Protecting the right to use bio-identical hormones in your heart disease prevention program

If you've been following the Track Your Plaque program, you know that we are advocates of "bio-identical hormones", i.e., hormone replacement using forms that are identical to the naturally-occuring human form.

In other words, we find it criminal that pharmaceutical manufacturers continue to promote use of non-identical hormones despite a probable increased side-effect and complication profile (a la Premarin). This unhappy situation persists because bio-identical hormones cannot be patent protected, meaning profits cannot be protected. Synthetic hormones can be patented and profits protected, thus their popularity among drug companies.

If that's not bad enough, Wyeth Pharmaceuticals--maker of synthetic hormone preparations, Premarin and Prempro--has filed an FDA petition to disallow the use of bio-identical hormones as prepared and dispensed by "compounding pharmacies". These are specialty pharmacies that mix and dispense hormones like estrogens (human estradiol, estriol, and estrione) and testosterone. They do so only with a doctor's prescription. Most are members of the Professional Compounding Centers of America (www.pccarx.com), a professional organization devoted to promoting quality-control over compounding practices.

Compounding pharmacies are occasionally guilty of compounding some suspect preparations. Witness the Fentanyl lollipops of 2002 in which the pain medication, Fentanyl, was put into lollipops for patients with chronic pain. This posed obvious dangers to any children who unsuspectingly ate the lollipops.

But the majority of compounding pharmacies are not guilty of such exotic practices. Most are simply pharmacies who might, for instance, mix a specific dermatologic preparation according to the orders of a dermatologist. Likewise with bio-identical hormones.

We have extensive experience with such a pharmacy in Madison, Wisconsin, the Women's International Pharmacy. They have filled hundreds of hormone prescription for us. They are responsible in their dispensing practices, in our experience. In fact, they have been at least as good, if not better, than other pharmacies we've dealt with.

We believe in protecting our rights to prescribe and you to use the choice of hormone preparations you and your doctor desire. This should include bio-identical hormones. The transparent profit motive from Wyeth should raise the hairs on your neck.

If you would like to post your comment to the FDA, there's a little time left. The folks at Womens' International Pharmacy have made it easy by posting links on their website. Go to http://www.womensinternational.com and just follow the instructions.



Here's a sample of some of the objections citizens have raised to Wyeth's petition:


I have been taking bioidentical hormones for two years. Bioidentical Hormones have been a great relief to me without the risk. I consult with my Physician who prescribes bio-identical hormones specifically for me, and my pharmacist prepares them. Without this medication and I would not be able to sleep; I would not be able to work due to the constant hot flashes. Without this medication, I find that I have less tolerance and I am considerably disagreeable. I also have problem with my memory without them. I want the bioidentcial hormones for the health benefits they provide. I urge you to not be swayed by Wyeth's petition. The product Premarin made by Wyeth, is made from pregnant horses not natural sources. Wyeth's hormones have been shown to cause cancer. I would not expect my government and its officials to submit to the highly funded petitioning of a pharmaceutical company who product is threatened by bioidentcial hormones. I do not expect my government to approved Wyeth's petition and leave me no choice of bioidentcial hormones and only the choice of Wyeth's cancer causing drugs Preamrin and Prempro. I ask that the FDA reject Wyeth's petition Docket #2005P-0411.

Another petitioner writes:

As a woman I take exception to Wyeth accusing the Compounding Pharmacy industry of unsafe practices. As a citizen of the United States I expect the FDA to stand up for my rights and the rights of all women who have found or in the future may seek consistent, safe and effective treatment with bioidentical hormones. Eliminating options by bowing to a large pharmaceutical company like Wyeth is not in the public interest and would deprive hundreds of thousands of American women from access to bioidentical hormones. Synthetic hormone replacement has been proven unequivocally unsafe in a government sponsored study and should not be forced as the sole treatment option for women. I hereby request the FDA rule against Wyeth's request. The FDA should not close down the bioidentical option of healthcare. I welcome studies of bioidentical hormones even though they are already FDA-approved and have been working effectively for decades. We already have the proof - hundreds of thousands of women, who over the past two decades have chosen bioidentical hormones based on their physicians' assessments. They are living proof that bioidentical hormones are safer and more effective and reliable than synthetic hormone drugs.

