The myth of small LDL

Annie's doctor was puzzled.

Despite an HDL cholesterol of 76 mg (spectacular!) and LDL of 82 mg, her CT heart scan showed a score of 135. At age 51, this placed her in the 90th percentile.

Not as bad, perhaps, as her Dad might have had, since he died at age 54 of a heart attack.

So we submitted blood for lipoprotein testing. Surprise! over 90% of all her LDL particles were small. (By NMR, they're called "small". By gel electropheresis, or the Berkeley Lab test, or VAP (Atherotech) technique, they're called "HDL3".)

What gives? Traditional teaching in the lipid world is that if HDL equals or exceeds 40 mg/dl, then small LDL will simply not be present.

Well, as you can see from Annie's experience, this is plain wrong. Yes, there is a graded, population-based effect--the lower your HDL, the greater the likelihood of small LDL. But small LDL is remarkably persistent and prevalent--regardless of your HDL.

We've seen small LDL even with HDLs in the 90's! I call small LDL the "cockroach" of lipids. If you think you have it, you probably do. Getting rid of small LDL requires a specific bug killer. (Track Your Plaque Members: Read Dr. Tara Dall's interview on small LDL.)

Don't let anybody blow off your request for lipoprotein testing just because your HDL is high. That's just not acceptable. Loads can be wrong even with a favorable HDL.

My stress test was normal. I don't need a heart scan!

Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief.

But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern.

I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished.

But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"

What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test.

Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)

Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack.

So, yes, Katy would benefit from another heart scan despite her normal stress test.

The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque.

But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.

Patient-napping: Yet another reason to stay clear of hospitals!

When I started practicing medicine around 20 years ago, it was common practice to alert a physician when their patient was seen in an emergency room.

If John Smith, for example, went to the emergency room with chest pain, the physician who had an established relationship with the patient--knew their history, had managed their health and illnesses, etc.--was notified, even if the hospital ER had no relationship with the physician. It was not uncommon for the patient to then be transferred to the hospital where their own doctor practiced.

Though cumbersome at times, it preserved the relationship of the patient with their doctor.

Over the past few years, this practice has crumbled. Nowadays, hospitals and their employed physicians (and other unscrupulous physicians acting in the name of profit) "fail" to notify the physician with an established relationship.

Guess what happens? The patient all too often ends up being put through the gamut of testing and procedures.

Why? For hospital profit, of course. If failure to notify a doctor who's had a 10-year long relationship with the patient is "overlooked" or, even more commonly, it's "unsafe" to transfer the patient because the patient is too "unstable" to be transferred, then this patient becomes ripe for picking--heart catheterization, stents, bypass surgery, etc. Ten's, if not hundreds, of thousands of dollars can be reaped by this deception. I call it "patient-napping".

I see this at least several times every month. As hospitals are becoming increasingly competitive, and as they put pressure on their physicians to churn patients for revenues, you're going to see more and more of this.

As always, what is your protection from this expanding influence of hospitals and the doctors too meek to stand up to them? Education and information. Arm yourself with an understanding of what is accomplished in hospitals, when you truly need them, and when you don't.

Take it one step further. At least from a heart disease standpoint--the #1 profit-maker for hospitals--aim to 1)identify your coronary plaque, then 2) seize control over your coronary plaque and reduce your risk for heart attack and heart procedures as much as humanly possible. That's the goal of the Track Your Plaque program.

Don't believe the negative press on fish oil



A British Medical Journal study released in March, 2006 has prompted a media flurry of reports on the worthlessness of fish oil. (Hooper L, Thompson RL, Harrison RA et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: a systematic review. BMJ March,2006)

Don't believe it for a second.

First of all, the study was a re-analysis of the existing published scientific literature. It was not a new study. It included a wild conglomeration of different clinical observations, as the studies examining fish oil over the years have been extraordinarily heterogeneous--in populations examined, omega-3 supplement (e.g., fish vs. capsule), period of observation, endpoints measured.

