A curious case of coronary plaque regression and progression

John received a coronary stent in 2003 following a small heart attack. The artery causing the heart attack was a diagonal artery, a branch of the important left anterior descending coronary artery (in the front of the heart). His cardiologist at the time advised him, "Take Lipitor and we'll do stress tests every year. Come back if you have any more chest pain." That was the full extent of John's preventive care.

He came to me for a second opinion and, naturally, we enrolled him in our program. We began by obtaining a CT heart scan score, though we had to exclude the stented diagonal artery. His score: 471. At age 51 and physically active, John had 7 additional abnormal lipoprotein patterns identified. We counseled John on better approaches to food choices, his weight target, fish oil, and correction of all lipoprotein patterns.

Two years later, John's repeat heart scan score: 511 . John was initially disappointed with the increase. But a closer look yielded something entirely different: the right coronary artery and circumflex (no stents) showed 20-30% reduction in their scores. The increase in total score was entirely due to substantial increase in score just outside the stent, in the left anterior descending artery. In other words, all of the increase in score was due to growth of a plaque at the mouth of the stent in the diagonal artery.

This is curious: profound regression of plaque with a big drop in score in the "un-instrumented" arteries, but tremendous growth of plaque and an increase in score in the "instrumented", or stented, artery, all in the same person's heart.

I don't know how controllable this specific situation in the left anterior descending and stented diagonal will be, and I'm unaware of any specific strategies to impact on this situation. The whole world of tissue growth within or around stents is littered with high hopes followed by failures. The drug-coated stents have been the only partial solution to this problem, though that's precisely the sort of stent John received.

Is there a message here? The message I take from this is that you and I should work like mad to keep from receiving a stent. Once they're implanted, we have less control over our coronary future. We can indeed regress ("reverse") coronary plaque. But we may not be able to regress the sort of tissue that grows in response to a stent implantation.

When is a heart scan score of 400 better than 200?

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score is 500--a bad score that carries a 5% or more risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score but not with the same dangers of Tom's much higher score.

Tom follows a powerful heart disease prevention program like the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods; takes fish oil; raises his blood vitamin D level to >50 ng/ml, etc. One year later, Tom's heart scan score is 400, a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor but nothing else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice the score, or 200 points higher, compared to Harry. Who's better off?

Tom is better off. Even though he has a significantly higher score, Tom's plaque is regressing. It is therefore quiescent with its components being extracted, inflammation subsiding, the artery is in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, excessive constrictive factors are constantly causing the artery to pinch partially closed, fatty materials are accumulating and triggering a cascade of abnormal responses.

This is therefore a peculiar situation in which a higher score is actually better than a lower score. It reflects the power of adhering to a preventive program. It also demonstrates how two scans are better than one because they show the rate of increase given a particular preventive approach.

Warning: Your cardiologist may be dangerous to your health!

Warren had a moderately high LDL cholesterol for years and took a statin drug sporadically over the past 7 years. Finally retired from a successful real estate investment business, he had a CT heart scan to assess his heart disease status.

Warren's score: 49. At age 59, this put him in the lowest 25%, with an estimated heart attack risk of 1% per year or less--a relatively low risk. At this heart scan score, the likelihood of an abnormal stress test was less than 3%, or a 97% likelihood of a normal stress test. Most would argue that a stress test would be unproductive, given its low probability of yielding useful information. In other words, there would be a 97% probability of normal blood flow through Warren's coronary plaque, and less than 3% likelihood that a stent or bypass surgery would be necessary.

Warren was also without symptoms. He hiked and biked without any chest discomfort or breathlessness. A prevention program like Track Your Plaque to gain control over future coronary plaque growth was all that was necessary and Warren had high hopes for a life free of heart attack and major heart procedures.

Then why did he go through a heart catheterization?

Warren did indeed undergo a heart catheterization on the advice of his cardiologist. When I met Warren for another opinion, it became immediately obvious that the heart catheterization was completely unnecessary. Then why was this invasive procedure done? There can only be a few reasons:

--The cardiologist didn't truly understand the meaning of the heart scan score. "We need to do a 'real' test."

--The cardiologist was terrified of malpractice risk for underdiagnosing or undertreating any condition, no matter how mild.

--The cardiologist wanted to make more money. Talking about heart disease prevention is a money-saving, not a money-making, approach.

