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.

Homocysteine and coronary plaque

If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.

More Vitamin D and HDL

I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.