The results were skewed by inclusion of a moderate-sized British study by Burr et al in men with angina. In this study, no benefit was demonstrated and, in fact, a negative effect--more heart attack and death--was observed with fish oil. This was not news, since the study was published in 2003. It's results have been a mystery to everyone, since its unexpected negative result for fish oil was so starkly different from virtually every other study that preceded it (suggesting a study flaw or statistical fluke).

Nonetheless, the Burr study served to throw off the overall analysis. It diluted the dramatic and persuasive outcome of the GISSI-Prevenzione Study of 11,000 people in which a 28% reduction in heart attack and 45% reduction in cardiovascular death was observed. Note that the substantial numbers of the GISSI make the study's outcome nearly unassailable.

Another important fact: fish oil is among the most powerful tools available to correct elevated triglycerides. Drops of 50% are common. Recall that triglycerides are a necessary ingredient to create the nasty LDL, as well as VLDL, Intermediate-density lipoprotein, and an undesirable shift from large to ineffective small HDL. Reducing triglycerides is therefore crucial for your plaque control program.

This re-analysis serves to prove nothing. Such analyses can only pose questions for further study in a real study like GISSI: a randomized (random participant assignment), controlled (treatment vs. placebo or other treatment) study.

The weight of evidence remains heavily in favor of fish oil, not only as helpful, but fabulously beneficial, particularly for anyone aiming to reduce coronary plaque.

How important is high blood pressure?


Control of blood pressure is crucial for coronary plaque control and stopping your heart scan score from increasing.

Dr. Mehmet Oz (of Oprah fame and a cardiac transplant surgeon at Columbia University) made graphic point of this on the ABC TV news show, 20/20, last evening on an episode called "Our Bodies: Myths, Lies, and Straight Talk". (See a summary on the ABC News 20/20 website at http://abcnews.go.com/2020/story?id=2109291&page=1)

Although I believe he somewhat overstated the case for hypertension (proclaiming "If you're going to remember one number, if you're going to focus and fixate on one number in your entire health profile, it better be your blood pressure"), he made the point that a blood pressure of 115/75 is what you should have for optimal health.

I couldn't agree more. Unfortunately, the old advice that desirable blood is 140/90 or less is absolutely wrong. At this level, we see flagrant increases in heart scan scores. We also progressive enlargement of the thoracic aorta, the large vessel that leaves the heart and branches to provide the major arteries of the body. Growth of the aorta to an aneurysm is also common at these formerly acceptable blood pressure. (The diameter of your aorta in the chest is an easily obtainable measure on your CT heart scan.)

The blood pressure you need for halting and reversing plaque growth on your heart scan is indeed 115/75 or less. (Not so low, however, that you're lightheaded.) This is the blood pressure that you were meant to have evolutionarily. It's also the blood pressure that helps tremendously in keeping your aorta from enlarging.

Watch for an upcoming exhaustive report on blood pressure and its plaque-raising effects and how to reduce it using nutritional strategies on the www.cureality.com membership website.

Is your doctor in cahoots with the hospital?

I got a call from a doctor about a patient we've seen in past.

"I've got Tricia in the office. She's been having some kind of chest and abdominal pain. I think it's esophageal reflux, but just to be safe I'm sending her to the hospital."

I advised this physician that, given Tricia's low heart scan score, she was unlikely to be having a coronary "event" like heart attack or unstable symptoms. It wasn't impossible, but just highly unlikely.

As the patient was without symptoms at the moment and had driven herself to his office, I offered to perform a stress test immediately. (Though stress tests are of limited usefulness in people without symptoms, they can be useful provocative maneuvers in people with symptoms of uncertain significance.)

The doctor declined. Tricia was, after all, in his office and he was responsible for any decisions despite any objections I voiced. Well, Tricia was directed by her doctor to go to a local hospital, though one with an especially notorious reputation for putting virtually anyone they can get their hands on through as many procedures as possible.

