Take a niacin "vacation"

I've been seeing a curious niacin phenomenon that has not, to my knowledge, been reported anywhere in the medical literature.

People with lipoprotein(a), or Lp(a), are best treated with niacin, particularly given the relative lack of other effective therapies. I now have seen approximately 10 people with great initial responses to niacin, only to observe Lp(a) levels slowly drift back up to the starting level over a period of 2-3 years.

In other words, if starting Lp(a) is 200 nmol/l (approximately 80 mg/dl), drops to 70 nmol/l on niacin. Then, over 2-3 years of treatment, it drifts back to 200 nmol/l. Very frustrating.

Somehow, your body's Lp(a) manufacturing mechanism circumvents the niacin, sort of like antibiotic resistance (without the bacteria, of course).

My response to this, though untested, is to have people take an occasional "niacin vacation". I don't mean take a trip to the Bahamas while on niacin. I mean take 2 weeks off from niacin every three months or so. My hope is that the occasional vacation from niacin will allow the body to continue to respond and suppress "resistance". When resuming niacin, you may have to escalate the dose gradually to avoid re-provoking the "flush".

The same "resistance" seems to develop to testosterone in males: an initial drop followed by a gradual increase. Curiously, I've not seen this in females with estrogens, which seems to generate a durable Lp(a) suppressing effect. For this reason, an occasional testosterone "vacation" might also be considered.

So far, I've advised several people to try this. The long-term success or failure, however, is uncertain. I know of no other solutions, however.

If you have Lp(a) and are on long-term niacin, you should consider talking about this issue with your physician. Like many aspects of Lp(a), while fascinating in its complexity, much remains uncertain. Stay tuned.

When LDL is more than meets the eye

Jerry wanted to know what to do with his LDL cholesterol of 112 mg/dl. "My doctor said that it's not high but it could be better."

So I asked him what the other numbers on his lipid panel showed. He pulled out the results:

LDL cholesterol 112 mg/dl

HDL 32 mg/dl

Triglycerides 159 mg/dl


I pointed out to Jerry that, given the low HDL and high triglycerides, his calculated LDL of 112 was likely inaccurate. In fact, if measured, LDL was probably more like 140-180 mg/dl. LDL particles were also virtually guaranteed to be small, since low HDL and small LDL usually go hand-in-hand (though small LDL can still occur with a good HDL).

So Jerry's LDL is really much higher than it appears. To prove it, Jerry will require an additional test, preferably one in which LDL is measured, such as LDL particle number (NMR), apoprotein B, or "direct" LDL.

It's really quite simple. Jerry likely has a high number of LDL particles that are too small. This pattern confers a three- to six-fold increased risk for heart disease.

Treatment requires more than just reducing LDL. Small LDL--an important component of this pattern, responds, for instance, to a reduction in processed carbohydrates like wheat products (breads, breakfast cereals, pretzels, etc.), NOT to a low-fat diet. Weight loss to ideal weight, especially loss of abdominal fat, will yield huge improvements in these numbers. Niacin may be a necessary component of Jerry's treatment program, since it increases LDL size and raises HDL.

For more discussion on measures superior to LDL cholesterol, see my upcoming editorial, Let Dr. Friedewald Lie in Peace (an expansion of a previous Heart Scan Blog). It will be posted on the Cardiologist on Call column on the Track Your Plaque website within the next week.)

Oil-based vitamin D


As time passes, I gain greater and greater respect for the power of restoring vitamin D blood levels to normal, i.e. 50-70 ng/ml. Just yesterday, I saw several people with blood levels of <10 ng/ml--severe deficiency.

Vitamin D deficiency this severe poses long-term risk for osteoporosis, arthritis, colon cancer, prostate cancer, inflammatory diseases, diabetes, and heart disease. Vitamin D appears to make coronary plaque reversal--reduction of your heart scan score--easier and faster.

But it is important that you take the right kind of vitamin D. Several of the people I saw yesterday with vitamin D levels of somebody living in total darkness were taking vitamin D, but they were taking tablets. Tablets are the wrong form. Powder-based tablets, in my experience, yield little or no rise in blood levels. Some preparations generate a small rise but the dose required is huge.

