World record heart disease reversal

A quick but important note.

Track Your Plaque Members:

Keep your eyes on the Track Your Plaque Member website for details and images of our most recent huge success story. Track Your Plaque participant, Neal, dropped his score more than anyone else before.

Although reduction of heart scan score is an everyday event around here, a 51% drop in score deserves to make news!

We will post the images of Neal's heart scans on the www.cureality.com Member website in the coming days.

Dose of fish oil

Dosing for fish oil is a perennial point of confusion. However, it's quite simple.

The active ingredients in fish oil are DHA and EPA, the so-called omega-3 fatty acids. Of course, if there's anything else in your capsules, such as omega-6, omega-9, or linolenic acid, these should not count towards the sum of EPA + DHA, since they do not exert the same benefits as the omega-3s.

The basic suggested starting dose for the Track Your Plaque program is 1200 mg of EPA+DHA. This is usually provided by taking 4 x 1000 mg capsules of fish oil, providing 180 mg EPA, 120 mg DHA per capsules, for a total of 1200 mg EPA+DHA.

About a third of people, however, will require greater doses of omega-3s to reduce triglycerides, VLDL, and/or intermediate-density lipoprotein (IDL). Most people will do fine with an increase to 1800 mg EPA+DHA, usually provided by 6 x 1000 mg standard capsules. A very occasional person (about 1 in 100) will require even higher doses.

If you ever decide to change your fish oil preparation, or if you change to a more concentrated form or another form such as liquid fish oil (e.g., Carlson's), paste (e.g., Coromega), or syrup (e.g., Pharmax Frutol), then you will need to examine the label to determine the dose of EPA+DHA. If, for instance, a teaspoon of liquid fish oil provides 360 mg EPA and 240 mg DHA, that's a total of 600 mg omega-3s per teaspoon. If your EPA+DHA dose is 1200 mg per day, then two teaspoons a day should provide it. Always adding up the EPA+DHA content of whatever preparation you choose will therefore allow you to mix, match, or change your dose whenever you like.

Niacin scams

As most of you know, niacin (vitamin B3) is an important tool for many in the Track Your Plaque program.

Niacin:

--raises HDL cholesterol
--reduces small LDL
--reduces lipoprotein(a)

And it's the most potent agent we have for all three patterns, despite just being a vitamin. Niacin also reduces LDL cholesterol, VLDL, IDL, triglycerides; reduces heart attack risk dramatically either alone or in combination with other agents.

Unfortunately, some people who are either afraid of the "hot flush" side effect, or experience excessive degrees of it, have resorted to two preparations sold in stores that have none of these effects.

Most notorious is "No-flush" niacin, also known as inositol hexaniacinate. This compound is an inositol sugar molecule complexed with 6 ("hexa-") niacin molecules. Unfortunately, it exerts none of niacin's effects in the human body. No-flush niacin has no effect on HDL, small LDL, or Lp(a), nor on LDL or heart attack.

In short, no-flush niacin is a scam. It's also not cheap. I've met people who have spent hundreds of dollars on this agent before they realize that nothing is happening, including a flush.

Likewise, nicotinamide does not work. It sounds awfully close to the other name for niacin, nicotinic acid. But they are two different things. Like no-flush niacin, nicotinamide has no effect on HDL, small LDL, Lp(a), etc.

Though I've discussed this issue in past, somehow these two "supplements" seem to sneak back into people's consciousness. You walk down the health food store aisle and spy that bottle of X-brand No-flush niacin, promising all the benefits of niacin with none of the bother. Then you remember that rough night you spent a few months back when the hot flush lasted longer than usual. That's when some people end up buying this agent making extravagant--and false--promises.

For now, for all its imperfections, niacin is still a pretty darn good agent for these patterns. Remember that the best strategy to minimize the hot flush effect is to drink plenty of water. We generally recommend taking the dose at dinner along with water. If the hot flush occurs, drink two large glasses of water (total volume 16-24 oz). Nine times out of ten, the flush is gone. It also dissipates the longer you take niacin.

