(Lack of ) Quality of nutritional supplements

In my last post, I blogged about how we must not confuse marketing with truth. They are often two different things.

A patient I saw today was absolutely convinced that his fish oil was the best available in the world: purer, uncontaminated by mercury or pesticides--"not like that other crap on the shelves." I asked him how he knew this. "They say so," he proudly declared.

Do you recognize this? He fell for the marketing. While there may be some truth in the manufacturer's claims, you can't believe it from the mouth of the manufacturer. True judgements about quality and purity have to come from an independent source like Consumer Reports, Consumer Lab, or the FDA.

But the FDA doesn't regulate the quality and purity of nutritional supplements. On the positive side, this has allowed supplement manufacturers to keep costs down, not having to navigate arcane and complex regulatory restrictions.

On the negative side, a fair number of supplement manufacturers get away with 1) producing supplements that fail to contain the stated amounts of ingredients, occasionally containing none of the essential ingredient(s), 2) contain contaminants like lead, and 3) make extravagant and often unfounded claims like "superior", "more effective", and "purer". (DHEA, for instance, is a particular landmine of poor quality. I recently suggested that a patient take DHEA; despite consistently taking 50 mg of a specific brand for several months, the blood level of DHEA-S didn't budge one bit--there was likely little or none in the capsule.)

The Fanatic Cook at http://fanaticcook.blogspot.com has posted some very insightful discussions on this issue and the proposed FDA regulations of supplements. They're worth perusing.

I really wish regulation weren't necessary and that the industry could have policed itself. But it clearly has failed and perhaps federal oversight is not such a bad thing, as long as the FDA regulations restrict themselves to oversight over quality and purity and not to efficacy. It's the efficacy regulation that could hogtie innovation in supplement development.

Marketing and truth are not the same

I often remind people: Don't confuse marketing with the truth.

Today, I spent a total of probably an hour and a half dissuading patients that some crazed piece of marketing trying to sell them something was not the same as truth.

I spent approximately 40 minutes alone with a woman who was absolutely convinced that:

--Nattokinase would cure her of all heart disease. It does not. Despite the promising health benefits of natto and vitamin K2 supplementation, nattokinase is a scam with no basis in science nor logic.

--Niacin destroys your liver and homeopathic remedies are superior. Quite simply, homeopathy = quackery. No rational thinking scientist endorses the utter nonsense practiced in this strange and outrageous set of practices that requires you to suspend all reason.

--Sufficient vitamin D is obtainable through a "potent" multivitamin. I know of no multivitamin preparation that even begins to provide the dose of vitamin D that is actually required by adults, nor is it absorbed since these D preparations are powder based.

--Fish oil will poison you with mercury. Accordingly, one brand of fish oil claims to be the only safe form. Those of you following these posts, or the reports of the USDA and FDA, as well as the reports of Consumer Reports and Consumer Lab (www.consumerlab.com) know that, unlike fish itself, there is no mercury in fish oil capsules.

--All coronary atherosclerotic heart disease is caused by heavy metal poisoning. Thus chelation with EDTA represents a cure for heart disease.


People are inundated with marketing that promise extravagant cures, remove need for any medication, make you smarter, sexier, thinner, and on and on.

If you see a TV ad for Ford that says they make the best cars in the U.S., do you immediately run out and put a For Sale sign on your GM car and buy a Ford? No, of course not. You recognize the ad for what it is: marketing. It may be true, but a TV commercial is not enough to convince you.

Then why would an ad promising extraordinary cures for cancer or heart disease convince you that this is true? It should not. Marketing ads should only serve to alert you to the possibility of value or benefit, but should never-- never--stand alone as proof. Take marketing for what it is: marketing of a product or service, not a scientific report, not a factual report, not news.

Marketing is advertising. Period.

More on erectile dysfunction

Several facts on erectile dysfunction and coronary plaque:


If you have erectile dysfunction, there's at least a 50% chance you also have coronary plaque.

If you have coronary plaque by a CT heart scan, there's a 50% chance you have erectile dysfunction.

If you have symptomatic coronary disease (chest pains, breathlessness, prior heart attack), there's a 90% chance you also have erectile dysfunction.


