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.

Wheat-free pumpkin bread

Try this recipe for a wheat-free, gluten-free yet healthy "bread." Unlike many gluten-free foods that send blood sugar skyward, this will not.

Ingredients:
2 cups ground almond meal (Buy it from Trader Joe's--70% cheaper than other grocery stores.)
1/2 cup ground flaxseed
1/2 cup sour cream (full-fat, of course)
15 oz canned pumpkin (Trader Joe's is bisphenol A-free)
2 medium to large eggs
1/2 cup chopped walnuts or pecans
4 tablespoons butter, melted
2 teaspoons baking powder
2 teaspoons cinnamon
1 teaspoon nutmeg or allspice
Dash of salt
Choice of non-nutritive sweetener (I used 3 teaspoons Trader Joe's stevia extract powder, the one mixed with lactose. Two tablespoons of Truvia, 1/2 teaspoon of the more concentrated stevia extract, or 1/2 cup Splenda are other choices. You can taste the mixed batter to gauge sweetness if in doubt.)

Preheat oven to 350 degrees F. Grease baking pan (e.g., 10 x 6 inch). The pan should be big enough so that the mix will not be more than 2 inches deep, else it will require much longer to bake. (If you have only smaller pans, you will need to cook longer while the pan is covered with aluminum foil.)

Mix all ingredients thoroughly in large bowl. Pour mix into greased baking pan.

Cover with aluminum foil and bake for 30 minutes. Remove foil and bake for additional 30 minutes or until inserted toothpick or knife comes out dry.

Serve with cream cheese or as is.

(I'd have some pictures, but the kids and I ate it up before I thought to take any photographs.)

Vitamin D: Deficiency vs optimum level

Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.

Dr. Dowd hits a bullseye with this remark:

The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?

Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.

I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)

The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.

Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.

Large LDL counts, too

Chad is a 43-year old father of five kids.

Earlier this year, he developed chest pain that got worse and worse. He ended up with a total of five stents in all three coronary arteries. After a devastating experience with Lipitor that resulted from a ruptured tendon, he came to me for an option.

Chad's lipoproteins:

Slow Burn works

I have been impressed with the results I've been obtaining with Fred Hahn's Slow Burn strength training technique.

Because I have limited time to hang around the gym, any technique that provides outsized results in a limited amount of time, I have to admit, appeals to me. In past, I'd be lucky to squeeze in one or two strength training sessions per week, devoting the rest of the time to biking outdoors, biking on a sedentary bike (while playing XBox), jogging, or doing strenuous yard work like digging trenches and planting shrubs.

Over the years, I've gradually lost muscle, since the strength training effort suffered with my time limitations.

So Fred's time-efficient Slow Burn idea struck a chord. Having now done it with some regularity, usually 1-2 times per week since mid-September, I have gradually added back visible muscle. My Slow Burn workouts, involving 8-10 different movements, seem to have restored the muscle I've lost, with a very modest time effort.

It took a little getting used to. After Fred showed me how to do the movements--slow motion movement in both the "positive" and "negative" directions, with smooth, non-jerking transitions, one set per muscle group, each taken to muscle exhaustion--it left me unusually tired and sore the next day. This surprised me, given the limited time involved. Breathing is also very important; the usual exhale-during-the-positive, inhale-during-the-negative pattern is replaced by breathing freely during the entire set. I didn't get this at first and ended up with headaches that got worse with each set. Breathing freely relieved me from the effect.

I have strength trained since I was around 15 years old. Back in the early 1970s, I had about 2000 lbs of barbells and dumbbells in my garage in New Jersey, while also driving back and forth to the Morristown, NJ, YMCA to train with friends. The Slow Burn movements forced me to break habits established over nearly 40 years of conventional strength training.

I've also played around with mixing conventional movements with Slow Burn movements to keep it fresh. This also seems to work.

If you're interested in giving it a try, here's an animation that demonstrates what Slow Burn movements look like. Fred has also produced an excellent 3-DVD set of videos that more fully describe the practice.