Media mis-information

This is an excerpt from a popular health website, EverydayHealth.com:


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 cholesterol…

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. It is also inexpensive. 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.

Many people begin treatment at low doses (250 mg twice a day, for example) and, over six weeks or so, gradually build up to an amount that lowers lipid levels, anywhere from 1,000 to 2,500 mg split between two doses during the day. This gradual approach may help build tolerance to side effects such as facial flushing. Although niacin is available over the counter, you should not use it in quantities sufficient to lower cholesterol without a physician’s supervision. It is important to test liver function and levels of blood sugar and uric acid before beginning niacin therapy and during the course of treatment.


(Bold emphasis mine.)

At http://www.everydayhealth.com/publicsite/index.aspx?puid=548e8630-32d6-41dd-91a7-48e1cbac65ad&p=4




After an enticing headline, the article goes on to scare the pants off you. It also sounds like accurate information, delivered in an unbiased way, cold and straight.

If we were to use niacin this way, it would indeed be intolerable for most. Do not follow the above nonsensical advice. But that may have been the intention from the start.


Very telling are the fact that, both above and below the article were colorful advertisements for Lipitor, complete with Dr. Robert Jarvik’s (inventor of an implantable mechanical heart) soothing, professorial image.

Did they want to bait us with promising information about cholesterol and niacin, only to throw water on our fire and steer us towards something else?

That would be typical drug company marketing.

All in all, I’m grateful for the attention the media provides for health issues. Perhaps many people wouldn’t even be aware of niacin and other healthy strategies if some website, newspaper, or magazine article hadn’t talked about it.

But I do worry about bias. Was this an unbiased report? Or was it more like much of the physician-directed mail I receive, cleverly concealed propaganda from the drug manufacturers? Who wrote it? No author is listed. Could it have been ghost written by someone in the drug company itself, or an arm of the drug company? That’s a very common practice for the literature physicians receive, glossy, high-class materials paid for by drug companies, written by drug company-owned companies, but no company logo or name listed.

My point: Be skeptical of what the media tells us. There’s usually a good deal of truth in the reporting, but there’s also often just enough mis-information or slanting of content to make you behave or believe a certain way. “If niacin is this dangerous, maybe I really should take the Lipitor.”

A dirty little secret

Here's a dirty little secret many people don't know about.

If I implant a stent, I might get paid somewhere around $2000 for the heart catheterization, stent implantation, femoral artery closure device, hospitalization charges. That's not too bad.

But what if I'd like more? What if I'd like to squeeze this unsuspecting patient for more, or actually his/her insurance company?

Easy: Add on complex procedures to the basic procedure that yield more professional charges. For instance, I could perform laser angioplasty, a procedure that adds another couple thousand dollars. I might pull out the old rotational atherectomy device, a high-speed diamond tipped drill that also adds substantial professional charges. I might also use the intracoronary ultrasound device, an otherwise helpful device, but I might pull it out to use on everybody.

With the exception of ultrasound, all the "add-on" procedures were more popular in the early and mid-1990s--before they were shown in clinical studies to provide no advantage, perhaps even add to procedural risks.

Thus, a patient might undergo a heart catheterization, balloon angioplasty with stent implantation into the proximal left anterior descending coronary artery (LAD), followed by laser angioplasty of the mid-LAD, followed by intracoronary ultrasound of the vessel. Next, rotational atherectomy of the circumflex, followed by stent and ultrasound. Total charges for this 2-3 hour procedure? Somewhere around $8000 to the cardiologist. Of course, hospital charges are far more.

Ironically, patients are invariably impressed. Hearing that they went through all sort of high-tech procedures makes them grateful for receiving the benefits of the skills of their cardiologist. Of course, they would like have done as well with a far simpler procedure. Perhaps they didn't need the procedure at all.