Coronary disease is characterized by a dysfunctional state of the "endothelium", or inner lining of the coronary arteries. Erectile dysfunction is characterized by dysfunction of the endothelium of the penile circulation. Same phenomenon, different territories. (There are other differences, of course, but the two conditions share this fundamental phenomenon.)


If you have any doubts about the physiologic effects of the supplement, l-arginine, just give it a try if you have erectile dysfunction. The erection enhancing effects alone should convince you that a genuine artery-dilating effect is exerted by this very powerful nutritional supplement.

If l-arginine fails by itself to restore full erectile capacity, there are additional strategies, both nutritional and medical, that you can consider.

Our newest Track Your Plaque Special Report on erectile dysfunction is coming out any day now.

High LDL cholesterol--only

As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?

In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.

Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation.

Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque.

Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits.

In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life.

Heart disease = statin deficiency

Judging from the conversations I hear from colleagues, what I hear from the media, and drug company advertising, you'd think that heart disease has one cause--a deficiency of statin drugs.

As their thinking goes, if you have coronary disease, you need a statin drug (Lipitor, Zocor, Crestor, pravachol, etc.). If you have progressive coronary disease, you need more statin drug. If you have a heart attack while on a statin drug, you need even more statin drug.

Some "experts" have even proposed that we do away with LDL cholesterol and we just give everybody a statin drug at high doses.

Does this make any sense to you?

Doesn't it make better sense that if someone has progressive heart disease or heart attack while on a statin drug, then target the other causes largely unaffected by a statin drug? Perhaps if LDL cholesterol remains high on the statin drug, then a higher dose is justified. But more often than not, it's not a high LDL on statin drugs that responsible, it's other causes. And there's many of them: low HDL, VLDL, IDL, Lp(a), deficiency of omega-3 fatty acids, inflammatory processes, vitamin D deficiency, among others. (An important exception to this is when the conventional calculated LDL substantially underestimates true LDL as measured by LDL particle number by NMR, apoprotein B, or 'direct' LDL.)

Imagine someone has pneumonia. After 2 weeks of antibiotics, they are only partly better. The solution: a higher dose of the same antibiotic--but never question if it was the right antibiotic in the first place. That's what is going on in heart disease.

The doctors have been brainwashed into believing this $22 billion dollar per year bit of propaganda. The drug companies actively try to recruit the public into believing the same. Don't fall for it.

The statin drugs do indeed have a role. But they are not the complete answer. More of the same when disease progresses makes no sense at all.

Fish oil and mercury

I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor, or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.

How much omega-3s are enough?

The basic dose we advocate for the Track Your Plaque program is 1200 mg per day of EPA + DHA, the essential omega-3 fatty acids.

1200 mg EPA+DHA is generally obtainable by taking 4 capsules of 1000 mg of fish oil, since the majority of preparations contain 180 mg EPA and 120 mg DHA per capsule.

But how will you know if a higher dose wouldn't be even better?

The principal parameter to look at is triglycerides. If triglycerides remain above 60 mg/dl, we usually consider increasing fish oil.

Another measure that's very important is intermediate-density lipoprotein, or IDL, also called "remnant lipoproteins" on a VAP panel. Persistence of any IDL or remnant lipoproteins is reason to consider more fish oil. Most commonly, if there is some persistence of either, we increase fish oil to 6000 mg per day of a standard preparation, or 1800 mg/day of EPA+DHA.

The only time we see persistence of IDL or remnant lipoproteins with this higher dose is when triglycerides are really high. If starting triglycerides are, for instance, 500 mg/dl, then even this higher dose may be insufficient. This is when more highly concentrated preparations of fish oil may be necessary, occasionally even the prescription form, Omacor. (We currently use Omacor only when high doses of EPA+DHA are required, most because of its outrageous cost. Two capsules per day costs around $120 per month; three capsules per day to provide 1800 mg/day of EPA+DHA costs $180 per month. I think this is outrageous and so we use it only when absolutely necessary.)

You might even argue that a higher dose of 1800 mg EPA+DHA, or 6000 mg of a standard capsule, might be preferable for more assured reduction of heart attack risk--even when triglycerides and IDL are perfectly under control. I wouldn't argue with you. But you won't observe any measurable feedback that tells you that a heightened effect is being obtained. I take that dose myself, in fact, despite the fact that elimination of wheat products and weight loss was sufficient to drop my triglycerides to the target level. I figure it's a small additional effort for added peace of mind.

