An exercise in optimism

Followers of the Track Your Plaque program already know that maintaining an optimistic viewpoint is important in gaining control over coronary plaque.

In fact, I believe that, in many cases, a sense of optimism may make or break your CT heart scan score-reducing efforts. Pessimists rarely drop their score, while optimists do so all the time.

This week posed a challenge to my optimism. I spent the last week on jury duty hearing the details of a murder case. For four days, I listened to blow-by-blow testimony about the totally pointless, unprovoked death of a young man by a drug-dealing thug. Much of the witness testimony was from people who shared the hopeless, violent world of the defendant.

I was, however, completely impressed by the dedication of the prosecuting attorney, a 50-some year old man who was clearly deeply dedicated to his mission and didn't once provide any indication that he was grandstanding or looking for some personal glory. He was doing his job and trying to obtain justice for the fallen victim. I was equally impressed by the judge, who seemed unfazed by the events but carefully explained why the system worked the way it did. After the trial, he provided some further insights to us jury members and I saw him as a human being who, like the prosecutor, was trying to make a small contribution to making the world better.

Though many of the witnesses who testified against the defendant shared his world, I was impressed with their courage in coming forward. They face the threat of reprisals, I'm sure, for coming forward to the law and testifying against a known career criminal. Several of them said that they were not after any reward, but simply wished to do the right thing and provide testimony that proved damning against the defendant.

I acted as the jury foreman and I was proud of how the jury members listened carefully, asked intelligent and probing questions, and then helped us render a confident and expeditious sentence: guilty.

If anything, despite the tragic circumstances, I was much heartened at how all the participants in this process played their part and justice (at least in the legal sense) was served.

Let optimism prevail, even in dire circumstances.

No need to re-invent the wheel

I seem to be repeating myself lately, but I think this does bear repeating:

There's no need to re-invent the wheel when it comes to gaining control over your heart scan score.

The Track Your Plaque program is the most powerful approach known to help you gain control over your coronary atherosclerotic plaque and CT heart scan score, bar none. While 100% of people do not drop their score, more and more people every week are doing so. (One of the admitted weaknesses of the Track Your Plaque website is our failure to list more success stories; we're working on it.)

The basic program is quite simple:

--The Rule of 60 for lipids (LDL 60 mg/dl; HDL 60 mg/dl or greater; triglycerides 60 mg/dl or less)

--Identify hidden causes of plaque, esp. small LDL, Lp(a), and IDL, followed by specific corrective action

--Fish oil--minimum 1200 mg per day of EPA + DHA

--Normal vitamin D3 blood levels (We aim for 25-OH-vitamin D3 of 50-60 ng/ml)

--Normal blood sugar (<100 mg/dl)

--Normal blood pressure (<130/80)

--An optimistic attitude



Much of the other stuff--vitamin K, matrix metalloproteinase reducing strategies, flavonoid strategies, exercise-induced hypertension, etc.--are, for the majority, fluff. Their real role is in people who may have failed in stopping the rise of their heart scan score just doing the basics of the program.

If you neglect the basics, hoping to find some magic potion, I'm afraid the overwhelming likelihood is that you will fail. I've seen it happen time and again. Someone will come to my office with an extraordinary list of supplements--hawthorne, dozens of anti-oxidants, EDTA, concentrated flavonoid preparations, and on and on. Not only is it shockingly expensive to do this, it's also unnecessary and foolhardy. This kind of unfocused, hocus-pocus in the hopes of getting it right fail time after time.

The Track Your Plaque program, while not foolproof, is the best I know of. Stick to the basics and wander off when the basics fail. But there's extraordinary power in just achieving the basics.

Are we a front for drug companies?

I was shocked recently when someone accused me and the Track Your Plaque website of being nothing more than a front for the drug industry, that we are promoting concepts with the hidden pharmacuetical agenda behind us.

Don't make me laugh. How in the world that kind of impression could be gotten from either the Heart Scan Blog or the Track Your Plaque website is beyond me.