A physician and user of bio-identical hormones writes:

Wyeth, the filer of this complaint, is trying to prevent women from being able to choose less expensive compounded options for hormone replacement. There is medical evidence that in modifying the structure of their drugs (such as Premarin and Prempro) so that they could be patented, they may have introduced factors that cause the health risks identified in the Women's Health Initiative. This complaint appears to be filed for commercial purposes because of the market share that has shifted from Wyeth's products to bio-identical products from compounding pharmacies. If the complaint were upheld, patients and their doctors would not have a choice in hormone treatments. Wythe's commercial strategy of trying to eliminate the 'competition' from compounding pharmacies is against the public interest and in the interest of its own corporate profits. Women and their doctors should be able to choose between patented formulations such as those offered by Wyeth, bioidentical formulas available from compounding pharmacies, and no hormone treatment. I have been taking bio-identical hormones for several years and have had excellent results in improving my symptoms. I have been unable to take other synthetic hormones in the past, and am very concerned that my best treatment option will be taken away.

If you get a 64-slice CT coronary angiogram

With new 64-slice CT scanners popping up everywhere nowadays, be sure to get your heart scan with it.

The new scanners do indeed provide wonderful images of the coronary arteries. But, say you have a 20% blockage in one artery by a coronary angiogram generated on one of these devices. What will you do in 1, 2, or 3 years when you want to know if you have progressed? Should you have the CT angiogram repeated?

Well, if you did you'll be exposed to a large dose of radiation--appropriate for a diagnostic test, but not for a screening test. The radiation exposure is not that different from undergoing a full conventional cardiac catheterization, or up to 100 chest x-rays.

"20% blockage" is also, contrary to popular opinion, not a quantitative measure. It is just an estimate of the diameter reduction at one spot. That number says nothing about the lengthwise extent of plaque. It also says nothing about the potential for "remodeling", the phenomenon of artery enlargement that occurs as plaque grows. In other words, if you had another CT coronary angiogram a year later and was told that your blockag was still 20%, in reality you could have had substantial plaque growth but it would not be reflected in that value.

People will come to me after having a CT angiogram for an opinion. Unfortunately, I send them back to their scan center to get a simple coronary calcium score. That measure is easy, quantitative, precise, and can be repeated yearly if necessary to track progression. (Track Your Plaque--I hope most of you get this by now.) Some physicians poke fun at the heart scan, or calcium, score--it's old, boring, only a measure of hard plaque. None of that's true. The coronary calcium score is a measure of total plaque (hard and soft). And when you are empowered to learn how to control and reduce your score, then it's the most exciting number in your entire health program!

Don't fall for the hype. If you go to a scan center and they insist on a 64-slice CT scanner, or if your doctor orders one, you should insist on getting a calcium score out of the test. Just ask. If they refuse, go somewhere else. Centers that refuse to generate a score have one thing on their mind: identifying people with severe blockages sufficient to obtain the downstream financial bonanza--angioplasty, stents, and bypass surgery.

If you have hypertension, think Lp(a)

Clair has coronary disease.

Clair first came to attention at age 57 when she suffered a large heart attack involving the front of her heart (the "anterior wall") two years ago. Her cardiologist implanted a drug-coated stent. Her doctors advised her to "cut the fat" in her diet, exercise, and take Lipitor.

One year later, she required a stent to another artery (circumflex). At this point, Clair was thoroughly demoralized and terrified for her future. Her first heart attack left her heart muscle with only 50% of normal strength.

She came to my office for another opinion. Of course, one of the first things we did was to identify all causes of her heart disease. No surprise, Clair had 7 new causes not previously identified, including low HDL (37 mg/dl), a severe small LDL particle pattern (75% of all particles were small), and Lp(a).

Her blood pressure was also 190/88, despite her relatively slender build and 3 medications that reduced blood pressure. That's a Lp(a) effect: Exagerrated coronary risk along with unexpected hypertension that often seems inappropriate.