If you're going to take vitamin D, take a preparation that yields genuine and substantial rises in blood levels. This requires an oil-based capsule. I commonly see blood levels of 25-OH-vitamin D3 rise from, say, 10 ng/dl to 60 ng/ml when oil-based capsules are taken.

The most common dose I prescribe to patients is 2000 units per day to females, 3000-4000 units per day to males in non-sun exposed months. Ideally, your dose is adjusted to blood levels.

The Vitamin Shoppe preparation pictured here is one I've used successfully and generates bona fide rises in blood levels. And it costs around $5. Just be sure the preparation you buy is oil-based.

For rapid success, try the "fast" track

Have you tried fasting?

Before your eyes glaze over, let me tell you what I mean. I don't mean a water-only fast for two weeks while you drool over all the temptations around you and you feel sorry for yourself.

I also don't mean the juice fasts that some people use that turn into fruit juice fasts of pure sugar.

Here's another way to do it. Usually, 48 hours of doing this will yield several benefits:

--Weight loss of 1 lb. You will likely experience an even greater weight loss of 2-4 lbs, but much of this will be water loss.

--If you're like me and share a heightened sensitivity to sugars and carbohydrates (like wheat), you may find out just how awful you feel when you eat certain foods. Many people tell me they feel absolutely wonderful when they fast--clearer thinking, increased energy, improved mood. Not the constant gnawing urge to eat they expected.

--After your fast is over, you look back and realize just what large portions of food you were eating. You'll be content with smaller quantities--and enjoy it more.


The "fast" I've used successfully includes two foods:

1) Vegetable juices--that you either juice yourself or purchase. V8 or its equivalent works pretty well. Though purchased V8 is not the best, it's better than nothing and does work reasonably well. If you juice your own vegetable juices, watch out for the diarrhea if you're unaccustomed to vegetable juices. Four 8 oz glasses per day works well.

2) Soy milk--for a source of protein and modest quantity of sugar and fat. I like the Light Silk Soymilk (Vanilla) which contains 80 calories, 2 g fat (0.5 g monounsaturated), 7 g sugar, 6 g protein per 8 oz glass. Four 8 oz glasses of soymilk also work well. In my neighborhood, 8th Continent is another good choice.


Sip both of these throughout the day. Of course, drink water in unrestricted amounts.

What can you expect in your coronary plaque control/heart scan score reversal program? When the fast is over, a rise in HDL, reduction in small LDL, reduction in triglycerides, reduction in blood sugar and insulin, and a smaller tummy. This strategy can be useful to kick-start weight loss efforts or as a periodic way to maintain control over weight and lipid/lipoprotein patterns.


Nutritional Composition Silk Soymilk--Vanilla

Nutrition Facts
Serving Size 1 cup (240mL)
Servings per container 8 H/G OR 4 QT

Amount per Serving

Calories 70
Calories from Fat 20

% Daily Value
Total Fat 2g 3%
Saturated Fat 0g 0%
Trans Fat 0g
Polyunsaturated Fat 1g
Monounsaturated Fat 0.5g

Cholesterol 0mg 0%
Sodium 120mg 5%
Potassium 300mg 8%
Total Carbohydrates 8g 3%
Dietary Fiber 1g 4%
Sugars 6g
Protein 6g
Vitamin A 10%
Vitamin C 0%
Calcium 30%
Iron 6%
Vitamin D 30%
Riboflavin 30%
Folate 6%
Vitamin B12 50%
Magnesium 10%
Zinc 4%
Selenium 8%

No flush = No effect



"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."


That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.

"Black holes" on heart scan


Lots of smokers, especially younger smokers, rationalize their habit by telling themselves that they'll stop if and when any hint of adverse health effects develop.

The problem is that, even in the first decade of smoking, dramatic and profound effects can develop--but you won't know it.

One of the most graphic examples of this I see every day in people who have heart scans. While CT heart scans are, of course, for identification of coronary plaque/coronary disease, they're also great for visualizing the lungs.

This man is a light smoker. The lungs are the black tissues (that's normal) on either side of the (white) heart in the center. Now, note the holes in the lung tissue. That's what they literally are: holes left by the destrucive, tissue-eating effects of cigarette smoking.

