What's the best lipoprotein test?

This is a frequent question from Track Your Plaque Members and others interested in improving their heart disease prevention program beyond that of simple-minded cholesterol testing.

I obtain lipoprotein testing every day on patients. I can tell you with the confidence of having done thousands of these tests that plain, old-fashioned cholesterol testing is like relying on riding a scooter to work compared to an 8-cylinder modern automobile. The scooter might get you there, but any rain, snow, or long distance to travel and you can just forget it.

All too often, lipoprotein testing uncovers abnormalities that standard cholesterol testing simply fails to uncover.

So, among the various lipoprotein tests available, which is best?


There are three commercial tests available today:

1) Gel electropheresis (GGE)--often known by its "brand" name as the Berkeley lipoprotein profile, after Berkeley HeartLabs. GGE uses a gel with an electric field applied to cause lipoproteins to migrate, based on particle size and charge.

2) Vertical auto-profile (VAP)--a form of centrifugation, or high-speed spinning of blood plasma to separate lipoprotein particles.

3) Nuclear magnetic resonance (NMR)--the idea of putting plasma in an NMR (also known as MRI) device to characterize blood proteins.

All three tests do an excellent job. All are competitively priced. All have validating data--lots of it--to justify their broad use (though health insurers, in their vast wisdom, would still have you believe that the tests are "experimental").

But is one better?

Having done many of all three (though least of VAP), I am partial to Liposcience's NMR. (By the way, I receive no fees from Liposcience to use their test, nor to promote it in any way.)

I believe NMR is superior in a few ways:

1) I believe that the LDL particle number is the best way to truly quantify LDL, better than apoprotein B and "direct" LDL.

2) It provides what I believe to be more accurate small LDL measures.

3) It provides intermediate-density lipoprotein (IDL), a post-prandial, or after-eating, measure not available on the other two.

Perhaps I'm biased because I use the NMR most frequently. But I've used it because I felt it yielded superior, more clinically believable, data.

In truth, all three laboratories do an excellent job and you'd be served fine by obtaining any of the three. But my heart goes to NMR.

Vitamin K2, aspirin, fish oil and blood thinning

An interesting question came up from one of our Track Your Plaque Members on the Forum.

"I am now taking 9 mg of vitamin K1 and 1000 mcg of K2.

Does taking this supplement with this much K1 have a counteracting effect on the thinning/anticlotting properties of aspirin and fish oil that I also take?"


Great question (along with lots of other greater discussions we have on the Forum.)

The answer: Vitamin K should have no effect on the platelet-blocking effects of aspirin or fish oil. The majority of blood clot inhibiting effects of aspirin and fish oil arise from their ability to keep blood platelets from "clumping" (just like the TV commercials for Plavix).

Vitamin K, on the other hand, participates in the liver production of blood clotting factors (like II, VII, IX, and X, among others for you curious ones).

Thus, vitamin K-dependent clotting factors and platelet-blocking are two separate pathways to forming blood clots. Some of us refer to the difference as "red clots" from the vitamin K pathway and "white clots" from the platelet pathway, since they really do have this different physical appearance.

The vitamin K2 conversation, like that about vitamin D, is fascinating for its potential to provide the missing link between the tightly-tied fortunes of bone health and atherosclerosis. Why is someone with a high CT heart scan score far more likely to have osteoporosis? Vitamin D and K2 deficiency may provide the missing link for many people.

"Drug no cure for gluttony"

That's the headline I'd like to see associated with rosiglitazone, brand name Avandia.

The recent negative press, whether deserved or not, surrounding the prescription drug rosiglitazone for pre-diabetes and diabetes highlights the fact that drugs never--never--substitute for what we can achieve with lifestyle changes.

Typically, rosiglitazone reduces blood sugar a few milligrams, reduces C-reactive protein, and very modestly reduces triglycerides and its associated evil lipoprotein friends. It also causes an average weight gain of 8 lb in the first year of use.

What will weight loss achieve, especially if accomplished through dramatic reduction or elimination of processed carbohydrates and wheat products, along with fish oil supplementation, vitamin D normalization, and exercise? Extraordinary benefits, far superior to what is achievable with this drug. In fact, while rosiglitazone is a Band-Aid for this process, the lifestyle changes can represent a cure in many or most instances.

It should come as no surprise that a drug that does nothing more than increase sensitivity to insulin cannot erase the devastating effects of an unhealthy life. Take rosiglitazone but neglect exercise, don't bother with vitamin D, indulge in pretzels and breakfast cereals, gain more weight . . . It serves the drug company's agenda better than it serves health.

Rosiglitazone not so rosy?