In fact, I saw several patients just this week with lipoprotein(a), Lp(a), and exagerrated high blood pressure (hypertension). It's not that uncommon.

Though it has not been described in the medical literature, our experience is that hypertension is a prominent part of the entire Lp(a) "syndrome".

Lp(a) is responsible for much-increased potential for coronary disease (coronary plaque). It increases in importance as estrogen recedes in a woman (pre-menopause and menopause) and testosterone in a man, since both hormones powerful suppress Lp(a) expression (though why and how nobody knows).

I believe that Lp(a) is also responsible for hypertension that most commonly develops in a persons mid-50s and onwards, often with a vengeance. 3 or 4 anti-hypertensive medications and still not controlled.



Role of l-arginine

L-arginine may be more helpful in this situation than others. L-arginine, recall, is the supply for your body's nitric oxide, a powerful dilator of the body's arteries and thereby reduces blood pressure. We use 6000 mg twice a day, a large dose that requires use of powder preparations rather than capsules.

More reading about l-arginine and nitric oxide is available through Nobel laureate, Dr. Louis Ignarro's book, NO More Heart Disease : How Nitric Oxide Can Prevent--Even Reverse--Heart Disease and Stroke, available at Amazon.com ( http://www.amazon.com/gp/product/0312335814/104-1247258-6443909?v=glance&n=283155).




Will l-arginine truly reverse heart disease on its own? No, I don't believe so. Contrary to Dr. Ignarro's extravagant claims, I find l-arginine a facilitator of plaque regression, i.e, it helps other strategies achieve regression, but it does not achieve regression or reversal by itself. (Note that Dr. Ignarro is a lab researcher who studies rats and has never treated a human being.)

But l-arginine may have special application in the person with lp(a), particularly if hypertension is part of the syndrome.


Note: As always, please note that I talk frankly about l-arginine and other supplements and medications but have no hidden agenda: I am not selling anything, nor am I affiliated with any source/website/store etc. that sells these products. If I advocate something, I do so because I truly believe it, not because I'm trying to sell something. I make this point because so much nonsense is propagated in the media because of profit-motive. That's not true here.

Dr. Ornish: Get with the program!


In the era up until the 1980s, most Americans indulged in excessive quantities of saturated fats: fried chickem, spare ribs, French fries, gravy, bacon, Crisco, butter, etc.

Along came people like Nathan Pritikin and Dr. Dean Ornish, both of whom were vocal advocates of a low-fat nutritional approach. In their programs, fat composed no more than 10% of calories. This represented a dramatic improvement--at the time.


In 2006, a low-fat diet is a perversion of health. It means over-reliance on breads, breakfast cereals, pasta, crackers, cookies, pretzels, etc., the foods that pack supermarket shelves and that now constitute 70-80% of most Americans' diet.

Dr. Ornish still carries great name recognition. As a result, his outdated concepts still gain media attention. The June, 2006 issue of Reader's Digest, in their RDHealth column, carried an interview with Dr. Ornish in which he reiterates his fat-phobia.

However, on this occasion he takes a different tack. This time he rails against the "dangers" of fish oil and omega-3 fatty acids. "I've recently learned that omega-3s are a double-edged sword...In some cases, omega-3s could be fatal."

He goes on to say that, while he believes that fish oil may prevent heart attacks, it has fatal effect if you already have heart disease.

Does this make sense to you?

He's basing his views on a single, obscure study published in 2003 conducted in rural England that showed an increase in death and heart attack on fish oil. Most authorities have not taken these findings seriously, since they are wildly contrary to all other observations and because the study had some design flaws.

Despite the fact that this isolated study runs counter to all other, better-conducted studies seems not to matter to Dr. Ornish.

Clinging to the low-fat concept is like hoping 8-track tapes will make a comeback. It's not going to happen. We enjoyed the benefits while they lasted, appropriate for the era. But now, they're woefully outdated.

The overwhelming evidence is that fish oil provides tremendous benefits with little or no downside. In the Track Your Plaque program, fish oil remains a crucial supplement to gain control over your coronary plaque and stop or reduce your heart scan score. Ignore the doomsday preachings of Dr. Ornish.