Regardless of which of the three motivations was at work here, they're all inexcusable. A disservice was done to this man: he had an unnecessary procedure, incurred some risk of complication in the process, and gained nothing.

An ignorant or profit-seeking cardiologist is worse than the unscrupulous car mechanic who, when presented with an unknowing car repair customer, proceeds to replace the carburetor and rebuild the engine when a simple 5-minute adjustment would have taken care of the problem.

I estimate that no more than 10% of my colleagues follow such practices, but it's often hard to know who is in that 10%. Ask pointed questions: Why is the catheterization necessary? What is the likelihood of finding information useful to my health? What are the alternatives? (By the way, the emerging CT coronary angiograms can be a useful alternative in some situations like this.)

Track Your Plaque is your source for credible information. Be well armed.

I don’t have high blood pressure!

Art undeniably had high blood pressure.

At age 53, he had all the “footprints” of high blood pressure that’d been present for at least several years: abnormal patterns by EKG, abnormally thick heart muscle, and an enlarged aorta by an echocardiogram. These sorts of changes require many years to develop. Art’s blood pressure was 140/85 sitting quietly in the office.

“That’s about what my primary care doc gets, too. Whenever it’s high, he takes it again after a few minutes and it always comes down.”

Art tried to persuade me that his blood pressure was high today only because of the traffic on the way into the office. When I dismissed this as a cause, he insisted that stress he’d been suffering because of his teenage son was the cause. “I just know I don’t have high blood pressure!”




Who’s right here? Well, Art is not here to defend himself. But one fact is crystal clear: you cannot develop complications of high blood pressure unless you truly have high blood pressure!

In other words, Art’s abnormal changes in heart structure (thickened heart muscle and enlarged aorta) are serious changes that develop only with years and years of sustained blood pressure at least as high as the one in the office. His blood pressure almost certainly ranged much higher at other times, particularly during stressful situations like waiting in the check-out line at the grocery store, watching a suspenseful TV show, petty irritations at his job, and on and on.

Blood pressure does not have to be high all the time to generate complications of high blood pressure. It can be sporadic, variable, even occasional. Clearly, sustained high blood pressure is the worst situation that creates adverse consequences more quickly. But blood pressure that wavers from low to high only some of the time can still, given sufficient time, cause the very same unwanted effects.

Control of blood pressure is crucial to your coronary plaque control program. Blood pressure may be boring: not as exotic, say, as lipoproteins, and not as fun as talking about nutritional supplements. But neglect blood pressure issues and you will not gain full control over coronary plaque growth—-your heart scan score will increase.

Watch for an upcoming Special Report on the Track Your Plaque Membership website, a full detailed discussion of how to recognize when blood pressure is an important issue, along with a full discussion of nutritional methods to reduce it, often sufficient to minimize or eliminate the need for medication.

Are there any alternatives to niacin?

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?


This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.


The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.
All posts by william-davis

Human foie gras

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.



While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

Let go of my love handles

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Surviving a widow maker

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

Fred Hahn's Slow Burn

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?



Fred Hahn's latest book, adapting slow burn techniques for kids.

Can I stop my Coumadin?

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:


I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna


No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

Homegrown osteoporosis prevention and reversal

I don't like to stray too far off course from discussions of heart disease and related issues in this blog. But the question of bone health comes up so often that I thought I'd discuss the strategies available to everybody to stop, even reverse, osteoporosis.

Coronary atherosclerotic plaque and bone health are intimately interwoven. People who have coronary plaque usually have osteoporosis; people who have osteoporosis usually have coronary plaque. (The association is strongest in females.) The worse the osteoporosis, the greater the quantity of coronary plaque, and vice versa. The two seemingly unconnected conditions share common causes and thereby respond to similar treatments.

Incredibly, rarely will your doctor tell you about these strategies. Your doctor orders a bone density test, the value shows osteopenia or osteoporosis, and a drug like Fosamax or Boniva is prescribed. As many people are learning, drugs like this can be associated with severe side-effects, such as jaw necrosis (death of the jaw bone), a dangerous and disfiguring condition that leads to loss of teeth and disfigurement, followed by reconstructive surgery of the jaw and face. These are not trivial effects.

Note that drugs are approved by the FDA based on assessment of efficacy and safety, NOT proven equivalence or superiority to natural treatments.