If the excessive use of procedures and devices fails to benefit patients, why don't hospitals discourage it? Two reasons: 1) It's difficult to legislate or regulate decisions made on judgement, which can be a tough issue with many fuzzy edges, and 2) hospitals made oodles more money from the practice.

If you have a salesman in your new car lot and he outsells all his colleagues by 30-50% and makes you a couple hundred thousand a month more in sales. You've watched him at work and he's clearly good at it. But you suspect that he pushes the envelope of propriety frequently--badgering customers, add rustproofing to a little grandmother's car that will be driven 3000 miles a year, selling cars for prices far above what they would have sold for had the customer bargained more vigorously.
do you put a stop to it at the risk of pushing your star salesman away? Few would.

Only a minority of my colleagues are guilty of this despicable practice. I only know of a few who openly do it. Hopefully, you're not among their patients.

The party’s over

A good number of cardiology colleagues are vigorously bashing the outcome of the COURAGE Trial. Recall that COURAGE is the large clinical trial recently released that showed that, in people with stable angina (chest pains), people did equally well with “optimal medical therapy” as with stents.

The problem is that many of my colleagues wouldn’t know what to do in a world deprived of implanting 10 stents a day. Giving people nitroglycerin/statin drug/aspirin/beta-blocker day after day, week after week, would be an awfully dull world. All the excitement of the cath lab would be a lot more rare. We’d actually have to wait for a heart attack from some dumb smoker! All the money would disappear, too. After all, seeing a patient in the office pays, at best, $200 (and has to be stretched to cover overhead expenses like staff, malpractice insurance, and rent). Putting a stent in can pay $2000, $3000, $4000, often more. Put in several a day and—Wow! Now we’re talking money.

You can understand how upsetting it is to my colleagues who feel like the rug may be pulled out from underneath their practices and lives. Feel as sorry for them as you do for people who lose their jobs on an assembly line because of robotic technology. Or travel agents because everyone makes travel arrangements over the internet. Technology, in this information technology, marches on.

Cardiologists, cath labs, stent manufacturers, and the huge industry built around heart disease had their party. Now it’s time to clean the room and sober up. The party’s over.

The broader acceptance of “optimal medical therapy,” as lame as it is, will eventually open the door for many to demand for something even better. Ever hear of Track Your Plaque?

More on being wheat-free

Reducing or even eliminating the wheat in your diet can dramatically enhance the phenomenon of insulin resistance.

Insulin resistance is the evil process that lies behind low HDL, high triglycerides, small LDL particles, and VLDL and IDL. It’s also the process that makes us tired after meals, heightens inflammation that raises your risk of heart disease, stroke, diabetes, and caner. Insulin resistance is the culprit behind the bulge hanging over some 100,000,000 American belts.

Show me a person with a protruding abdomen and I’ll show you a bread lover, or some other form of wheat.

Why do I pick on wheat so much? Many of you among the more nutrition-minded would point out that wheat is just one group of food items among many other high-glycemic index foods, i.e., foods that yield a vigorous surge in blood sugar (glucose), followed by a sharp decline. Wheat enjoys the high-glycemic index company of corn, rice (white and brown), potatoes, among others.

I pick on wheat because, for most Americans, wheat is 90% of the high-glycemic index problem. (I’m assuming you’ve at least eliminated or dramatically reduced highly-processed sweets like candy, cookies, soft drinks, cakes, etc. That’s a no-brainer.) It’s not uncommon to have a wheat-based product with every meal, a wheat-based snack, 7 days a week. But few people have corn products (i.e., corn starch products) three times a day. Or rice three times a day.

Wheat has traded places with saturated fat sources as the chief scourge of diet. In 1985, we had dinners of spare ribs, cheeseburgers, French fries, and butter on our mashed potatoes. Hardly anybody eats that like anymore, at least amongst the web-savvy set.