Dr. Steve Nissen of the Cleveland Clinic published a study that suggests that the pre-diabetes and diabetes drug, rosiglitazone, may increase likelihood of heart attack by 43%.

I say "suggests" because the analysis was something called a "meta-analysis", a re-examination of data obtained by pooling unrelated studies and reanalyzing the data. Strengths of this sort of analysis: Sometimes trends that are not evident in smaller studies finally become evident in the larger numbers of participants obtained through pooling of data. Downside: Any statistician will tell you that a meta-analysis can only suggest an association, it cannot prove it.

Nonetheless, we are talking about people's lives. As they say, if you are taking this drug, also known by the brand name, Avandia, then talk to your doctor. I think that this is sound advice, as there are a number of factors to weigh in decision making. For instance, how far along the diabetic path are you? Have you had negative experiences with other agents?

It will, unfortunately, be months to years before confirmatory evidence on this question become available. In the meantime, Nissen will accuse the drug industry of pushing drugs through the FDA approval process without full safety data. GlaxoSmithKline, the manufacturer of Avandia, will counter with claims of weak data, the existing trials not confirming Nissen's findings, etc. We've seen it before.

My take on this is to step back and look at the broad picture. Do we need yet another reason to say that it's far better to maintain normal body weight, dramatically reduce reliance on processed carbohydrates and wheat, exercise, and following other insulin-sensitizing strategies, rather than rely on insulin-sensitizing drugs? (That's what rosiglitazone is supposed to do.) Metabolic syndrome, also known as pre-diabetes, or diabetes is present to various degrees in two thirds of all adults I meet. Nearly all of it is self-inflicted. Nearly all of it is curable with the above lifestyle strategies if undertaken early enough in the process.

A 190 lb, 5 foot 2 inch woman, or a 220 lb, 5 foot 10 inch man, both of whom are surprised that they have pre-diabetes really need to get a grip on reality and health. To me, it's no surprise that drugs do not reverse all the nasty manifestations of lifestyle gone berserk. It should also come as no surprise that the complex, chaotic physiologic mess created by metabolic syndrome and pre-diabetes is not perfectly managed by adding one drug.

The lipid distorting effects of weight loss

Roger experienced a near-fatal heart attack 6 years ago. He survived thanks to the quick action of bystanders who initiated CPR and called 911. An emergency catheterization was performed and a stent implanted into the closed right coronary artery. But that's not why I tell Roger's story.

Since then, Roger has become comfortable with the idea that he has heart disease. His initial commitment to good nutrition and exercise has waned, as it often does in us distractable humans. So Roger gained about 30 lbs through a long winter, inactivity, eating frozen dinners, and the cookies and baked goodies his daughters made him.

As a result of the weight gain and inactivity, Roger's HDL dropped to 32 mg/dl, triglycerides rose to 211 mg/dl, blood sugar crept up into the pre-diabetic range of 116 mg/dl. Undoubtedly, small LDL was out of control beneath the surface. His tummy reflected the weight gain, flaccid and overhanging his belt.

I read Roger the riot act. I reminded him of what he had experienced and nearly didn't survive. Weight loss and a re-invigoration of his nutrition and exercise efforts was going to be crucial.

Roger listened and took it to heart. Over three months, he lost 24 lbs, a phenomenal result. However, his repeat lipid panel showed an HDL of 28 mg/dl, triglycerides 234 mg/dl, blood sugar unchanged.

"I don't get it! I lose all this weight and the number get worse?!" Roger was understandably upset after his enormous effort.

I told Roger that after a profound weight loss, lipids can go berserk for up to two months after weight has stabilized. Typically, HDL drops and triglycerides rise--the opposite of what we want. But wait another two or so months after weight has stabilized and the numbers begin to look beautiful.

Why does this crazy effect happen? I really don't know and I've never heard a satisfactory explanation for it. But it is very real and quite predictable.

The lesson: after a substantial weight loss, be patient. Check your lipid numbers too soon and you might be confused or disappointed. If you do check them, bear in mind that additional time may need to pass before you see the weight loss fully reflected.

Cholesterol reduction and wheat

In my previous post, Identical twins and the explosive influence of weight , we witnessed an excellent example of the profound influence of food choices and weight control on lipoproteins. The heavier twin among these 35-year old male twins (Steve) had an LDL particle number over two-fold higher than his more slender counterpart (Alfred).

The heavier twin, Steve, got here through numerous and longstanding dietary excesses: fast foods, saturated fats, sweets, processed foods. The conventional answer to Steve's lipid dilemma would be to modestly reduce his reliance on saturated fat, exercise, and limit snacks.

How far would that get Steve? Not very far at all. With regards to his high LDL particle number of 2256 nmol/l (representing an "effective" LDL cholesterol of around 225 mg/dl), it would be reduced a little, perhaps 10%.

