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.
All posts by william-davis

America: The world’s diet laboratory

Low-fat, low-carb, high-protein, Pritikin, Ornish, Atkins, South Beach, Sonoma, Sugar-Busters, Weight Watchers, vegetarian . . . Have Americans tried them all?

We’ve witnessed the relative success of diet habits in selected regions world-wide: the longevity of the Japanese on a spare soy and fish-based diet; the reduced heart disease incidence of the French despite an indulgent food-centered culture; the extreme heart disease-free lives of the Cretan Greeks.

Contrast this with the startling failure of the American diet experiment: We’re all (speaking for the collective whole) fat, diabetic, and miserably mired in the diseases of obesity. We’ve experimented with every possible iteration of diet from grapefruit or cabbage only, to calorie deprivation (a al Weight Watchers), to restricting this or that element of diet. The “official” organizations have made their contributions, as well: the American Heart Association’s Therapeutic Lifestyle Changes (formerly Step I and II diets), a program eerily similar to what Americans are already eating and resulting in failure; the American Diabetes Association diet, incomprehensibly embracing carbohydrates when they are the root of the nutrition-habit-gone-wrong that caused the disease in the first place; the USDA and their Food Pyramid, encompassing a design that contains the germ of wisdom but is so heavily overweighted in grains that it is a sure-fire way to increase weight and heart disease were you to follow their recommendations.

What have we learned from our grand experiment, our nationwide misadventure in nutrition?

I believe that we’ve learned how not to eat: Processed snack foods, meals delivered in a fast-food setting with the offer to “super-size” your order, make-believe food ingested in your car eaten for the sake of staving off the inevitable hunger pangs. Few would argue that these are certain paths to obesity and poor health.

Certainly, if we’ve learned how not to eat, can we extrapolate just how to eat? And not just for weight loss, since most diets focus just on that, but on health, particularly heart health?

If Americans have so far failed to learn the lessons of the nutritional world, we certainly have not failed at talking about it. From books to blogs, websites, information gurus to infomercials, we certainly celebrate the capacity to share our experiences, our grief over our nutritional “misfortune,” despite a world of plenty.

Yet we swim in a sea of information. Can we sift through the chaff to discover the essential truth?

Let me articulate an extreme (extreme meaning closer to the truth, I hope) interpretation of nutritional wisdom:

--If it requires a label or nutritional analysis, reject it. The wondrous green pepper, or bottle of olive oil, for instance, require no such qualifications. Some exceptions: milk, yogurt, cottage cheese (unless, of course, you purchase straight from a local producer). I am always impressed with the contortions and frustrations people experience trying to decipher labels. Ironically, the healthiest foods don’t even require labels.

--If it is ingested in a rush, it’s likely to add to poor health. True food is meant to be consumed at leisure, not in haste to satisfy some irrational, unthinking impulse.

--Search for natural, whole foods. Natural, whole foods require no marketing. You pay a premium for a company to adorn a product with glitz, glamour, and appeal. Repackage Cocoa Puffs as chocolate flavored, round overly-processed wheat flour, sans marketing spin, and what is left? Processed foods are?intentionally?addictive. They are added to, modified, high-fructose corn syruped, etc. to increase desirability, but also create addiction. Eliminate them just as a smoker eliminates cigarettes.

--A corollary to the above issue: purchase foods that appear as if you had grown it or raised it yourself. If you were to grow corn in your backyard garden, you would eat it on the cob or some similar way. You would not grind it, pulverize, process it, nor serve it as cornstarch and add to a pile of chemicals to make breakfast cereal. Eat foods in their natural state, not the highly processed food-product that requires a colorful package and advertising to sell.

--Don’t keep bags of chips, boxes of breakfast cereal and crackers, frozen dinners, all “just in case.” Don’t allow yourself that opportunity because you will more than likely seize it. An alcoholic who keeps a secret bottle of gin hidden in the cabinet is well aware that it’s there and will eventually give in to impulse.

--When you eat meat, try to find free-range, organic products. Even better, purchase from a local producer who you trust.