Wheat has assumed the previous exalted role as chief scourge as a consequence of the low-fat consciousness of the 80s and 90s. It has since ballooned in importance in diet and, as a result, skyrocketed as a cause of obesity, insulin resistance, and coronary plaque growth.

What if you're already slender and have none of the above issues, especially small LDL particles? Then don't sweat the wheat issue.

Note: My comments on being wheat-free should not be confused with gluten sensitivity or celiac disease. These are allergies to wheat gluten that, if undiagnosed, wreak havoc on health to extremes. This phenomenon is separate and distinct from the far more prevalent issue I’m discussing.

Can you break the “Rule of 60”

In the Track Your Plaque program, we aim for conventional lipid values (LDL cholesterol, HDL cholesterol, and triglycerides) of 60—60—60, i.e., LDL 60 mg/dl, HDL 60 mg/dl or greater, triglycerides 60 mg/dl. Most participants do indeed reach these target values.

When I tell this to colleagues, they’re stunned. “You can’t possibly get those numbers in most people.” And I can sympathize with their plight. After all, they are stuck with relatively lame tools: statin drugs, the American Heart Association diet. I’d be surprised if they ever achieved 60—60—60.

But can you drop your heart scan score even if you don’t reach the 60—60—60 targets? Yes, you can. The Rule of 60 is only a guideline, a tool that helps more people achieve our goals. The Rule of 60 does not guarantee reversal (drop in heart scan score), nor does not achieving the targets completely destroy your chances.

We have had many people drop their scores even if they haven’t reached the targets. On the other hand, we’ve also had people who failed at first, only to see success once they achieved the 60 mg/dl targets.

But which one are you? That’s the problem. We possess limited capacity to predict who will or who will not drop their scores from the start. We know that there are factors that stack the odds in your favor (e.g., optimism, lack of Lp(a), ideal weight, vitamin D >50 ng/ml, etc.). We know that there are factors that make it tougher (overweight, Lp(a), pessimistic attitude, underappreciated hypertension, higher heart scan scores, etc.) But at the start, we just don’t know who truly needs to adhere to the Rule of 60. So we suggest that everyone, at least in the beginning, aim to achieve it.

I had an exception the other day. Rich did everything by the Track Your Plaque book. However, a starting low HDL of 27 only rose to 37 after one year of effort—way below our 60 mg/dl target. Yet a repeat heart scan showed 23% reduction.

Why would Rich be so successful despite a persistently very low HDL? There may be a number of reasons. One explanation could be that conventional measures of HDL fail to distinguish between what HDLs truly work and what do not. Look at ApoA1 Milano; remember this story? The people in the secluded mountain village of Limone-Sul-Garde in northern Italy have HDL cholesterols of 8-15 mg/dl yet do not experience excess vascular atherosclerosis, suggesting that what little HDL they have is super-effective.

Yes, large HDL seem to be more healthy and effective than small HDL, but perhaps there’s more to it. However, nobody has a HDL effectiveness test ready for us to use.

In the meantime, we continue to suggest that the Track Your Plaque Rule of 60 be considered as a means of making plaque reversal as likely as possible. You and your doctor can always adjust in future, depending on your heart scan score results.

Non-profit hospitals

Hospitals hide behind a veil of non-profit.

Ostensibly operating for the public good, most hospitals enjoy all the business advantages of non-profit status. This means that any profits that flow to the bottom line at the end of the year are not subject to tax. Hospitals point out that profit margins are modest, often ranging from 2-6%.

What they don’t tell you is that, regardless of non-profit status, lots of money can be paid out along the way. A hospital CEO who pays himself $4 million dollars a year can work for this non-profit organization. He can also direct the hospital in business expansion: pharmacies, extended-care facilities, medicine and medical supply distributorships. Your friendly hospital CEO, as well as his many administrators, can hold positions in hospital subsidiaries, complete with salaries and perks.

