as is true for some serious drinkers, he works more effectively while intoxicated.

Or Dr. ST, who proudly admitted to me one evening over dinner that he has accepted 6-figure payments from medical device companies on a number of occasions to use their products.

Or the manic ups and downs of Dr. J, who refers just about every patient he sees for emergency bypass surgery when in his down phase, mangles coronary arteries in daring angioplasties during his up phase.

How about 310-lb Dr. P, who hounds her patients about indulgent lifestyles? That would be excusable as innocent lack of self-insight if it weren't for her propensity to use heart procedures on patients as punishment. "I have no choice but to take you to the hospital."

Dr. M. manages to maintain the appearance of straight-and-narrow during the day, all the way to attending church twice a week with his children. His daytime persona effectively covers up his frequent visits to prostitutes.


We are ALL flawed. My colleagues are no different. But some circumstances cultivate the flaws, fertilize corruptibility, reward it. Such has become the state of affairs in healthcare for heart disease. Why? Is it the excessive potential for money-making that existed until recently? Is there something about the save-the-day mentality of heart disease that attracts imperfect personalities looking for the adrenaline-charged thrill but morphs over time into near-psychopathic lives?

It's not the end of the world. The fact that my colleagues' behavior has reached such extravagant lows signals a bottom: things are about to change.

In the meantime, let me tell you a few more secrets . . .



Copyright 2008 William Davis, MD

Fanatic Cook on the American Heart Association

The Fanatic Cook has posted a stinging criticism of the American Heart Association (AHA):

American Heart Association My Fat Translator

Beyond the nonsensical nutritional recommendations (e.g., substitute small French fries for large French fries), she lists the major financial contributors to the AHA, a Who's Who in the pharmaceutical and processed food industry.


"For an organization that brought in close to a billion dollars last year, you'd think they could come up with something a little more pronounced. If I was more cynical I'd say the AHA had an interest in keeping Americans fat . . . or at least dependent on a highly-processed, fast food diet, requiring drugs to tweak lab values."

To be sure, the AHA does a great deal of good in funding research and educating the public about the prevalence of heart and vascular disease. But their fund raising interests have clearly subverted the honesty of their nutritional advice. Sadly, it is the AHA dietary advice that hospital dietitians use in counseling people with heart disease after their heart attack, stent, or bypass surgery. After my patients are discharged from the hospital for any reason, I tell them to please forget everything the nice hospital dietitian told them. It is not okay to eat the factory farm-raised hamburger on the sugar-equivalent enriched flour bun. Low-fat ice cream is not a healthy substitute for full-fat ice cream.

The AHA is no different than the USDA and the American Diabetes Association, "official" organizations that have, in effect, sold out to industry.

Sleep for heart health

Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):



Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.

Is normal TSH too high?

There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.


In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.


Copyright 2008 Wiliam Davis, MD

Talking heads

Tne Philadelphia NBC affiliate's website carried this commentary from a colleague of mine:


Mark from the Lehigh Valley is curious about scans that can detect heart disease.

He asked, "I am in my early 50s. My father had a heart attack in his 40s. I am healthy with no symptoms of heart disease, should I consider a heart scan?"

"Well, Mark, occasionally family history needs to be considered more closely. If your father had coronary disease at a relatively young age at the absence of any known risk factor for heart disease for example diabetes, smoking, obesity, high blood pressure, than your level of risk should be considered more closely," Dr. Kevin Shinal, a cardiologist, said.

"There are a number of studies available to access [sic] your level of risk. One such study is a calcium score. A calcium score is a form of a CAT scan that access [sic] the calcium burden or presence of calcium in your coronary arteries. It assigns you a score and score is translated into a level of cardiovascular risk," Shinal said.

But the doctor warned because Mark doesn't have active symptoms, the scan probably wouldn't be covered by insurance.



Was there an understandable answer in there? I certainly couldn't find it.

Why pick on some yokel responding inarticulately to the local media's quest for content? Because this is, all too often, what the public hears: Ill-informed blather from someone who has little or no understanding of the issues. Maybe this doctor wanted his practice group to get some free publicity. "Doctor, could you just answer a few questions from viewers?"

Unfortunately, it's not just local media who are guilty of consulting with know-nothings with only passing knowledge of an issue. National media are guilty of it, too. The need to fill airtime with content is better filled with talking heads who present a compelling story, whether or not it is accurate or insightful, rather than an expert with deep insight into a topic who might not present as pretty a story. I've seen this countless times. A good portion of my day, in fact, is occupied responding to patient questions based on the misinformation presented in some media report.

My message of this brief rant: Be very careful of the messages delivered by the media, even if provided by some supposed "expert." In fact, I regard "experts" in health about as believable as politicians. Sure, sometimes they provide accurate information. But they often do not, or provide information with limited understanding. Or, worse, information intended to serve some hidden agenda.

Were the media to ask me to respond to the question, however, I would say:

"Yes, you should absolutely have a heart scan--yesterday! With your family history, there is no other way to accurately, easily, and inexpensively quantify the amount of coronary atherosclerosis in your heart's arteries. A stress test only uncovers advanced disease. A heart catheterization is overkill and absolutely not indicated in an asymptomatic man. Judging the presence of heart disease from cholesterol values is folly.

"What's left? A CT heart scan. So, yes, you need a CT heart scan ASAP with no doubt whatsoever."

But they didn't ask.