--For anyone with patterns like low HDL, small LDL, high triglycerides, and blood sugar >100 mg/dl, following a diet that is as free of wheat products as possible will yield enormous benefits. Wheat is a part of all breads, virtually all breakfast cereals, pretzels, crackers, bagels, cookies, cupcakes, pancakes, waffles, etc. Going wheat-free is also a surprisingly effective weight loss strategy.

That’s just a few thoughts. The approach we use in the Track Your Plaque program helps achieve weight loss, but also helps correct lipoprotein patterns, often dramatically.

Many diets have failed to keep pace with the changing nutritional habits of Americans. In 1960, we ingested close to zero high-fructose corn syrup. We’re now approaching 80 lbs per year per American. Breakfast cereal in 1950 consisted of a handful of products, eaten intermittently; today, it is a staple with enough products to fill a modern supermarket’s entire aisle. Meats have changed, thanks to the factory farm phenomenon feeding its animals corn in inhumanely restricted conditions, a dietary shift for livestock that has modified the fat composition to something far different than 50 years ago, not to mention the antibiotics and other chemicals used to accelerate growth and fight off infection from the artificial, overcrowded conditions.

The American nutritional shift, along with rampant obesity, have also caused a relatively new cause of coronary heart disease to explode: small LDL particles. The contribution of small LDL has been enormously underestimated, since most physicians don’t know what it is, don’t know how to check for it, and don’t know what to do with it. Yet it has emerged as the number one cause for heart attack and heart disease nationwide.

Stay tuned for our rewritten New Track Your Plaque diet to be released as a Special Report on the www.cureality.com website in future.

Dr. Jarvik, is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to scare the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Niacin bad. Lipitor good. Even celebrity doc says so. Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he serves as spokesman (or at least figurehead) for this $13 billion dollar a year drug? Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs?

Jarvik has never--never--actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from? It's beyond me. Perhaps it was the thousands of dollars likely paid to him. That will make an "expert" out of just about anybody.

Robert Bazell, science reporter, for CNBC, made this report on the Jarvik-Lipitor connection in his March, 2007 report, Is this celebrity doctor's TV ad right for you?

Mr. Bazell writes:

On May 16, 1988, an editorial in the New York Times dubbed the artificial heart experiments, “The Dracula of Medical Technology.”

“The crude machines,” it continued, “with their noisy pumps, simply wore out the human body and spirit.”

Since then, in a series of start-up companies, Jarvik has continued his quest to make an artificial heart — as have several other firms. One competitor recently won FDA approval to sell its device for implantation in extreme emergencies.

Perhaps Jarvik’s chances of success with another artificial heart account for his willingness to serve as pitchman for Pfizer. I inquired, without success, to find the going rate for a semi- celebrity like Jarvik to appear in such ads. Thomaselli of Advertising Age said whatever it is, it is “infinitesimal” compared to Pfizer’s expenditures of $11 billion a year on advertising, much of it for Lipitor.

Why spend so much marketing Lipitor?

Because Lipitor is only one of six drugs in the class called statins that lower cholesterol. Many cardiologists say that for the vast majority of people any one of these drugs works just as well as the other. Two of them, Mevacor and Zocor, have already lost their patent protection so they cost pennies a day compared to $3 or more a day for Lipitor.

In 2010, when Lipitor loses its patent protection, it, too, will cost pennies a day, and Pfizer will no longer need Dr. Robert Jarvik.



So, is niacin so bad after all? Or is this Everyday Health report just another clever piece of advertising for Pfizer?

Is niacin as bad as it sounds?

A popular health newsletter, Everyday Health, carried this headline:

A Cholesterol-Busting Vitamin?

Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter?
Find out how niacin can help reduce choleseterol.


At doses way above the Recommended Dietary Allowance — say 1,000–2,500 mg a day (1–2.5 grams) — crystalline nicotinic acid acts as a drug instead of a vitamin. It can reduce total cholesterol levels by up to 25%, lowering LDL and raising HDL levels, and can rapidly lower the blood level of triglycerides. It does so by reducing the liver’s production of VLDL, which is ordinarily converted into LDL.


I'd agree with that, except that it is rare to require doses higher than 1000-1500 mg per day unless you are treating lipoprotein(a) and using niacin as a tool for dramatic drops in LDL. But for just raising HDL, shifting HDL into the healthy large class, reducing small LDL, and for reduction of heart attack risk, 1000-1500 mg is usually sufficient; taking more yields little or no further effect.