But I occasionally do need to state explicity: We do not promote drugs, neither this Blog nor the Track Your Plaque website has ever sought nor been backed by pharmaceutical money. The only money that supports this website is our own and that from paying Track Your Plaque members.

In fact, I am quite proud of the unbiased content and commentary on both venues. I challenge anyone to point out how and where there is any suggested relationship to a hidden source of commercial backing. I assure you, there is none.

If I say a drug is worth you and your doctor considering, then I say so with a true belief in it, not because somebody or some company paid me to say so. If I say a drug stinks, I believe that too. If we use a specific supplement in the program, it's because we believe it truly adds value to a plaque-reversal program. We receive no money from drug, supplement, or other commercial interests to promote their products. Period.

What is "normal"?

When it comes to laboratory values and medical testing, a common dilemma is knowing what is "normal." Let me explain.

First of all, when you receive a laboratory result for a test, a "reference range" or "normal range" is usually provided. Where did that range come from?

It varies from test to test. For instance, a low potassium is easy, because low potassium levels can lead to life threatening consequences, e.g., dangerous heart rhythms. High potassium likewise, because dangerous phenomena develop when potassium generally exceeds 5.5 mg/dl or so.

But what about something like HDL or LDL. Here's where confusion reigns. Often, "normal" is obtained by taking the average and saying that any value plus or minus two standard deviations (remember that painful class?) represents normal or reference range.

If that were true, what if we applied that principle to body weight. If we weighed several thousand adult women, the average would be in the neighborhood of 172 lbs (no kidding). Does that mean that 172 lbs plus or minus two standard deviations is normal? No, of course not.

There is therefore a distinction between "normal" and "desirable". For HDL cholesterol, your laboratory report might say that an HDL cholesterol of 40-60 mg/dl is normal. But is it desirable? I don't think so. The most frequent HDL level for a male with a heart attack is 42 mg/dl--hardly desirable.

Let's take triglycerides. The average triglyceride level in the U.S. is somewhere around 140 mg/dl. For those of us who do a lot of lipoprotein testing, we can tell you that triglycerides at this level, though generally regarded as being within the normal range, are associated with flagrant and obvious excesses of several abnormal lipoprotein particles that contribute to coronary plaque growth (VLDL and often IDL; small LDL; drop in HDL and shift towards small HDL).

So, always take the so-called "normal" or "reference" values on a lab report as crude guidelines that often have little or nothing to do with health or desirability. Unfortunately, many physicians are not aware of this and will declare any value within the normal or reference range as okay. An HDL of 40 mg is not okay. A triglyceride level of 140 mg is also not okay.

What is okay? What is desirable? That depends on the parameter being examined. From a basic lipid standpoint, of course, we regard desirable as 60-60-60. Desirability from a lipoprotein standpoint we will cover in a more thorough Track Your Plaque Special Report in future.

The wisdom of the masses

My sister sent me these quotes:



"We don't like their sound, and guitar music is on the way out."

Decca Recording Co. rejecting the Beatles, 1962


"Stocks have reached what looks like a permanently high plateau."

Irving Fisher, Professor of Economics, Yale University, 1929


"Airplanes are interesting toys but of no military value."

Marechal Ferdinand Foch, Professor of Strategy, Ecole Superieure de Guerre, France


"Everything that can be invented has been invented."

Charles H. Duell, Commissioner, US Office of Patents, 1899



No doubt, conventional wisdom can often be laughably (tragically?) wrong. The problem is that, as absurd as all the above sentiments seem to us now and in retrospect, they represented the view of many people years ago. These views were held by many, including many people in positions of power and decision-making responsibility.

A more relevant but nonetheless laughable and widely held belief in 2007: coronary heart disease should be treated with hospital procedures.

Why is a disease that requires 30 years to develop treated only at the final moments with a procedure? Do you only change your car's oil when the engine is on its last legs? Or, do periodic, relatively effortless oil changes during the life of the car make better sense?

I witness just how brainwashed the public has become with this crazed notion when I meet someone socially at, say a fundraiser or cocktail party. When they ask what I do, I tell them I'm a cardiologist. The invariable response: "Oh, what hospital do you work out of?"