(Watch for an article I wrote updating the benefits of fish oil for Life Extension magazine.)

The cholesterol fallacy

Evan spotted the kiosk set up in the middle of the local mall. "Free cholesterol screenings. Know your heart health!" the sign declared.

It was a free cholesterol screening being offered by a local hospital.

The friendly nurse behind the kiosk had Evan fill out a form, then pricked his finger. Five minutes later, she reported to him with a smile, "Sir, your cholesterol is 177--your heart's fine! We get concerned when cholesterol is over 200. So you're in a safe range."

What the nurse failed to recognize is that Evan's HDL was 30 mg, a low value that actually places him at high risk for heart disease. Low HDL also signifies high likelihood of the small LDL particle pattern, a marked predisposition towards pre-diabetes and diabetes, a probable over-reliance on processed carbohydrates in his diet, a dramatically increased probability of hidden inflammation (e.g., elevated C-reactive protein), increased tendency for high blood pressure. . .

In other words, Evan's "favorable" total cholesterol is, in truth, nonsense. It's misleading, falsely reassuring, and provided none of the insight that a real effort might have yielded. Like hippies, tie-dye, other relics of the 1960s, total cholesterol needs to be put to rest. It has served many people poorly and been responsible for countless deaths.

When you see a kiosk or other service like this, even if it's free, run the other way.

"Heart disease a growth business"





So announced a Boston newspaper recently, featuring a story about new heart program at a local hospital.

They were announcing how a hospital had entered the cardiovasculare procedure game and how it would boost their bottom line. The article discussed how the hospital administration was anticipating "a surge in patients from the baby boom generation."

To justify this new program, the article quoted an administrator from another hospital: "Cardiovascular issues is [sic] the number one cause people sought treatment at our hospital."

The hospital featured in the story had spent $13.5 million dollars to develop their program.

Do you think they'll make it back?

You bet they will--many times over. Hospitals are businesses, complete with a bottom line, an expectation of profit and an eye towards growth.

The hospitals in the city where I live (Milwaukee, Wisconsin) are, as in Boston and elsewhere, very aggressive--expanding into new territories, hiring new "salesmen" (physicians), all to capture more marketshare and produce more "product" (your coronary angioplasty, stent, bypass surgery, defibrillator, etc.).

The equation for hospital profits is tried and true. Ignore your heart disese risk and you can help your local hospital grow its business. Neglect to get your heart scan and you can help your hospital pay down its debt. Get a heart scan, then do nothing about it, and you may even justify a pay raise for the hospital administrators for record revenue growth and profit.

Hospitals are a growth business because of the failure of most people and their doctors to 1) identify hidden coronary disease (CT heart scan to obtain your heart scan score), then 2) seize control over it (the Track Your Plaque program or, at least, your doctor's guidance along with your efforts at prevention).

Unless you do so, you are highly likely to help your hospital boost its annual goal for procedures.

The myth of small LDL

Annie's doctor was puzzled.

Despite an HDL cholesterol of 76 mg (spectacular!) and LDL of 82 mg, her CT heart scan showed a score of 135. At age 51, this placed her in the 90th percentile.

Not as bad, perhaps, as her Dad might have had, since he died at age 54 of a heart attack.

So we submitted blood for lipoprotein testing. Surprise! over 90% of all her LDL particles were small. (By NMR, they're called "small". By gel electropheresis, or the Berkeley Lab test, or VAP (Atherotech) technique, they're called "HDL3".)

What gives? Traditional teaching in the lipid world is that if HDL equals or exceeds 40 mg/dl, then small LDL will simply not be present.

Well, as you can see from Annie's experience, this is plain wrong. Yes, there is a graded, population-based effect--the lower your HDL, the greater the likelihood of small LDL. But small LDL is remarkably persistent and prevalent--regardless of your HDL.

We've seen small LDL even with HDLs in the 90's! I call small LDL the "cockroach" of lipids. If you think you have it, you probably do. Getting rid of small LDL requires a specific bug killer. (Track Your Plaque Members: Read Dr. Tara Dall's interview on small LDL.)

Don't let anybody blow off your request for lipoprotein testing just because your HDL is high. That's just not acceptable. Loads can be wrong even with a favorable HDL.