But after that positive comment comes this:

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. . . However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.


Strange. After a headline clearly designed to pull readers in, clearly stating niacin's benefits, the article then proceeds to share the pants off you with side-effects.

But look to the side and above the text: Ah . . . two prominent advertisements for Lipitor, complete with Dr. Robert Jarvik's photo. "I've studied the human heart for a lifetime. I trust Lipitor to keep my heart healthy."

Sounds like bait and switch to me. "You could try niacin--if you dare. But you could also try Lipitor."

Who is Dr. Jarvik, anyway, that he stands as the spokesman (or at least figurehead) for this $13 billion dollar a year drug. Of course, he is the 1982 inventor of the Jarvik artificial heart, surely an admirable accomplishment. But does that qualify him to speak about heart disease prevention and cholesterol drugs? Jarvik has, never actually prescribed Lipitor, since he never completed any formal medical training beyond obtaining his Medical Doctor degree, nor has he ever had a license to practice medicine. He does, however, continue in his effort to provide artificial heart devices, principally for implantation as a "bridge" to transplantation, i.e., to sustain a patient temporarily who is dying of end-stage heart failure.

So where does his expertise in heart disease prevention come from?

Omega-3 fatty acids: Frequency vs. quantity

I believe I have been observing an unexpected phenomenon: When it comes to fish oil and omega-3 fatty acids, the frequency of dosing may be as important, perhaps more important, than the actual dose.

First of all, why advocate omega-3 fatty acids from fish oil? There’s a list of lipid/lipoprotein reasons, including reduction of triglycerides and triglyceride-containing particles (VLDL, intermediate-density lipoproteins), reduction of small LDL, and increase in HDL. There’s also solid benefit in reduction of heart attack risk, reduction in death from heart attack, and reduction in stroke. There are also anti-inflammatory benefits and improvements in mood, reduction in depression.

Fish oil is a crucial ingredient in the Track Your Plaque program. I am honestly uncertain of just how much success we would give up if fish oil were NOT a part of the program, but I am unwilling to find out. The data are simply too compelling to not include omega-3 fatty acids from fish oil. Of course, supplementation of omega-3 fatty acids assumes greater importance in a modern world in which your food has become terribly depleted of the omega-3 fraction of oils. (Cultures that rely heavily on fish or wild game probably would not benefit to the same extent, since these foods contain omega-3 fatty acids.)

But I believe I have observed a curious effect over the past year or two. With the proliferation of many different preparations of fish oil that provide seemingly endless choices—low-potency fish oil, high-potency fish oil, paste forms of fish oil like Coromega, liquids such as Carlson’s, etc.¾I’ve observed that frequency of dosing may exert as much of an effect as the dose.

For example, someone might take the basic, low-potency preparation like Sam’s Club that contains 180 mg EPA and 120 mg DHA per capsule, four capsules per day. That yields a total of 1200 mg EPA and DHA per day. This is our minimum dose that provides the basic heart attack-reducing effect, though with modest effect on triglycerides and associated patterns.

Say someone switches to a high-potency preparation of 360 mg EPA and 240 mg DHA, providing a total of 600 mg omega-3 fatty acids per capsule, or twice the dose of the low-potency preparation. Would you expect double the effect?

Curiously, no. What I have observed, however, is that more frequent dosing may provide a larger effect. The least effective dosing is once per day; twice per day is far more effective. Three times per day¾though cumbersome¾provides even greater effect.

So, which is more important: dose or frequency?

I can’t say for certain, since my observations are informal and have not been obtained by a formal statistical analysis of our data. That will come with time.

For the present, suffice it to say that, if you are struggling with suppression of patterns like increased triglycerides, IDL, or low HDL, then at least twice- or three-times-per-day dosing might be worth considering, even before you increase the dose further.

Best: Greater dose, or higher-potency preparation, combined with higher frequency.

Lipoprotein testing

This is an update of a post I made about a year ago. However, I'm reposting it since the question comes up so often.