Yes, most hospitals are officially non-profit. But that’s a designation for tax purposes. It does not mean that hospitals are non-lucrative.

I believe that it’s time for hospitals to drop the façade of “Saint” in their names or other religious names—Methodist, Baptist, Jewish, All Saints’. More accurate would be something like “ABC Medical Enterprises, Inc.” That way, the public would be quicker to recognize that they are dealing with a business run by people eager to make more money.

Wheat five times a day

Terri couldn't understand why her weight wouldn't drop.

At 5'3", 208 lbs., she had the typical mid-abdominal excess weight that went with small LDL, low HDL, high triglycerides, a post-prandial (after-eating) fat clearance disorder, high blood sugar, increased c-reactive protein, and high blood pressure.

She claimed to have tried every diet and all had failed. So we reviewed her current "strict" diet:

"For breakfast, I had Shredded Wheat cereal in skim milk. No sugar, just some cinnamon and a little Splenda. For lunch, I had low-fat turkey breast sandwich--no mayonnaise--on whole wheat bread. For snacks, I had pretzels between breakfast and lunch, and a whole wheat bagel with nothing on it before dinner. For dinner, we had whole wheat pasta with tomato sauce and a salad. While we watched TV, I did have a couple of whole wheat crackers.

"I don't get it. I didn't butter anything, I didn't sneak any sweets, cakes, I didn't even touch cookies. And I love cookies!"

Did you see the pattern? I pointed out to Terri that what she was doing, in effect, was eating sugar 5 or more times a day. Many of her meals, of course, contained no sugar. All were low fat. But the excessive wheat content yielded quick conversion to sugar--glucose--immediately after ingestion.

Repeated surges of blood sugar like this trigger the excessive insulin response that yields low HDL, higher triglycerides, small LDL, etc., everything that Terri had.

Terri was skeptical when I suggested that she attempt an "experiment": Try a four week period of being entirely wheat-free. This meant more raw nuts and seeds, more lean proteins like low-fat yogurt and cottage cheese, chicken, fish, lean red meats, more vegetables and fruits.

After only two weeks, Terri dropped 5 1/2 lbs. She also reported that the mood swings she had suffered, afternoon sleepiness, and uncontrollable hunger pangs had all disappeared. The mental cloudiness that she had experienced chronically for years had lifted.

What happened was that the load of sugar from wheat products, followed by an insulin surge then a precipitous drop in sugar, and finally fogginess, irritability, and cravings for food all disappeared. With it, the entire panel of downstream phenomena (small LDL, CRP, etc.) all faded.

Though she started out intending to complete a four week trial, I believe that, having seen the light, she will continue to be wheat-free, or nearly so, for a lifetime.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.

The costs of doing drug business?

Here's a telling situation.

Liz had been on prescription niacin, Niaspan, 1500 mg per day (3 x 500 mg tablets) for several years to treat her severe small LDL pattern and familial hypertriglyceridemia (triglycerides 500-1000 mg/dl). Because her health insurance had been paying for the "drug," she insisted on taking the prescription form.

A change in insurance, however, meant that the Niaspan was no longer covered. Her pharmacy wanted to charge $227 per month.

Liz came to the office in tears, worried that she was going to have to choke up $227 per month. I reminded her that, as I had told her several years ago, she could easily replace the Niaspan with over-the-counter Sloniacin or Enduracin. Both release niacin over approximately 6 hours, just like Niaspan.

Here are the prices I've seen with Sloniacin, 100 tablets of 500 mg:

Walgreens: $15.99
Walmart: $12.99
Costco: $8.99

So the most expensive source, Walgreens, would cost Liz just under $15.99 per month to take 1500 mg per day.

$15.99 versus $227.00 per month for preparations that are highly similar. Hmmmmmm.

