Do stents prevent reversal?

I've seen this phenomenon several times now: A highly-motivated Track Your Plaque participant with a stent in one artery will do all the right things--lose weight, achieve 60:60:60 in basic lipids, identify and correct hidden lipoprotein disorders, take fish oil, correct vitamin D, etc.

Follow-up heart scan shows dramatic reduction in scoring in the two arteries without stents--30% per artery. But the artery with the stent will show marked increase in scoring above and/or below the stent. (It's impossible to tell what happens in or around the stent itself from a calcium scoring standpoint, since steel looks just like calcium on a CT heart scan.) In other words, there is marked plaque growth in the vicinity of the stent, despite the fact that dramatic reversal of atherosclerosis has occurred in other arteries without stents.

Should we take this to mean that a stent destroys the opportunity for atherosclerotic plaque reversal in the stented artery? I don't know, but I fear this may be true. What dangers does this different sort of plaque pose? Is it the result of the injury imposed at time of stent implantation, some modification of flow or biologic responses as a result of the presence of the stent?

These are all unanswered questions. But I believe that it is yet another suggestive piece of evidence that the best stent is no stent at all.

At what score should I have a heart cath?

This question comes up frequently: At what specific heart scan score should a heart catheterization be performed? In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necesary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should autmatically prompt a major heart procedure like heart catheterization in a person without symptoms.

Niacin makes NY Times

In the wake of the crash and burn of Pfizer's torcetrapib, media attention has turned up the miracles of . . .good old niacin. The NY Times carried a well-written report on niacin in its recent report, An Old Cholesterol Remedy Is New Again.


(Read the entire report at http://www.nytimes.com/2007/01/23/health/23consume.html?em&ex=1169701200&en=670fa84ae2ea648c&ei=5087%0A)

Among their comments:

...torcetrapib worked primarily by increasing HDL, or good cholesterol. Among other functions, HDL carries dangerous forms of cholesterol from artery walls to the liver for excretion. The process, called reverse cholesterol transport, is thought to be crucial to preventing clogged arteries.

Many scientists still believe that a statin combined with a drug that raises HDL would mark a significant advance in the treatment of heart disease. But for patients now at high risk of heart attack or stroke, the news is better than it sounds. An effective HDL booster already exists.

It is niacin, the ordinary B vitamin.

In its therapeutic form, nicotinic acid, niacin can increase HDL as much as 35 percent when taken in high doses, usually about 2,000 milligrams per day. It also lowers LDL, though not as sharply as statins do, and it has been shown to reduce serum levels of artery-clogging triglycerides as much as 50 percent. Its principal side effect is an irritating flush caused by the vitamin’s dilation of blood vessels.

Despite its effectiveness, niacin has been the ugly duckling of heart medications, an old remedy that few scientists cared to examine. But that seems likely to change.

“There’s a great unfilled need for something that raises HDL,” said Dr. Steven E. Nissen, a cardiologist at the Cleveland Clinic and president of the American College of Cardiology. “Right now, in the wake of the failure of torcetrapib, niacin is really it. Nothing else available is that effective.”

In 1975, long before statins, a landmark study of 8,341 men who had suffered heart attacks found that niacin was the only treatment among five tested that prevented second heart attacks. Compared with men on placebos, those on niacin had a 26 percent reduction in heart attacks and a 27 percent reduction in strokes. Fifteen years later, the mortality rate among the men on niacin was 11 percent lower than among those who had received placebos.

'Here you have a drug that was about as effective as the early statins, and it just never caught on,' said Dr. B. Greg Brown, professor of medicine at the University of Washington in Seattle. 'It’s a mystery to me. But if you’re a drug company, I guess you can’t make money on a vitamin.'



Of course, you and I don't have to wait for the media to endorse something. I'm nonetheless thrilled that this hugely helpful vitamin is gaining greater recognition. My preferred form nowadays is over-the-counter SloNiacin (Upsher Smith). Weve seen no liver side-effects and a minimal quantity of flushing. It's also reasonably priced, $13.99 for 100 tablets of 500 mg at Walgreen's. That's a lot cheaper than prescription Niaspan at $130 for 60 tablets.

Perhaps the notoriety will cut back on the silly responses from some physicians that I still hear about from patients: "My doctor said to stop the niacin because it's going to destroy my liver."

Wheat: the nicotine of food

Yes, we know that wheat contributes to creating small LDL, drops HDL, raises triglycerides, and VLDL. We also know it indirectly slows the clearance of after-eating fats from the blood (curious, I know). Wheat products also increase inflammation (C-reactive protein), raise blood sugar, and contribute tremendously to diabetes.

What many people don't know is that wheat products also have an addictive quality: have one donut and you want another. It's true for bread, breakfast cereals, pretzels, cookies, etc. How many times have you had just one Oreo cookie?