Repentance for past sins

If you are new to the Track Your Plaque program and would like to jump start your effort, or if you are struggling with losing weight and excess weight is a part of the situation that created your CT heart scan score, then don't forget about fasting.

Fasting is the cessation of eating. However, recall from the Track Your Plaque Special Report, Fasting: Fast Track to Control Plaque at http://www.cureality.com/library/fl_04-012fasting.asp, there are many variations on fasting that permit some intake of healthy foods. (Thus, they are not, in the strict sense, "fasting". Accurate or no, there are variations that may be more palatable or do-able in the real world by real people.)

My personal favorite method to fast is to use a low-sugar, low-fat soy milk such as Light Silk, available at most major grocery stores. This high-protein, low-fat, low-sugar soy milk takes the edge off hunger and provides a minimal quantity of calories. A minimum of 72 hours is required for substantial results. (My one reservation about this brand of soy milk is that the Fanatic Cook claims that the manufacturer, Dean Foods, is a factory farm operation that abuses livestock--a discussion for another day.)

Fasting yields more than weight loss. It refreshes your appreciation for food. It reawakens you to the amount and quality of food you've been putting in your body. Fasting also allows you to recognize just how bad you might feel from the diet you were eating.

You also emerge from a fast with a reduced appetite and a renewed sense of appreciation for food. It makes the discipline of healthy eating a lot easier when you break your fast.

I tell people that fasting is not punishment. It is a form of enlightenment, of re-experiencing food and life. Fasting allows you to "catch up" on all the indiscretions you've been guilty of over the years.

It also provides enormous advantage in gaining control over coronary plaque.

A fanatic for Fanatic Cook

If you haven't already done so, I'd urge you to peruse the wonderfully insightful, sophisticated, and biting commentary provided by the Fanatic Cook Blog at http://fanaticcook.blogspot.com.

She (I assume it's a she) has been discussing the proposed Safe Food Act recently, an effort to address all the dangers in foods that have come to attention lately, like melamine in pet food and E. coli in bagged spinach. Her most recent post is:

Nebraska Farm Bureau Thinks Food Safety Act Bad Idea, the latest in a series of posts exploring this issue.

I'd like to know who the Fanatic Cook is, or "Bix" as she calls herself. (I assume it's a "she" but I don't really know that for a fact.) I've corresponded with her and she prefers to remain anonymous for unspecified reasons. I'd like to know who this person is both for a more secure sense of credibility, as well as I'd simply like to know who can write so intelligently and why. I suspect that she's a professional nutrition scientist or something along those lines, since the level of insight into many scientific issues is quite impressive. Her Blogs will make great material for a book, if compiled and organized. Watch out for this one.

Erectile dysfunction and coronary plaque

Erectile dysfunction (ED), previously known as "impotence," and coronary atherosclerotic plaque go hand in hand.

A recent study in men with advanced coronary disease showed that 93% experienced ED. The participants in the Track Your Plaque program, for the most part, do not have advanced coronary atherosclerosis, but have an earlier form detected by a CT heart scan.

What proportion of men with asymptomatic coronary plaque as measured by a CT heart scan have ED? Around 50%. In other words, it's not a rare occurrence.

The conversation about ED (and even its renaming from impotence) really gained momentum with the development of ED-drugs like Viagra and Cialis. The drugs are reasonably effective and safe. However, you will hear little about all the strategies that can either precede your need for these drugs and/or enhance your response to these drugs if the response is partial. That part of the conversation, of course, doesn't yield loads of drug company revenues.

One of the most helpful and specific nutritional supplements available that can partially restore the nitric oxide-deficiency of ED is l-arginine. L-arginine is the body's source of nitric oxide (NO), the master dilator (relaxing agent) for all arteries of the body. NO dilates penile arteries, it dilates coronary arteries. Lack of NO disables the penile capacity for erection and encourages growth of coronary atherosclerotic plaque. Track Your Plaque Members are already familiar with l-arginine as a facilitator of coronary plaque regression.

We will detail the supplements that you can use safely in your Track Your Plaque program to both enhance erectile function if you suffer ED, as well as impact positively on coronary health, in an upcoming and detailed Special Report on the www.cureality.com website.
Cureality | Real People Seeking Real Cures

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.