Large new clinical study launched to study. . .niacin


Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.

How is that new? Well, this time niacin comes with a new spin.

Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin.

The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.

In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable.

But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush.

Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available.

You don't have to wait. You already have niacin and aspirin available to you.

The dark side of CT heart scans

"I just got a heart scan!" declared Eric to his doctor. He handed the report to him.

"Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."


I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong.

There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)

Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk.

If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.

Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.

The dirty little secret about aneurysms

Jake had an abdominal aneurysm identified--by accident.

While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.

Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."

Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged.

How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."

Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery.

If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying.

But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it?

Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult.

The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise.

More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.

Heart scan scores dropping like stones!!

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.

Pre-diabetes: An explanation for explosive coronary plaque growth

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."


Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.


Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.
All posts by william-davis

Getting your dose of fish oil right

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

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

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

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

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

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

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

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

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

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

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

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

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

Easy: She follows her own advice.

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

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

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

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

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

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

More on this concept can be found at:

What's worse than sugar?

The Wheat-Deficiency Syndrome


Nutritional approaches: Large vs. Small LDL

Are you wheat-free?

Statin drug revolt

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

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

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

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





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

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

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

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

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

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

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

Join the revolt!

Lovaza Rip-off

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

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

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

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

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

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

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

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

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

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



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

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

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

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

--Wheat and sugars make us diabetic!

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


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

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

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


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

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

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

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

Another case of aortic valve disease reduced with vitamin D

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

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

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

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

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

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

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

I've posted about this peculiar phenomenon previously:

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

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

A formal trial at some point would be invaluable.

Track Your Plaque Program Data Tracking Tools

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



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

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

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

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

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

Yet another reason to avoid fructose

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

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

Two Moms

Two lovers


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

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

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

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

Increased blood levels of uric acid have been shown to:

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

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

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

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

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

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


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

Free the Animal

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



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

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

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

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

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

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

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

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

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

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

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



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

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

I'd recommend:

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

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

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

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

Low Thyroid and Plaque

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

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


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

Correcting the subtle levels of low thyroid:

1) Makes LDL reduction much easier

2) Facilitates weight loss

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

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

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

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

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Overweight, hungry, diabetic, and fat-free

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis


Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil



Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.