In order of importance (greatest to least), here are strategies that I believe are important to regain or maintain bone health. Indeed, I have seen many women increase bone density using these strategies . . . without drugs of any sort.

1) Vitamin D restoration--Vitamin D is the most important control factor over bone calcium metabolism, as well as parathyroid function. As readers of this blog already know, gelcap forms of vitamin D work best, aiming for a 25-hydroxy vitamin level of 60-70 ng/ml. This usually requires 6000 units per day, though there is great individual variation in need.

2) Vitamin K2--If you lived in Japan, you would be prescribed vitamin K2. While it's odd that K2 is a "drug" in Japan, it means that it enjoys the validation required for approval through their FDA-equivalent. Prescription K2 (as MK-4 or menatetranone) at doses of 15,000-45,000 mcg per day (15-45 mg), improves bone architecture, even when administered by itself. However, K2 works best when part of a broader program of bone health. I advise 1000 mcg per day, preferably a mixture of the short-acting MK-4 and long-acting MK-7. (Emerging data measuring bone resorption markers suggest that lower doses may work nearly as well as the high-dose prescription.)

3) Magnesium--I generally advise supplementation with the well-absorbed forms, magnesium glycinate (400 mg twice per day) or magnesium malate (1200 mg twice per day). Because they are well-absorbed, they are least likely to lead to diarrhea (as magnesium oxide commonly does).

4) Alkaline potassium salts--Potassium as the bicarbonate or the citrate, i.e., alkalinizing forms, are wonderfully effective for preservation or reversal of bone density. Because potassium in large doses is potentially fatal, over-the-counter supplements contain only 99 mg potassium per capsule. I have patients take two capsules twice per day, provided kidney function is normal and there is no history of high potassium.

5) An alkalinizing diet--Animal products are acidic, vegetables and fruits are alkaline. Put them together and you should obtain a slightly net alkaline body pH that preserves bone health. Throw grains like wheat, carbonated soft drinks, or other acids into the mix and you shift the pH balance towards net acid. This powerfully erodes bone. Therefore, avoid grains and never consume carbonated soft drinks. (Readers of this blog know that "healthy, whole grains" should be included in the list of Scams of the Century, along with Bernie Madoff and mortgage-backed securities.)

6) Strength training--Bone density follows muscle mass. Restoring youthful muscle mass with strength training can increase bone density over time. The time and energy needs are modest, e.g., 20 minutes twice per week.

Note that calcium may or may not be on the list. If on the list at all, it is dead last. When vitamin D has been restored, intestinal absorption of calcium is as much as quadrupled. The era of force-feeding high-doses of calcium are long-gone. In fact, calcium supplementation in the age of vitamin D can lead to abnormal high calcium blood levels and increased heart attack risk.

These are benign and easily incorporated strategies. They are also inexpensive. I challenge any drug to match or exceed the benefits of this combination of strategies. Keep in mind that strategies like vitamin D restoration provide an extensive panel of health benefits that range far beyond bone health, an effect definitely NOT shared by prescription drugs.

Your enlarged aorta

The thoracic aorta lives happily within the chest.

The aorta is the main artery of the body that emerges from the heart, located just under the sternum. It is the "tree trunk" from which all the major arteries branch off to the rest of the body: the arms, brain, abdominal organs, pelvis, and legs. The aorta receives the high-pressure blood ejected directly out of the heart muscle.

However, there are evil forces in the body that work to weaken the aorta. When the aorta is weakened, it enlarges. Enlarged aortas also tend to grow atherosclerotic plaque. Plaque in the aorta poses long-term risk for stroke and and mini-strokes ("transient ischemic attacks," or TIAs), due to fragmentation.

There are many enlarged aortas in this world. I see at least several every week. It is fairly common, particularly in people with high blood pressure and cholesterol abnormalities, as well as those who are overweight. Smokers get it really bad.

Conventional thinking is that, once an aorta enlarges, it will inevitably continue to enlarge at the average rate of 2.0 mm per year (resulting in 1.0 cm enlargement over 5 years). For this reason, conventional discussions on the topic of thoracic aortic aneurysms all say something like "Enlarged aortas should be monitored yearly. Surgical replacement should proceed when the aorta reaches a diameter of 5.5 cm."