Do your part to save on healthcare costs

While many of the factors that drive the relentless increase in health care costs are beyond individual control, you are still able to exert personal influence over costs. Just as in political elections, your one vote alone may not count; it's the collective effort of many people who share similar opinions that results in real change.

I just got the new monthly premium for my high-deductible health insurance: Up $300 per month, putting my family's total premium over $2000 per month---for four healthy people. (My son fractured his wrist playing high school hockey earlier this year; that may explain at least some of the increase.)

I'm going to shop around for a better deal. However, shopping is likely to only stall the process. It will not address the systemic problems with healthcare that continue to drive premiums up and up and up.

So what can you do to help keep costs down? Here are a few thoughts:

Never accept a prescription for fish oil, i.e., Lovaza. Just buy far less costly over-the-counter fish oil. I treat complex hyperlipidemias, including familial hypertriglyceridemia, ever day. I NEVER use prescription fish oil. A typical 4 capsule per day Lovaza prescription adds around $280 to $520 per month to overall health costs (though your direct out-of-pocket costs may be less, since you shove the costs onto others in your plan).

Never accept a prescription for vitamin D. Prescription vitamin D is the mushroom or invertebrate form anyway. Just buy the human (cholecalciferol, D3) form from your health food store or "big box" store. They yield consistent increases in 25-hydroxy vitamin D levels, superior to the prescription form. And they're wonderfully inexpensive.

Eliminate wheat from your diet. If there is a dietary strategy that yields unexpected and outsized benefits across a wide spectrum of health, it's elimination of this thing we're sold called "wheat," you know, the genetically-transformed, high-yield dwarf mutant that now represents 99% of all wheat sold. Blood sugar drops, pre-diabetics become non-prediabetics, diabetics reduce need for medication or become non-diabetic, cholesterol values plummet, arthritis improves, acid reflux and irritable bowel symptoms improve or disappear, just to mention a few. Wheat elimination alone, I believe, would result in incalculable savings in both healthcare costs and lives saved.

Be sure to obtain iodine. In the fuss to cut salt use, everyone forgot about iodine. Lack of iodine leads to thyroid disease, usually hypothyroidism, that, in turn, causes cholesterol values to increase, weight to increase, and heart disease risk to double, triple, or quadruple. Iodine supplementation is easy and wonderfully inexpensive.

Over time, I hope that all of us can help develop the effort to self-direct more and more of our own health. Our Track Your Plaque program has shown me that, not only can people take the initiative to direct aspects of their own health, they can do it better than 99% of doctors.  

I'm sure there are many, many other ways to help reduce costs. Any suggestions?
All posts by william-davis

Brainwashed!

At a social gathering this weekend, as we humans like to do, someone asked me what I did for a living. I told him I was a cardiologist.

"What hospital do you work at?" he asked.

This is invariably the response I get whenever I tell people what I do. I wouldn't make much of it except that it happens just about every time.

This indicates to me just how successful hospitals, my colleagues, cardiac device manufacturers, and others supporting the status quo in heart care, have been in persuading us that the place for heart disease is the hospital--period.

Tense families, drama, high-tech...It all takes place in the hospital.

Yet the people destined to be the fodder for hospital heart care are presently well, mostly unaware of what the future holds. Also unaware that heart disease is readily, easily, inexpensively, and accurately identifiable. Ask anyone in the Track Your Plaque program who's had a CT heart scan.

We all need to rid ourselves of the idea that the hospital is the place for heart disease. If the coronary plaque behind heart attack is easy to detect and controllable, there's little or no need for the hospital for the vast majority of us.

In the majority of instances of coronary disease, the hospital should be the place for the non-compliant and the ill-informed, and not for those of us sufficiently motivated to know and do better. The formula is simple: 1) Quantify plaque with a CT heart scan, 2) Identify the causes, then 3) Correct the causes.