How can I get my lipoproteins tested?
This question came up on our recent online chat session and comes up frequently phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. That’s the best way. However, it is also the most difficult. Lipoprotein testing, despite over a decade of considerable scientific exploration and validation in thousands of research publications, still remains a sophisticated tool that only specialists in lipids will use. But this provides you with the best information on you’re your lipoproteins mean.
2) If you don’t have a doctor who can provide lipoprotein testing and interpretation, go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (ultracentrifugation). None of them will provide you with the names of actual physicians. They can provide you with the name of a local representative who will know (should know) which doctors in your area are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.

3) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area. One drawback: Most lipidologists have been heavily brainwashed by the statin industry and tend to be heavy drug users.

4) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method and, frankly, it is very time consuming. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s better than nothing.

5) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60. It’s sometimes a necessary compromise.

Our discussions on the Track Your Plaque Forum have impressed me with the difficulty many people encounter in getting lipoproteins drawn and interpreted. Some of our Members have been very resourceful identifying blood draw laboratories around the country, such as Lab Safe, that will at least provide the blood draw service.

I wish it was easier and we are working on some ideas to facilitate this nationwide. It will take time.

In 20 years, this will be a lot easier when doctors more commonly use lipoprotein testing. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

Is it exercise or diet?

Wayne, a 61-year old retired school superintendent, had been an exercise fanatic all his adult life. If not running long distances and occasional marathons, he'd bike up to 70 miles a day. He did this year-round. In cold weather, he set his bicycle up on an indoor device and also ran on a treadmill and added weight training.

That's why it was kind of surprising that he sported a large belly. At 5 ft 8 inch and 190 lbs, that put his Body Mass Index (BMI) also high at 28.8 (desirable <25). You'd think that vigorous, almost extreme, exercise like this would guarantee a slender build.

Wayne also had lipoproteins to match: triglycerides 205 mg/dl, LDL 176 mg/dl but LDL particle number much higher at 2403 nmol/l (an effective LDL of 240 mg/dl); 75% of LDL particles were small.

I asked Wayne about his diet. "I eat healthy. Cheerios for breakfast usually. Some days I'll skip breakfast. Lunch is almost always a sandwich: tuna, turkey, something like that on whole wheat bread or a whole wheat bagel. Chips, too, but I guess that's not too healthy. Dinners vary and we eat pretty healthy. Almost never pizza or junk like that."

"Pasta?" I asked.

"Oh. sure. Two or three tiems a week. Always whole wheat. With a salad."

Wayne was well aware of the conventional advice for whole grains and, indeed, had been trying to increase his intake, particularly since his basic cholesterol numbers had been high in past. To his surprise, the more he tried at diet, the more LDL seemed to go up, as did triglycerides.

I see this situation every day: The obsession with processed carbohydrate foods, worsened by the message perpetuated by the American Heart Association, the USDA Food Pyramid, Kraft, Kelloggs, Post, etc. Eat more fiber, eat whole grains.

NY Times columnist, Jane Brody, chronicles her (embarassing) mis-adventure following the same mis-guided advice in Cutting Cholesterol, an Uphill Battle.

According to the USDA Food Pyramid, Wayne is not getting enough grains and whole grains, particularly since he is highly physically active. Consistent with the message given by the food industry: "Eat more!"

The food industry-supported Whole Grain Council advises:

Whole Grains at Every Meal
The US Dietary Guidelines recommend meeting the daily requirement by eating three "ounce-equivalents" of breads, rolls, cereals or other grain foods made with 100% whole grains. A slice of bread or a serving of breakfast cereal usually weighs about an ounce.

Want an easier way to think about it? Just look at your plate at each meal, and make sure you've included some source of whole grains. That's why our slogan is "Whole Grains at Every Meal."



By this scheme, if you are overweight, it's because you lack fiber and you're too inactive. "Get up and go!" It's not the diet, they say, it's you!

See through this for what it is: Nonsense. Wayne was overweight, packing 20 extra pounds in his abdomen from his over-dependence on processsed carbohydrates--"whole grains"--not from inactivity.

Instant heart disease reversal


What if reversal of heart disease--regression of coronary atherosclerotic plaque--were achievable instantly? Just add water and--voila!!