I tell them I don't, that I take care of the majority of heart disease right from the office. 99% of the time I get a puzzled look. If we had comic bubbles above our heads revealing our internal thoughts, it would read "Yeah, right. What a kook."

The notion that coronary heart disease is something that is manageable with simple tools for the majority of us in the early stages is entirely foreign to almost everybody. The hospitals and the medical industry have so succeeded in dazzling the public with images of staff in scrubs, rushing from emergency to emergency, lights flashing, scalpels flying. . . how can you possibly accomplish this at home or anywhere outside of the high-tech world of the hospital?

Well, I'm a cardiologist and I do it every day. We all need a figurative dose of electroshock therapy to shake ourselves of this crazy notion.

How important is l-arginine?

Perhaps more than any other supplement, l-arginine causes frustration and confusion. It’s difficult to find, sometimes quite expensive, and some preparations cause loose stools.

Just how necessary is it?

L-arginine, you’ll recall, is a source of nitric oxide, or NO. Though it’s the same stuff as in car exhaust, NO provides a critical signaling role in your body’s cells that regulate a multitude of functions. Among the important roles of NO is to powerfully dilate, or relax, arteries. A constant flow of NO is required for health, particularly since each molecule persists only a few seconds.

L-arginine is the body’s source of nitric oxide. In addition, a peculiar but very effective blocker of l-arginine called asymmetric dimethylarginine, or ASDM, has recently been discovered to prevent the production of NO. Varied conditions like hypertension, diabetes, high cholesterol, excessive saturated fat or processed carbohydrate intake all lead to heightened levels of ASDM, often several-fold greater levels, and thereby effectively blocking NO production.

The “Arginine Paradox” is the name that some researchers in this field have given to the unusual property of l-arginine supplementation to “overpower” the blocking effects of ASDM. This is somewhat unusual in biologic systems in that an agent that blocks a receptor cannot usually be outmuscled by providing excess material for a reaction. Kind of like hoping that your car runs faster simply by topping up the gas tank.

Concrete observable benefits have been made for l-arginine in clinical trials, such as arterial relaxation that results in arterial enlargement (which can actually be seen in the cath lab); anti-inflammatory effects; reduction of blood pressure; enhancement of insulin responses, etc. All of these effects can be connected to beneficial properties that may facilitate atherosclerotic plaque regression and, indeed, there are limited data to document that this is true.

Drug companies may be greedy, but they’re not stupid. They’ve been vigorously pursuing this line of research for some years, a research path that led inadvertently to the erectile dysfunction agent, sildenafil (Viagra), and all its subsequent competitors. (Erectile dysfunction is another expression of endothelial dysfunction, since male erections are driven by the ability to dilate penile arteries.) The wonderful properties of NO enhancement continue to occupy research labs around the world.

Wow. So what’s the reluctance? In the early years of the Track Your Plaque program (meaning just a short 7-8 years ago), I was thoroughly convinced that l-arginine was a crucial, necessary part of a plaque regression program. Without it, you would rarely succeed. With it, the odds were tipped in your favor.

However, something curious has emerged recently. I’ve seen more and more people dropping their heart scan scores. Not just a little bit, but a huge amount. Witness our most recent record holder, Neal, who dropped his score 51% in 15 months. Just five years ago, this magnitude of reversal was unimaginable. Granted, Neal is our record holder, but others are obtaining 10, 18, 24, 30% drops in scores all the time. Many have done it without l-arginine.

Now, how about the people who have failed to stop a rising score? Would they do better with l-arginine as part of the mix? I believe so, but sometimes we never quite know except in retrospect. It has been a great dilemma for us trying to predict from the starting gate who will or who won’t drop their heart scan score.

My view from the trenches is that l-arginine packs its greatest atherosclerosis-fighting punch in the first year or two of use, when “endothelial dysfunction” is likely to be present (abnormal artery constriction). But as all other strategies take hold—fish oil, correction of lipid and lipoprotein abnormalities, weight loss (big effect), vitamin D (another very big effect), etc.—endothelial behavior improves over time. Perhaps l-arginine becomes a less necessary component over time.