Notice, however, that 72% of all Steve's LDL particles are small (1639/2256). This is the pattern that responds dramatically to a sharp reduction in processed carbohydrates, especially wheat-containing products.

If Steve were to eliminate all wheat products--all breads, breakfast cereals, pretzels, cookies, cakes, pasta, crackers--LDL particle number will drop dramatically, perhaps 50%, often more depending on the magnitude of weight loss. Small LDL will respond most obviously and will be sharply reduced, perhaps disappear. Incidentally, these changes might not be well reflected by the conventional calculated LDL cholesterol, since small LDL particles are well-concealed by standard measures.

Reducing corn products, white and brown rice, and potatoes would also add to the effect. But, in 2007, wheat products represent 90% of the problem for the majority of people. Reducing or eliminating wheat therefore yields the biggest effect by a long shot.

Steve therefore represents an excellent example of how reducing processed carbohydrates, esp. wheat-containing products, can yield an unexpected and paradoxical reduction in LDL cholesterol as evidenced by the highly accurate LDL particle number (or apoprotein B). Reducing saturated fat sources also helps, but it certainly will not yield the kind of results most people need. You've got to be smarter than the simple-minded conventional advice.

Identical twins and the explosive influence of weight

A Track Your Plaque member, Eugene, brought this fascinating story to my attention.

Eugene has two nephews, identical twins aged 35 years. Despite their similar personalities and appearances, somehow these two drifted apart in weight with Steve outweighing Alfred by 30 lbs.

Eugene explains:

These guy's are big not, but overly fat. Just big. One is about 30 lbs heaver than the other. They live 2 blocks apart, they ate the same (together) meal the night before the blood work. Their mother is a type 2 diabetic with a heart condition. Steve does not eat as well as his twin, junk food and a lot of processed starches.


Their results:



LDL-Particle number
Alfred 900
Steve 2256

Small LDL-P
Alfred 400
Steve 1639

HDL-C
Alfred 44
Steve 36

Triglycerides
Alfred 85
Steve 355

Metabolic Syn.
Alfred no
Steve yes


Glucose

Fasting
Alfred 93
Steve 112

1hour
Alfred 134
Steve 206

2 hour
Alfred 105
Steve 172


Identical twins begin with the very same genetic background. As these two graphically illustrate, weight can have a profound influence in the genetically susceptible.

LDL particle number alone is 250% greater in the heavier twin. The dreaded small LDL particle is over 400% worse! Look also at the dramatic differences in blood sugar.

If you ever had any doubts about the importance of excess weight and nutrition, just remind yourself of this fascinating illustration.

Thanks, Eugene.

Low-fat diets raise triglycerides

Martin, a hospital employee, knowing that I fuss a great deal with lipids and lipoproteins, showed me his lipid panel because the result triggered a "panic value" for triglycerides at 267 mg/dl. He asked if he should go on a serious low-fat diet.

I asked Martin what he had for breakfast: a whole wheat bagel with no-added-sugar jam. Lunch: a turkey sub on whole grain bread, no mayonnaise. Snacks: baked chips, pretzels ("a low-fat snack!").

In years past, if person developed high triglycerides levels, a very low-fat diet was prescribed. Someone would come to the hospital, for instance, with abdominal pain from pancreatitis (an inflamed pancreas)due to the damaging effects of triglyceride levels >1000 mg/dl. For this reason, many people still believe that all instances of elevated triglycerides should be treated with a reduction in fat intake.

This is absolutely wrong. While a fat restriction may reduce triglycerides in genetically-programmed responses when triglycerides are >1000 mg/dl, lesser levels of high triglycerides of, say 250 or 300 mg/dl, do not respond to dietary fat restrictions as a sole strategy.

Yes, a reduction in unhealthy fats (saturated, trans, polyunsaturated) helps. But a reduction in fats of all sorts is not necessary and can, in fact, worsen the problem. We learned this lesson years ago with the Ornish diet and similar ultra low-fat approaches. When you reduce fat intake significantly to <10% of calories, triglycerides go way up. In those days, it wasn't uncommon to see triglycerides skyrocket past 200 or 300 mg/dl on these diets.

Why are triglycerides important? Triglycerides are an ingredient in creating the lipoproteins VLDL, IDL, small LDL. Elevated triglycerides trigger a drop in HDL, a shift towards small, ineffective HDL, and contribute to heightened inflammation. Higher triglycerides also tend to go hand in hand with lipoproteins that persist for extended periods (12-24 hours or longer) in the blood after a meal.