My stress test was normal. I don't need a heart scan!

Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief.

But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern.

I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished.

But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"

What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test.

Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)

Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack.

So, yes, Katy would benefit from another heart scan despite her normal stress test.

The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque.

But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.

Patient-napping: Yet another reason to stay clear of hospitals!

When I started practicing medicine around 20 years ago, it was common practice to alert a physician when their patient was seen in an emergency room.

If John Smith, for example, went to the emergency room with chest pain, the physician who had an established relationship with the patient--knew their history, had managed their health and illnesses, etc.--was notified, even if the hospital ER had no relationship with the physician. It was not uncommon for the patient to then be transferred to the hospital where their own doctor practiced.

Though cumbersome at times, it preserved the relationship of the patient with their doctor.

Over the past few years, this practice has crumbled. Nowadays, hospitals and their employed physicians (and other unscrupulous physicians acting in the name of profit) "fail" to notify the physician with an established relationship.

Guess what happens? The patient all too often ends up being put through the gamut of testing and procedures.

Why? For hospital profit, of course. If failure to notify a doctor who's had a 10-year long relationship with the patient is "overlooked" or, even more commonly, it's "unsafe" to transfer the patient because the patient is too "unstable" to be transferred, then this patient becomes ripe for picking--heart catheterization, stents, bypass surgery, etc. Ten's, if not hundreds, of thousands of dollars can be reaped by this deception. I call it "patient-napping".

I see this at least several times every month. As hospitals are becoming increasingly competitive, and as they put pressure on their physicians to churn patients for revenues, you're going to see more and more of this.

As always, what is your protection from this expanding influence of hospitals and the doctors too meek to stand up to them? Education and information. Arm yourself with an understanding of what is accomplished in hospitals, when you truly need them, and when you don't.

Take it one step further. At least from a heart disease standpoint--the #1 profit-maker for hospitals--aim to 1)identify your coronary plaque, then 2) seize control over your coronary plaque and reduce your risk for heart attack and heart procedures as much as humanly possible. That's the goal of the Track Your Plaque program.

Don't believe the negative press on fish oil



A British Medical Journal study released in March, 2006 has prompted a media flurry of reports on the worthlessness of fish oil. (Hooper L, Thompson RL, Harrison RA et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: a systematic review. BMJ March,2006)

Don't believe it for a second.

First of all, the study was a re-analysis of the existing published scientific literature. It was not a new study. It included a wild conglomeration of different clinical observations, as the studies examining fish oil over the years have been extraordinarily heterogeneous--in populations examined, omega-3 supplement (e.g., fish vs. capsule), period of observation, endpoints measured.

The results were skewed by inclusion of a moderate-sized British study by Burr et al in men with angina. In this study, no benefit was demonstrated and, in fact, a negative effect--more heart attack and death--was observed with fish oil. This was not news, since the study was published in 2003. It's results have been a mystery to everyone, since its unexpected negative result for fish oil was so starkly different from virtually every other study that preceded it (suggesting a study flaw or statistical fluke).

Nonetheless, the Burr study served to throw off the overall analysis. It diluted the dramatic and persuasive outcome of the GISSI-Prevenzione Study of 11,000 people in which a 28% reduction in heart attack and 45% reduction in cardiovascular death was observed. Note that the substantial numbers of the GISSI make the study's outcome nearly unassailable.

Another important fact: fish oil is among the most powerful tools available to correct elevated triglycerides. Drops of 50% are common. Recall that triglycerides are a necessary ingredient to create the nasty LDL, as well as VLDL, Intermediate-density lipoprotein, and an undesirable shift from large to ineffective small HDL. Reducing triglycerides is therefore crucial for your plaque control program.

This re-analysis serves to prove nothing. Such analyses can only pose questions for further study in a real study like GISSI: a randomized (random participant assignment), controlled (treatment vs. placebo or other treatment) study.

The weight of evidence remains heavily in favor of fish oil, not only as helpful, but fabulously beneficial, particularly for anyone aiming to reduce coronary plaque.

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.

I'll supply the tar if you supply the feathers

The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.