How common are the holes (or emphysematous "blebs", as they're called in medical lingo)? Very common. You'll even see them in 30-somethings who've smoked only a few years.

These are holes that have nothing in them. The lung tissue that was destroyed to create the hole will never grow back, even when smoking stops. The holes in this example are actually small to average in size. I've seen much bigger. And this only represents the early stages of lung tissue destruction. A long-time heavy smoker shows all other sorts of abnormalities.

Whenever I show these "black holes" to people who smoke, they are horrified and I've actually gotten many people to quit. Take the opportunity to quit as soon as you can if you smoke.

Small LDL--a persistent bugger

Sometimes, small LDL is easy to get rid of. Take niacin, for instance, and it can simply disappear from your body.

But other times, it can be aggravatingly persistent. Several times every day, in fact, I need to run through the checklist of strategies to reduce small LDL with patients.

How important is small LDL? In my experience, it is among the most potent causes behind coronary plaque known. It's a big part of the explanation why some people at an LDL of cholesterol of X mg/dl will have heart disease, while others with the same X mg/dl of LDL will not. When present, small LDL particles are much more likely to trigger atherosclerotic plaque formation. Small LDL particles magnify Lp(a)'s ill-effects tremendously. The data vary but small LDL probably increases heart attack risk at least three-fold.



Here's a checklist of strategies that I advise patients to consider to minimize the small LDL pattern:


--Lose weight to ideal weight--This is very important and effective.


--Fish oil--A relatively small effect unless triglycerides are high to begin with.




--Reduction of wheat products--This can provide a BIG effect. More precisely, a reduction in high-glycemic index foods is effective. But the biggest day-to-day high-glycemic food culprits are wheat products like breads, pasta, crackers, chips, pretzels, and breakfast cereals. "You mean whole wheat bread makes small LDL?!" Yup.


--Reduction of sweets--For the same reasons as reducing wheat products.


--Add raw almonds and walnuts--1/4 to 1/2 cup per day.




--Replace wheat products with OAT products, especially oat bran. This does NOT mean oat-containing breakfast cereals with added sugar and wheat, e.g., Honey Nut Cheerios, Cracklin' Oat Bran Cereal, etc. You might as well eat candy. Buy oat bran as plain oat bran--nothing added. Use it as a hot cereal or added to yogurt, "breading" for chicken, etc.




--Vitamin D--A variable effect, likely resulting from its beneficial effects on "insulin resistance".


--Exercise


--Niacin--Very effective but not always enough.


Among the choices, my favorites are weight loss, niacin, and reduction of wheat products. Those will give you the biggest bang for your buck.

Red badge of courage

A group of 60- and 70-somethings were standing in the anteroom to the cardiac rehabilitation center. All (males) had their T-shirts pulled up, comparing their coronary bypass scars.

It reminds me of war veterans comparing their war wounds. The scars of suffering, of having "conquered" and won a war with a common enemy, a badge of courage.

This is part of the broad social acceptance of bypass surgery and other major procedures for heart disease. Hospitals support it. They do it for the psychological support for patients enduring a difficult process. Often, talking about a shared experience can be a helpful purge for the fears and frustrations of a traumatic event.

Curious thing, though. I've actually had people request bypass surgery simply because all their friends have had one. No kidding. "I just figure my time is coming. I might as well get it over with."

Get the picture? We've had a battle with heart disease and the hospitals have won. The enormous success of hospitals over the last 20 years is not because of delivering babies, it's not from psychiatric hospitalization, it's not from cancer treatment. It's from heart disease. The largest floors in the hospital are usually the cardiac floors. The bulk of revenues and profit are from heart disease.

If I manufacture widgets and each widget I sell makes me scads of money, guess what? I want to sell more and more widgets. I'll persuade people they need my widgets even if they don't. Perhaps I'll even persuade them that buying one is a noble cause. Maybe I'll subtly suggest that I am a charitable operation and I only sell my products for the public good. I could even name my company after a saint. Personal profit--absolutely not!

Ignore the hype. See hospitals and their "products" for what they are: A necessary service--some of the time; profitable products that they hope to sell to more and more people most of the time.