This is because an aortic diameter of 5.5 cm is associated with much greater likelihood that the aorta will rupture (fatal within minutes) or the internal lining will tear, a "dissection." The surgery is a major undertaking that involves opening the chest and usually replacing the aortic valve and inserting a synthetic aorta. The procedure is high-risk, especially if any branch arteries are involved.

So putting a stop to any further aortic enlargement is a worthwhile goal. Unfortunately, conventional thought is that there is nothing you can do to stop the inevitable growth of the thoracic aorta.

Nonsense. There are a number of efforts you can make to halt further increase in aortic diameter. (My experience in this is anecdotal and unpublished, but now numbers several hundred patients.)

There are two categories of factors that cause the aorta to increase in diameter:

1) Internal pressure--Think of blood pressure as the internal inflating pressure on this "balloon." Keeping the "inflating pressure," i.e., blood pressure, low exerts substantial effect on slowing growth of aortic diameter. I aim for normal BP or lowish BP (less than 130/80, preferably 100/70).

2) Factors that weaken the aortic wall--Processes like inflammation, glycation, lipoprotein deposition, and nutritional deficiencies will serve to weaken the supportive tissue of the aorta. For that reason, correction of lipoprotein abnormalities (e.g., small LDL and lipoprotein(a)), reductions in carbohydrate intake and thereby blood glucose/glycation, and "normalization" of vitamin D, vitamin C supplementation (for collagen crosslinking), and omega-3 fatty acids all play a role.

To push even farther, there may be additional advantage to following strategies that impair the production and activity of a crucial enzyme that lives within the aortic wall: matrix metalloproteinase, or MMP. MMP degrades the collagen and other supportive tissues within the aorta, weakening it and permitting expansion. Blocking MMP may prove to be among the most powerful new strategies to halt aortic expansion.

Compounds that have potential MMP-inhibiting effects include:
--Vitamin D--A substantial effect
--Resveratrol--One of the polyphenols from red wine
--Doxycycline--This old antibiotic often used for acne treatment has, in preliminary studies, shown important MMP-blocking effects and slowed aortic expansion.

Anyway, there you have it. A bit complicated, but a "recipe" that has failed me only rarely.

Extreme carbohydrate intolerance

Here's an interesting example of what you might call "extreme carbohydrate intolerance."

May is a 44-year woman who has now had her 7th stent placed in her coronary arteries. She lives on a diet dominated by breads, breakfast cereals, muffins, rice, corn products, along with some real foods.

Her conventional lipid panel and other lab values:

Total cholesterol 346 mg/dl
Triglycerides: 877 mg/dl
HDL cholesterol: 22 mg/dl
LDL cholesterol: incalculable
(Recall that LDL cholesterol is usually a calculated, not a measured value. The excessively high triglycerides make the standard calculation invalid--more invalid than usual.)

Fasting blood glucose: 210 mg/dl
HbA1c (a reflection of previous 60-90 days average glucose): 7.2% (desirable 4.5% or less)
ALT (a "liver enzyme"): 438 (about five-fold normal)


At 5 ft even and 138 lbs (BMI 27.0), May appears small. But the modest excess weight is all concentrated in her abdomen, i.e., in visceral fat.

By lipoprotein analysis via NMR (Liposcience), May's LDL particle number was 2912 nmol/L, or what I would call a "true" LDL of 291 mg/dl. (Drop the last digit.) Of the 2912 nmol/L LDL particles, 2678 nmol/L, or 92%, were small.

The bad news: This pattern of extremely high triglycerides, extremely high LDL particle number, low HDL, predominant small LDL, and diabetes poses high-risk for heart disease--no surprise. It earned her 7 stents so far. (Unfortunately, she has made no effort whatsoever to correct these patterns, despite repeated advice to do so.)

The good news: This collection is wonderfully responsive to diet. LDL particle number, small LDL, triglycerides, blood glucose, and HbA1c drop dramatically, while HDL increases. Heart disease will at least slow, if not stop.

It's amazing how far off human metabolism can go while indulging in carbohydrates, particularly a genetically carbohydrate-intolerance person. (Actually, I wouldn't be surprised if May's diet, as bad as it seems to you and me, still fits within the dictates of the USDA food pyramid.) The crucial step in diet to correct this smorgasbord of disaster is elimination of carbohydrates, especially that from wheat, cornstarch, and sugars.

What's for breakfast? Egg bake

Heart Scan Blog reader and dietitian, Lisa Grudzielanek, provided this recipe in response to the post, What's for breakfast?