There’s no doubt that uncertainty still surrounds the use and science surrounding l-arginine. However, if you’re interested in stacking the odds in your favor, particularly during the first year or two of your plaque-reducing efforts, I think that l-arginine is worth considering. It is cumbersome, it can be expensive, some preparations may even be foul. But in the big picture of life, with hospitals trying every possible ploy to get your body on a table for a procedure, doctors perverting their mission by signing employment contracts with hospitals and agreeing to usher you into the hospital as a paying patient whenever possible, and drug companies viewing you and me as a market for medications which may or may not be helpful, l-arginine is surely not that big a burden.

Track Your Plaque and non-commercialism

If you're a Track Your Plaque Member or viewer, you may know that we have resisted outside commercial involvement. We do not run advertising on the site, we do not allow drug companies to post ads, we do not covertly sponsor supplements. We do this to main the unbiased content of the site.

We've seen too many sites be tempted by the money offered by a drug company only to see content gradually drift towards providing nothing more than cleverly concealed drug advertising. I personally find this deceptive and disgusting. Ads are ads and everyone knows it. But when you subvert content, secretly driven by a commercial agenda, that I find abhorrent.

That said, however, I do wonder if we need the participation of some outside commercial interests to help our members. In other words, many (over half) of the questions and conversations we have with people is about what supplement to take, or what medication to take. While we cannot offer direct medical advice online (nor should we) because of legal and ethical restrictions, I wonder if could facilitate access to products.

Many people struggle, for instance, with trusted sources for l-arginine, vitamin D, fish oil. Other people struggle with finding a heart scan center because of the changing landscape of the CT scanning industry. Could we somehow provide a clear-cut segment of the website that clearly demarcates what is commercial and non-Track Your Plaque-originated, yet at least provides a starting place for more info?

Ideally, we would have personally tried and investigated everything there is out there applicable to the program. But that's simply impossible at this stage.

I feel strongly that we will never run conventional ads on the site. Nor will we ever permit any outside commercial interest to dictate what and how we say something. The internet world is full of places like that. Look at WebMD. I find the site embarassing in the degree of commercial bias there. We will NEVER sell out like that, regardless of the temptation. People with heart disease are all conducting a war with the commercial forces working to profit from them--hospitals, cardiologists, drug companies, medical device companies (yes, even they advertise to the public, e.g., implantable defibrillators--no kidding). Genuine, honest, unbiased information is sorely needed and not from some kook who either knows nothing about real people with real disease, or has a hidden agenda like selling you chelation.

I'd welcome any feedback either through this Blog or through the contact@cureality.com.

The nattokinase scam

A conversation about vitamin K2 commonly leads to confusion. Several people have asked about something called nattokinase.

The scientific data on the potential role of vitamin K2 deficiency in causing both osteoporosis and vascular calcification is fascinating. Along with vitamin D3, vitamin K2 may be an important factor in regulation of calcium metabolism. Supplementation may prove to be a major strategy for inhibition of vascular calcification.

Obtaining K2 in the diet is tricky, since it's present in just a handful of foods: egg yolks, liver, traditional cheeses, and natto. This is where the confusion starts.

Natto is a Japanese fermented soy product. I've had it and it's quite disgusting. Nonetheless, Japanese who eat natto experience less fracture. (A parallel study in heart disease has not been performed.) Natto is also a source of another substance called nattokinase.

Advocates (otherwise often known as supplement distributors) claim that nattokinase is a "fibrinolytic", or blood clot-dissolving, preparation that "improves blood flow, protects from blood clots, and prevents heart attacks and strokes."