I wonder what the $211.01 extra per month goes towards? Admittedly, Abbott Labs, the current company selling Niaspan (after Abbott acquired Kos), has invested in a few clinical trials, such as ARBITER-HALTS6. But does supporting research justify this much difference, a difference that amounts to $2532 over a year? If just 100,000 patients are prescribed Niaspan at this dose (a typical dose), this generates $253 million.

Is the cost of developing and marketing a supplement-turned-drug that great? Is this justifiable? Is it any wonder that our health insurance premiums continue to balloon?

I use Sloniacin and Enduracin almost exclusively.

Measurement

A crucial component of self-empowerment in healthcare is to be able to measure various health parameters. More and more measurement tools are entering the direct-to-consumer arena.

Quantification of various phenomena is important in managing many aspects of health. Imagine a carpenter trying to build a house without the use of a tape measure, level, or other measuring tools. In health, as in building a house, measurement, adjustment, and correction are critical.

Among the most helpful health measurement tools:

Blood glucose meters--Blood glucose meters aren't just for diabetics. They are among the most powerful weight loss tools available.

Blood pressure cuffs--There's no better way to assess blood pressure than to assess it under all the varied conditions of life: When you're tired, when you're excited, when you're upset, when you're happy, hungry, stomach full, morning, night. This is a lot better than the one isolated measure in the doctor's office.

Digital thermometers--Your first a.m. oral temperature is a great way to assess thyroid status. We aim to maintain first a.m. oral temperature around 97.3 degrees F, the normal human temperature upon arising that reflects normal thyroid function. (No, Dr. Broda Barnes fans, axillary temperatures should NOT be used due to flagrant variation from right armpit to left armpit, modifying effects of clothing and ambient temperature, etc. Oral temperature tracks internal, "core," temperature fluctuations reliably, including circadian variation, far better than axillary temperatures.)

Fingerstick blood tests--An incredible number of blood tests are now available just by performing a simple fingerstick in your kitchen or bathroom. You can get 25-hydroxy vitamin D, lipids, thyroid measures (TSH, free T3, free T4), hormones (DHEA, testosterone, estrogens). And the list is growing rapidly. Salivary tests are also growing in number for many of the same measures.

A variation on fingerstick blood tests are devices like CardioChek that allow you to do a fingerstick, but also run the test on your own device at home. (The CardioChek device tests total cholesterol, triglycerides, and HDL.)

Urine pH--You can dipstick your own urine to assess the relative acidity or alkalinity of your lifestyle. Acid pH (7 or below) suggests that diet is weighed too heavily in favor of animal products and grains. An alkaline pH (above 7) suggests plentiful vegetables and fruits, not counteracted by animal products and grains.

There are many more, including the ZEO device to monitor sleep quality, RESPeRATE for reduction of blood pressure, HeartMath to manage stress and augment the parasympathatic (relaxation) response. We've come a long way compared to the health monitoring devices of just 25-30 years ago.

Anyway, that's a partial list. Given the rapid advances in technology that allow such home tests, I anticipate a much longer list in the coming few years.

For some perspective on how far these devices have come, here's a great graphic of an early sphygmomanometer, or blood pressure gauge.


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

At 5 ft 7 inches, he weighed in at 273 lbs, putting his BMI at a sobering 42.8. (A BMI of 30 or above is classified as "obese.") In addition to lipoprotein(a), Jack had an extravagant quantity of small LDL (the evil "partner" of lipoprotein(a)), high triglycerides, and blood sugars in the diabetic range. With a heart scan score of 1670, Jack had little room for compromises.

Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.

So I taught Jack how to check his blood sugars using a fingerstick device, what I call the most important weight loss tool available. I asked Jack to check his pre-meal blood glucose and his one-hour after-meal blood glucose and not allow the after-meal blood glucose to rise any higher than the pre-meal. For example, if blood glucose pre-meal was 115 mg/dl, after-meal blood glucose should be no higher than 115 mg/dl.

If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.

Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.

What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.

Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger.

The two kinds of small LDL

You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.