Lisa, by the way, is one of the rare dietitians who understands that organizations like the American Dietetic Association have made themselves irrelevant. She therefore advocates diet principles that work, not just echoing the idiocy that emanates from such organizations, often driven by economics more than science. Lisa works in the Milwaukee area and has proven a useful resource person for my patients who have required extra coaching in the Track Your Plaque diet principles.

Egg Bake
My favorite breakfast is what I call an "egg bake." Others may refer to it as a "quiche."

Take a variety of fresh vegetables. This time of year is great for farmers' markets.

I typically use fresh chopped organic spinach, bell peppers, red & white onions, scallions, broccoli, mushrooms, cherry tomatoes halved and, if desired, meat (nitrite-free ham or leftover chicken breasts).

1) Chop veggies and place in casserole dish.
2) Add meat and handful of cheese of your choice.
3) Scramble 8 eggs & little bit of milk & pepper.
4) Add to casserole dish and mix/coat veggies with egg mixture.
5) Put in oven at 450 degress for 30 minutes.

Yummy, ready to eat breakfast that is so easy for the work week.

What's for breakfast?

If you eliminate wheat from breakfast and otherwise adhere to a low-carbohydrate dietary approach, what is there to eat for breakfast?

If you take out English muffins, bagels, all breakfast cereals, pancakes, waffles, and toast, what's left to eat?

Actually, there's plenty left to eat. It just may not look like the traditional American notion of "breakfast." (The traditional idea of breakfast was is, in part, due to the legacy of Dr. John Harvey Kellogg, who, in the latter part of the 19th century, ran a sanitarium in Battle Creek Michigan. He and his brother, Will Keith Kellogg, discovered the idea of turning grains into flakes, the birth of the breakfast cereal. Subscribe to the idea of breakfast cereal for breakfast and you subscribe to the ideas of a man who would administer four enemas for you today to cure your cancer or rheumatism.)

Here are a few ideas. By no means is this meant to be a comprehensive list, just a starting point for a few new breakfast food ideas.

--Eggs--Of course, eat the yolk. Eat three yolks. Scrambled, "fried," (not really deep-fried, of course), hard-boiled, poached, as an omelette. Add pesto, olive oil, vegetables, mushrooms, salsa.

--Ground flaxseed--As a hot cereal with your choice of water, milk (not my favorite because of insulin effects; the fat is immaterial), full-fat soy milk (yeah, yeah, I know), unsweetened almond milk. Add walnuts, blueberries, etc. Ground flaxseed is the only grain I know of that contains no digestible carbohydrates.

--Lunch and dinner--Yes, if you cannot have breakfast foods for breakfast, then have lunch and dinner, meaning incorporating foods you ordinarily regard as lunch and dinner foods into your day's first meal. This means salads, leftover chicken from last night, soup, raw vegetables dipped in hummus or guacamole, stir fry, etc.

--Cheese--For something quick, grab a chunk of gouda or emmentaler along with a handful of raw almonds, walnuts, or pecans. Because of the excess acidity of cheese (along with meats, among the most acidifying of foods), I usually try to include something like a raw pepper or avocado, foods that are net alkaline.

--Avocados--Cut in half, scoop out contents. They're quick and delicious, when available.

I hesitate to mention it, but I sometimes will have tofu, cubed and flavored with whatever is available--soy sauce, miso, pickled vegetables. My mother was Japanese, so I'm comfortable with this, though many people are not.

Anyway, that's a partial list that nonetheless can get you started on a wheat-free, low-carb breakfast.

If you are just starting out, you will notice a number of fundamental changes. You may first experience the characteristic "withdrawal" effect: mental fog and fatigue that lasts about a week. Energy then picks up, often substantially. This is followed by gradually reduced appetite: You will be far less hungry. You will require less food, less often, since appetite will be driven by physiologic need, not the appetite-stimulating properties of wheat (and cornstarch, high-fructose cornsyrup and sucrose).

By the way, do not skip breakfast unless it's part of an occasional fasting effort. Skip breakfast, wind down metabolism, get fat. I am impressed at how consistent skipping breakfast backfires in those who think that it helps you control weight.

I also welcome any suggestions on what you eat as part of your wheat-free, low-carb breakfast. (Thanks for the great suggestions on the last blog post, Anna.)