Don't you believe it. This is patent nonsense. There are several problems with this rationale:

--Any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. That's why all medically used fibrinolytics are given intravenously. Drug companies have struggled for years to encapsulate, modify, or somehow protect protein (or polypeptide) products taken orally from degrading this way. They've never succeeded. That's why, for instance, growth hormone (a polypeptide) remains an injection, not an oral agent. An oral growth hormone, by the way, would sell like mad, so the drug companies would very much like to figure out how to bypass the degradative effects of stomach acid. One of the "researchers" behind the nattokinase claims boasts that he has single-handedly figured out how to protect the nattokinase molecule in the gastrointestinal tract. However, he won't tell anybody how he does it. Right.

--Fibrinolytic agents are extremely dangerous. In years past, we used to treat heart attacks with intravenous fibrinolytic agents like tissue plasminogen activator, urokinase, streptokinase, and others. They have fallen by the wayside, for the most part, because of limited effectiveness and the unavoidable dangers of their use. Fibrinolytics are "dumb": they dissolve blood clots in both good places and bad. While they might dissolve the blood clot causing your heart attack, they also degrade the tiny clot in your cerebral (brain) circulation that was protective. That's why fatal brain hemorrhages, bleeding stomach ulcers, and blood oozing from strange places can also occur with fibrinolytic administration. Believe me, I've seen it happen, and I've watched people die from them.

The idea that a small dose taken orally is healthy is ridiculous. Even if nattokinase worked, why the heck would you take an agent that has known dangerous and very real consequences?

Don't let this idiocy reflect poorly on the K2 conversation, which, I believe, holds real merit and is backed by legitimate science. This is symptomatic of a larger difficulty with the supplement industry: Insane and unfounded claims about one supplement erodes credibility for the entire industry. It gives regulation-crazed people like the FDA ammunition to go after supplements, something none of us need. You and I have to sift through the nonsense to uncover the real gems in this rockpile, real gems like vitamin D3, omega-3 fatty acids from fish oil, and, perhaps, vitamin K2. But not nattokinase.

Blood pressure with exercise

Here's a frequently neglected cause for an increasing CT heart scan score: High blood pressure with exercise. Let me explain.

Paul's blood pressure at rest, sitting in the office or on arising in the morning, or at other relatively peaceful moments: 110/75 to 130/80--all in the conventional normal range.

We put Paul on the treadmill for a stress test. At 10 mets of effort (on the protocol used, this means 3.4 mph treadmill speed at 14 degree incline), Paul's blood pressure skyrockets to 220/105. That's really high.

Now, blood pressure is expected to increase with exercise. If it doesn't rise, that's abnormal and may, in fact, be a sign of danger. Normally, blood pressure should rise gradually in a stepwise fashion with increasing levels of exercise. But any blood pressure exceeding 170/90 is clearly too high with exercise. (Not to be confused with high blood pressures not involving exercise.) A handful of studies have suggested that a "breakpoint" of 170/90 also predicts heightened risk of heart attack over a long period.)

I see this phenomenon frequently--normal blood pressure at rest, high with exercise. This also suggests that when Paul is stressed, upset, in traffic congestion, under pressure at work, etc., his blood pressure is high during those periods, as well. I wouldn't be surprised to see other phenomena of underappreciated high blood pressure, like abnormally thick heart muscle (left ventricular hypertrophy), an enlarged thoracic aorta (visible on your heart scan), left atrium, perhaps even an abnormal EKG or abnormal kidney function (evidenced by an elevated creatinine on a standard blood panel).

Unfortunately, the treatments that reduce blood pressure are "stupid," i.e., they have no appreciation for what you are doing and they reduce blood pressure all the time, whether or not you're stressed, exercising, or sleeping.

Blood pressure reduction should begin with weight loss, exercise, reduction of saturated fats and processed carbohydrates (esp. wheat), magnesium replacement, vitamin D replacement. Think about CoQ10. After this, blood pressure medication might be necessary.

The message: Watch out for the blood pressures when you have a stress test. Or, if you have a friend who is adept at getting blood pressures, get a blood pressure immediately upon ceasing exercise. It should be no higher than 170/90.

Vitamin D2 vs. vitamin D3

An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.
All posts by william-davis

Fish oil: What's the difference?

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour. 

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.






To B or not to B

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.