"We don't believe in heart scans"

Tim's CT heart scan score was an earth-shattering 3,447, clearly in the upper stratosphere of percentile rank. Risk of heart attack: 25% per year. At age 58, it was a wonder that nothing had happened yet.

Tim went to the Cleveland Clinic for an opinion, long a powerful bastion of heart procedures. The consulting cardiologist told Tim, "We don't believe in heart scans. They're wrong too often."

An opinion from a widely-respected cardiovascular center. If they don't "believe" in heart scans, does that mean they "believe" in stents and bypass surgery? Does it mean that the thousands of research studies that have now been published on the value of heart scanning are pure fiction? Is there a choice to believe or not believe?

I continue to be shocked at the extraordinary ignorance on the topic of heart scanning among my colleagues. The number one killer of Americans and you still rely on stress tests?

Why this perception that heart scans are "wrong too often"? What this cardiologist means, I believe, is that when people are taken to the cath lab for catheterization, a substantial number of those with positive heart scan scores don't have "blockage". But I could have told him that even before the heart catheterization.

There is an expected and well-documented likelihood of finding significant "blockage" based on your heart scan score. At Tim's scary score of 3,447, what is the likelihood of "blockage" of 50% or more? It's around 40-50%. That means that half the people at this score will have a blockage sufficient to justify inserting stents or undergoing bypass surgery, half will not. There will indeed be many plaques, but none severe enough to block flow.

Does that make the heart scan wrong? I don't think it does. Just because you don't need a major procedure to "fix" blockages does not mean that no heart disease is present. Without preventive efforts, Tim's heart attack risk remains an alarming 25% per year--whether or not he gets stents or bypass. The only treatments that substantially reduce this risk (in an asymptomatic person) are preventive efforts, not procedures.

Yet cardiologists like the one Tim consulted at the Cleveland Clinic regard heart scans as something "he doesn't believe in". I would suggest a return to the textbooks and published literature and re-thinking how heart disease should be managed.

Heart scans should provide an opportunity for prevention, not an opportunity for profit.

More on the “Rule of 60”

Despite its apparent simplicity, there’s a lot of thought and wisdom in the Rule of 60.

What if you achieve only a single value in the Track Your Plaque “Rule of 60”? What if, for instance, you got LDL down to 60 mg/dl, but ignored the fact that your HDL was 41 mg/dl and triglycerides were up to 145 mg/dl? Can you still do pretty well?

Probably not. In fact, this specific combination of low HDL and high triglycerides tells me several things:

1) LDL is really much higher than suggested by the 60 mg/dl, which is a calculated value, often much higher. Recall that calculated LDL is prone to immense inaccuracy. When measured, the LDL is commonly somewhere between 120 and 160 mg/dl. However, when you raise HDL to 60 and reduce triglycerides to 60, much of the inaccuracy is removed, i.e., calculated LDL becomes more accurate. LDL can be measured as LDL particle number (NMR), apoprotein B, or direct LDL.

2) LDL particles are small. This is yet another reason why the weight-based LDL measures can be inaccurate. Imagine you have two identical glass jars full of marbles. One jar has small marbles, the other has large marbles, but both jars have the same weight in marbles. Which jar has more marbles? The one with small marbles, of course. The same phenomenon occurs with LDL particles: at the same weight, you can have different numbers of LDL particles. It’s the number of particles that better determine risk for heart disease, not the weight.

3) Triglycerides of 145 mg/dl is actually below the target advised by the National Cholesterol Education Panel Adult Treatment Panel-III guidelines, i.e., you’re okay by conventional standard. But look beneath the surface, and you’ll find that triglycerides at 145 mg/dl are associated with flagrant excesses of VLDL lipoprotein particles and a greater likelihood of a postprandial (after-eating) disorder (increased IDL or postprandial triglycerides), both of which add to coronary plaque.

4) This pattern is also commonly associated with higher blood sugar, higher blood pressure, increased inflammation (e.g., C-reactive protein), increased fibrinogen—all the facets of the metabolic syndrome, or pre-diabetes.

In fact, some of the most aggressive plaque growth—increasing heart scan scores—will occur with this specific pattern. So just achieving one facet of the Track Your Plaque Rule of 60 does not suffice. It’s the whole package that really stacks the odds in your favor of stopping or dropping your heart scan score.
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.