As you might guess, this doctor was closely associated with this hospital. He and his colleagues obtain incentives (or are penalized) if they do not generate revenue-producing procedures for the hospital.

So, guess what? Tricia ended up with several procedures, all of which yielded nothing--except $30,000 in revenues from Tricia's insurance company.

I harp on this deplorable state of affairs because it is utterly, painfully, and shamefully TRUE. Just look at the hospital and you'd better brace yourself for a series of tests that could cost you the equivalent of a nice 3 bedroom home. If they were truly necessary after the failure of preventive and other simple efforts, fine. But, all too often, they are driven by profit motives.

Could I have stopped this somehow from occurring? After all, Tricia was reasonably aware of the way we do things around here. I fear that even this failed to serve Tricia well. But I remain hopeful that, as we build broader awareness of these issues, that more and more people and physicians will stand up and refuse to tolerate the status quo.

Where is the Track Your Plaque program going?

I spend a lot of time worrying about how people can be helped to navigate through this program.

Take, for instance, the man in rural Texas who, while traveling in Dallas, got a heart scan on a whim. His score was 990. When he took the report back to his doctor, he got a smirk--and that's all. When he came to the Track Your Plaque program, he lacked a physician advocate to help him.

Or the woman from Florida who sought opinions from two reputable cardiologists for her heart scan score of 377. Both advised her that she needed a heart catheterization--despite her lack of symptoms, her 5-day-a-week exercise program, and normal stress test. She also lacks a physician advocate who acts on her behalf, helping her achieve success, rather than just churning her for money from hospital procedures.

For people like this and for others, I see the Track Your Plaque program evolving in several directions:

1) An online clinic--You enter and we take your "hand" and lead you step by step through the process, not only at the beginning, but over the months and years. This would help clear up some of the confusion and zigzags that some people experience trying to navigate through the program.

2) Develop physician and non-physician partners--The woman in Florida, for instance, could be referred to a doctor nearby who understands the program and is able to assist her. At present, this is virtually impossible because of the bias towards heart procedures, drugs as the sole treatment for heart disease risk, and the superficial physician-patient relationship. The majority of practicing physicians just don't understand the program despite the fact that it is based on sound clinical and experimental data. But it will in time.

Looking back, we've come a long way. I remember first having patients undergo heart scans 10 years ago. My colleagues laughed or called it "silly". The general public didn't know what they meant.

Now we're talking about how to broadcast the most powerful heart disease prevention program available in the world to a larger audience, but making it easier and more accessible. Mass media like Oprah's two hour-long spots helped, but we need to make the next leap. Not just identifying hidden heart disease to feed the hungry cardiovascular hospital procedure monster, but to educate/inform/empower the public on what to do with the scan once they've had it.

Who cares about triglycerides?

Walter's triglycerides were 231 mg. His LDL cholesterol was "favorable" at 111 mg, HDL likewise at 49 mg.

"Everything looks good," his doctor declared.

"Do you think the triglycerides are okay, too?" Walter asked.

"Well, the guidelines do say that triglycerides should be less than 150, but I believe you're close enough. Anyway, triglycerides don't really cause heart disease."


When I met Walter, I made several comments. First of all, in light of his heart scan score of 713, none of his numbers--HDL, LDL, or triglycerides-- were acceptable. But the triglycerides were glaringly and terribly too high.

Why? What exactly are triglycerides?

Triglycerides are a basic fat particle that, though they do not cause heart disease directly, trigger the formation of an array of abnormal lipoprotein particles in the blood that are among the most potent causes of heart disease known.

These abnormal lipoprotein particles include small LDL, VLDL, and IDL (intermediate-density lipoprotein--a really bad pattern). Excess triglycerides also cause HDL to drop. They also cause a distortion of HDL structure, causing the particles to become abnormally small. Small HDL is also useless HDL, unable to provide the protection that HDL is designed to do.