To my knowledge, it is not--yet. But I sometimes play with this idea in my head. I could imagine that such a program would consist of a few essential elements:

--A fast or semi-fast, or at least a very spare diet, over a period like 10 days to promote net catabolism. It is also supremely anti-inflammatory to restrict calories.

--High-dose vitamin D, e.g., 20,000 units per day of D3 to fully replenish depleted stores and achieve all the metabolism-correcting effects of D3 restoration.

--EPA + DHA at a higher than usual dose with frequent throughout-the-day dosing to encourage replacement of cellular lipid constituents with the more stable omega-3 fraction of fatty acids.

Beyond this, I'm uncertain. What role l-arginine, statins, niacin . . . conjugated linoleic acid? ApoA1 Milano infusions?

This is simply whimsical at this point. I don't know if such an approach would work. But if it did, you might imagine that it would offer an opportunity--for the properly motivated--as an alternative treatment for angina, advanced coronary disease, a means to pull someone back from the brink.

With the insights gained from our slow-but-powerful Track Your Plaque approach, perhaps we will also gain insights into how to accelerate such a process of reversal so that it is achievable in days, rather than months or years.

The small LDL epidemic

Ten years ago, small LDL was fairly common, affecting approximately 50% of the patients I'd see. For instance, an LDL particle number of 1800 nmol/l would be 40-50% small LDL in about half the people.

But in the last few years, I've witnessed an explosion in the proportion of people with small LDL, which now exceeds 80-90% of people. The people who show small LDL also show more severe patterns. 80-90% small LDL is not uncommon.

Why the surge in the small LDL pattern? Two reasons: 1) The extraordinary surge in excess weight and obesity, both of which favor formation of small LDL particles, and 2) over-reliance on processed carbohydrates, especially wheat-based convenience foods.

The constant media din that parrots such nonsense as the report on CNN Health website, Healthful Breakfast Tips to Keep You Fueled All Day, helps perpetuate this misguided advice. The dietitian they quote states:

"If you don't like what you're eating, you won't stick with it. If your choices aren't the most nutritious, small tweaks can make them more healthful. For example, if you have a sweet tooth in the morning, try a piece of nutty whole-grain bread spread with a tablespoon each of almond butter (it's slightly sweeter than peanut butter) and fruit preserves instead of eating foods that offer sweetness but little nutritional benefit, like doughnuts or muffins. If you enjoy egg dishes but don't have time to prepare your favorite before work, try microwaving an egg while toasting two slices whole wheat or rye (whole-grain) bread. Add a slice of low-fat cheese for a healthful breakfast sandwich that's ready in minutes. And don't overlook leftovers. If you feel like cold pizza (which contains antioxidant-filled tomato sauce, calcium-rich cheese, and lots of veggies), have it. It's a good breakfast that's better than no breakfast at all."

It sure sounds healthy, but it's same worn advice that has resulted in a nation drowning in obesity. The food choices advocated by this dietitian keep us fat. It also perpetuates this epidemic of small LDL particles.

If you have small LDL and its good friend, low HDL, it's time for elimination of wheat products, not some politically-correct silliness about increasing fiber by eating whole grains. Whole grains create small LDL! Or, I should say, what passes as whole grains on the supermarket shelves.

For some helpful commentary on this issue, see Fanatic Cook's latest post, Playing with Grains.

Mini-dose CTA?

I caught this little news report in the online edition of Canyon News , an LA paper, under the title Cedars-Sinai Develops Test to Prevent Heart Attacks .

They report that Dr. Daniel S. Berman M.D., chief of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai, reports that a new method of performing CT coronary angiography, "mini-dose CTA," has been developed that allows both coronary calcium scoring as well as CT coronary angiography (CTA) at a dose as low as 10% of standard dose. No technical details were provided.

Now, that may be worth knowing more about. If this is true, then CTA may indeed be useful as a "screening" procedure. However, we are going to need to know more: What devices are capable of doing this, what settings on the devices were used, etc. It does indeed come from a reputable source in Dr. Dan Berman, who is well known in nuclear cardiology circles.

We will try and dig for info. Stay tuned.
All posts by william-davis

What to eat: Part I

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.