Triglycerides respond very nicely to a dramatic reduction in processed carbohydrates, especially wheat and corn. Of course, wheat is the bulk of the problem, since it has grown to occupy an enormous role in many people's diet, not uncommonly eaten 3,4, or 5 times per day in various forms, as it has in Martin's diet. Eliminating all sources of high-fructose corn syrup is also helpful, since high-fructose corn syrup shoots triglycerides way up. (Recall that high-fructose corn syrup is everywhere: ketchup, beer, low-fat or non-fat salad dressings, breads, fruit drinks, sports drinks, breakfast cereals, etc.)

Curiously, it is a fat that also powerfully reduces triglycerides in the form of fish oil. In the Track Your Plaque program, fish oil, taken at truly effective doses of 4000 mg per day or more (to provide at least 1200 mg EPA+DHA), is our number one choice after reduction of processed carbohydrates for reduction of high triglycerides.

The dreaded niacin "flush"

As most anybody who takes niacin knows, it can cause a hot flushed feeling over the chest and face that is generally harmless, though quite annoying.

Many doctors are frightened by this response and will warn patients off from niacin. Some people who take niacin are so annoyed that they find it intolerable.

However, a very simple maneuver can relieve the hot flush in over 90% of instances: Drink water. Let me explain.

I usually instruct patients to take niacin at dinnertime. That way, food slows absorption modestly. I also ask them to drink water with dinner. If the flush occurs after dinner (usually 30-60 minutes later), then drinking two 8-12 oz glasses of water immediately breaks the flush within 3 minutes in the great majority of people. It's quite dramatic.

Doing this around dinner (lunch works just as well) allows sufficient time to clear the excess water from your body before bedtime and spare you the aggravation of disrupted sleep to urinate. Drinking plenty of water works most of the time. Only an occasional person will need to take a 325 mg uncoated aspirin to more fully break the flush. I generally suggest that patients keep the uncoated aspirin in reserve if the water doesn't provide relief within a few minutes.

Thankfully, the intensity of the niacin flush lessens, often disappears, with chronic use.

Why do some people develop the flush and other don't? It is believed that some people metabolize niacin more rapidly to a compound called nicotinuric acid, a niacin metabolite that causes dilation (relaxation) of skin capillaries--thus the flush. The rapidity of converting niacin to nicotinuric acid is determined genetically.

An occasional person really struggles with niacin to the point of intolerance. However, on the positive side, these people may also be "hyper-responders" to niacin, i.e., they show exagerated benefits in raising HDL, reducing small LDL, etc., from small doses such as 250 mg per day.

If you experience the hot flush of niacin, think water to put out the fire.

A cure for pessimism?

Followers of the Track Your Plaque program know that we place great value on having an optimistic outlook. Not only are you more likely to be happy and successful in life, you are also far more likely to drop your CT heart scan score. Virtually everyone who has succeeded in dropping their heart scan score dramatically has been an optimist, including our most recent record holder who dropped his score an astounding 51%.

But what if you are a pessimist, someone who gripes and complains about everything, sees the bad in other people, blames others for anything and everything that goes wrong--yet you still desire to drop your heart scan score? Are you a lost cause? Should you just give up?

I don't think so. I will admit that, of all the hurdles we encounter in trying to purposefully stop or reduce heart scan scores, overcoming a pessimistic attitude is probably the toughest. Tougher than being overweight, maybe tougher than even Lp(a).

Perhaps there's a solution in two years of psychotherapy sessions with a counselor, or exploring unresolved childhood conflicts with a psychologist, or an antidepressant drug. Pessimism is, after all, a deeply-ingrained pattern of behavior, something that can't be changed just by suggesting it or simple self-realization.

The closest thing I know of to a quick and relatively easy solution for converting a pessimist to an optimist is very simple:

Do good things for other people.

Something peculiar happens to the pessimist when he/she starts to help others. They are less threatened by other people (since much griping is really fear in disguise), begin to see others as vulnerable creatures who could use their help rather than sources of annoyance, and a kinship with others is acquired.

Doing good things can mean giving blood, donating money to the Sierra Club or other charity, volunteering with the Boy Scouts, tipping the hard working waitress trying to pay for college more generously, paying compliments to people around you, helping a neighbor carry the groceries when you see him struggling, showing a child how to make a paper airplane . . .

Good deeds can take a million different forms. But it must involve you personally. It can't mean delegating a helpful activity to your spouse. You must also do it frequently, not just once a year. It doesn't have to cost money, it doesn't have to involve a lot of time (though your personal bodily involvement does yield the greatest return in optimism). These are things anyone can do and help make the world around you a little better.

If taking these small steps towards an optimistic attitude are too much for you, then I would worry that you are destined to fail in dropping your heart scan score.

All posts by william-davis

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.