So Walter's elevated triglycerides are, in reality, a substantial red flag for an entire panel of abnormal particles that contribute to the growth of his coronary plaque.

So, if you get this kind of commentary on your triglycerides, ask for another opinion. (Track Your Plaque Members: Also see Triglycerides: Mother of meddlesome particles at http://www.cureality.com/library/fl_dp002triglycerides.asp.)

Total cholesterol and heart scans

Andy was fearful of heart disease in his life. At age 52, he'd already had four CT heart scans--one each year on or near his birthday.

Yet, when I looked at Andy's scans, his scores had been increasing 20-24% per year. Each and every score was greater by 20% or more over the previous.

So I asked Andy what steps he had taken to stop this relentless progression. "Well, I've always been real health conscious. But ever since my first scan, I really started sticking to a healthy diet, exercising nearly every day, and I take a bunch of supplements."

"What did your doctor advise?" I asked.

"Well, Dr. ---- said that nothing needed to be done, since my total cholesterol was always below 200."



Men's Health magazine's fabulous story about the folly of using total cholesterol to gauge heart disease risk.




Aaaauuuggghhh!! Wrong!

This man was, in fact, at rapidly escalating risk for heart attack. This rate of growth simply can't continue forever without igniting this bomb.

A total cholesterol below 200 is meaningless, as Andy's increasing coronary plaque proved. For instance, you can have a total cholesterol of 165 mg but with an HDL cholesterol of 27 mg. This would constitute very high risk for heart disease despite the low total cholesterol. The low HDL pattern is among the most common reasons for a misleading total cholesterol. Small LDL, high triglycerides, and lipoprotein (a) are other frequent reasons.

Andy, run the other way! Do not heed this doctor's advice! You need a solid answer to the question: Why exactly do I have coronary plaque in the first place?

Then, agree on a treatment program that corrects your specific causes.

Cardiologists out of touch

This weekend, I'm fulfilling some responsiblities I have every so often to some of the local hospitals. It gives me a chance to interact with many of my colleagues who are likewise "on call" for the weekend.

I tried to strike up several conversations with colleagues about how they were managing heart disease prevention. I received blank stares, puzzled looks, indifference. One colleague declared that 80 mg of Lipitor is all you need to know.

These same colleagues are the ones scrambling for the heart attack patients in the emergency room, climbing over one another for consultation in the hospital for patients with chest pain and heart failure. They're consumed with expanding the range of procedures they can perform.

Carotid stenting is hot. So is stenting of the leg arteries. Defibrillators have been a financial bonanza. Opportunities abound on how to add these procedures to a cardiologist's abilities.

But heart disease prevention? How about heart disease reversal?

Frankly, I'm embarassed by my colleagues' lack of interest. Imagine we had a cure for breast cancer--not a palliative therapy that just slows the disease down or prolongs life, but actually cures it once and for all. I would hope that all physicians and oncologists would learn how to accomplish this. What if instead they focused on learning new ways to remove breasts, administer new toxic chemotherapies, etc. but ignored the whole idea of cure?

This is what is happening with coronary plaque reversal. The answer is right in front of them, but the vast majority (99%) of cardiologists choose to ignore it. After all, prevention and reversal simply don't pay the bills.

That means that, in 2006, you simply cannot rely on your cardiologist to counsel you on how to achieve regression or reversal of coronary plaque. How about your internist, family physician, or primary care doctor? Well, they're busy doing pneumovax injections, Pap smears, managing knee and hip arthritis, low back pain, diarrhea, headaches, sinus infections and . . yes, dabbling in heart disease prevention.

And, for the most part, doing a miserable job of it. What you generally get echoes the drug manufacturers pitch: Take a statin drug, cut the fat in your diet.

Until the majority of doctors catch on, you're going to have to rely on sources like the Track Your Plaque program for better information.
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.