Curiously, elimination of wheat products, unlike elimination of nicotine, usually causes the cravings to disappear. In other words, if you stop smoking cigarettes, the desire to smoke doesn't go away. With wheat products, the often overwhelming desire for more wheat products often just goes away.

But most people are simply unable to dramatically reduce or eliminate wheat products from their daily diet and therefore struggle each and every day with excessive cravings for bagels, donuts, cookies, breads, etc.

Try this useful experiment: Eliminate wheat products for a month and see what happens. Most people drop blood pressure, lose the tummy excess, feel more alert, see a drop in blood sugar, experience improvements in lipoproteins, and regain control over appetite.

Good time for a heart attack?

Man Has Heart Attack At Right Place, Right Time

If Robert Ricard had picked the wrong restaurant for lunch, he might have died.

The 71-year-old Michigan man suffered a heart attack shortly after ordering a glass of wine with friends at Bentley's Roadhouse on Saturday.

Luckily, a disaster medical team was sitting nearby.



A TV station in Michigan reported the above story. You've heard these "if it wasn't for ___, so and so would have died" stories. They're reported in all cities at one time or another.

What amazes me about these common local stories is that they're accepted at all. The question that comes to my mind is "Why couldn't the heart attack have been averted in the first place?" Early identification then, as close as humanly possible, elimination of risk would have been a preferable path.

Of course, it may not be the role of the media to cast judgement on why and how the entire episode could have been completely prevented from occurring. But you shouldn't fall into the same trap of complacency. We cannot expect others to save us when the "big one" hits. Your best assurance is to never have one in the first place.

How good is the South Beach Diet?

I'm a fan of the South Beach Diet.

Though it is billed as a program for weight loss (for which it is very effective), it is really a program for health. The basic approach of South Beach involves:

Eat good fats — Choose good fats from olive oil, canola oil, peanut oil, flaxseed oil, walnut oil, avocados, nuts, and fish. Omega-3 (fish oil) supplements are also fine.


Eat good carbs — Good carbs include high-fiber, nutrient-dense fruits, vegetables, legumes, and whole grains.

Eat lean protein — Good sources include eggs, low-fat dairy, nuts, seeds, legumes, skinless white-meat poultry, fish, shellfish, lean cuts of meat, and vegetarian options such as tofu.

(From The South Beach Diet, Dr. Arthur Agatston)


There's no doubt that South Beach can yield dramatic weight loss. In my experience, the success in weight loss depends on 1) how unhealthy your diet was in the first place, and 2) how long you can stick to Phase I, the inital phase during which weight loss is most dramatic. Some people have to periodically cycle back to Phase I to break a "plateau" or to lose faster.

But South Beach is also healthy. It has all the ingredients of a healthy eating program: Low saturated and hydrogenated fats, rich in monounsaturated fats, high fiber, low- to moderate- glycemic index, vegetables and fruits, lean proteins.

The Atkins' diet, in contrast, while very effective for weiglht loss, is an unhealthy process. I've seen lots of bladder infections, constipation, skin rashes, and kidney stones. That's just in the short term. If you stick to the "induction phase" (the no carbohydrate, low fiber, indiscriminate fat initial phase) for an extended period, I suspect that other adverse internal phenemena also develop that might not show for years, like cancer. But--it does work for weight loss!

South Beach's Phase I is also carbohydrate restricted, but steers you towards healthier foods, such as healthy oils from olive and canola, raw or dry roasted nuts, and lean proteins and vegetables.

What really makes South Beach special, however, are its clever recipes. Dr. Arthur Agatston (the author) involved chefs from the restaurants in the South Beach area of Miami to help create healthy yet delicious recipes. We've tried many of them and, while they are different from traditional fare, are delicious and satisfying for the most part.

Criticisms? None, really. But, when my patients choose South Beach (which I often encourage), I often have to impress on them that the Track Your Plaque program is not about weight loss. It is about seizing control of a potentially life-threatening disease. It is a far more important goal with greater implications. Weight loss is just one aspect of a coronary plaque control effort. For this reason, we sometimes have to make changes in the South Beach program to allow for correction of specific lipoprotein patterns.

The most common modification is in people with small LDL particles. This pattern often does indeed respond to weight loss and/or niacin. However, it occasionally persists despite these efforts. We then will ask the patient to continue to restrict the re-introduction of wheat products, though it is allowed after Phase I in South Beach. In other words, for this specific and sometimes difficult to control lipoprotein pattern, a spedific modification of the off-the-shelf South Beach program is sometimes necessary. Of course, the diet is created to suit everybody. Lipoprotein analysis permits detailed insight into your patterns and it's only to be expected that specific modifications might be needed.

But, as written, you can do quite well in your plaque control program by sticking to South Beach.

Be patient with niacin

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)


Some recent samples:


Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.





Heart attack kills groom at reception
A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.






Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.






Heart-attack victim to return to Hamburg stage


Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.



That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.

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.