The Fanatic Cook: A fabulous Blog about food and nutrition

I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:

The Fanatic Cook at http://fanaticcook.blogspot.com/

I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)

Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.

There's also oodles of recipes, all for the taking.

Eggs: Good, bad, or indifferent?

Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)





A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.




Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Diabetes is Track Your Plaque's Kryptonite!


If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes.

I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes.

Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss.

Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range.

Roy's repeat heart scan showed a score of 482--a tripling of his original score.

Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth.

Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know.

The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)

Boy, was I wrong!

Around 10 years ago, I was talking to a balloon and stent manufacturer's representative, who was raving about some new device that was due for release to the market. Back then, the sky seemed the limit to cardiac device manufacturers, who were falling over themselves scrambling to design and market the next new device.

The angioplasty market then had ballooned (no pun intended) from nothing to a multi-billion dollar industry. Stents were just getting underway but clearly had potential for being at least as large.

But this was a time when preventive therapies were also beginning to get quite powerful. We had just gotten started doing CT heart scans and were excited about the possibilities, statin drugs were gaining evidence through clinical trials, and the power of many nutritional supplements was finally achieving validation. We were even learning the error of our prior low-fat ways.

So I broadly pronounced to the enthusiastic product representative, "In 10 years, balloons, angioplasty, and stents will occupy this little corner of cardiac care because prevention will have become so powerful. We won't talk about heart procedures. We'll talk about coronary plaque regression!"

I even advised the representative that he should consider a career change in anticipation of the coming wave of preventive strategies.

Was I ever wrong. Despite the power of heart disease prevention--which is indeed true--cardiac device and procedure technology has boomed, both in popularity as well as in revenue success. Device manufacturing and sales are hugely successful. Implanting devices into people is a hugely profitable enterprise.

Since my ill-timed comments to the salesman, Boston Scientific, a major manufacturer of stents and other cardiac devices, reported revenues of $6.2 billiondollars in 2005, a 12% increase over the prior year. Medtronic reported 2005 revenues of $11.3 billion, growing at 15% per year. Clearly, cardiac procedures are still quite popular--and profitable.

My timing was off, but not for long. The huge crest of change in preventive therapies is upon us. That's the premise behind the Track Your Plaque concept: heart disease prevention can't be found in a hospital, is not supported by cardiac device manufacturers, and is not being advocated by most cardiologists or primary care physicians. Yet the tools are getting better and better every day.

Those of you who succeed in halting or reducing your heart scan score are extremely unlikely to add to Boston Scientific's or Medtronic's revenues. Help me spread the word.

Don't forget how dangerous heart disease can be

Sometimes it's easy to get smug when coronary plaque is a reversible process.

When you see people day in, day out, week in, week out, drop their heart scan scores, reversing what could be a dangerous disease, you can sometimes lose sight of just how dangerous coronary disease can be.

Whether I like it or not, I maintain a reasonably active role in hospitals out of necessity. I do need their services occasionally for people with advanced heart disease when I meet them (when regression is not the initial conversation for safety reasons), or valve disease is diagnosed, or someone shows up with congenital or heart muscle diseases. In other words, although we focus on coronary issues, there's more to heart disease than just coronary disease.

This unfortunate case just served to remind me how powerful coronary disease can be. Elizabeth, an active 67-year old, finally came to the hospital after suffering 6 months of chest pain and increasing breathlessness. She hated hospitals and hadn't seen a doctor in 30 years since she was successfully treated for cancer.

In those 30 years, she'd been quite active with family and a small business. But she also smoked 2 packs of cigarettes most of those years.

After she was admitted to the hospital, it became clear that Elizabeth had experienced one, if not several, heart attacks along the way. The entire front 2/3 of her heart was non-functional. If that wasn't bad enough, two of her heart valves were severely diseased and dysfunctional: Her aortic valve barely opened (aortic valve "stenosis", or stiffness) and the mitral valve leaked severely (mitral valve "insufficiency", or leakiness). All of this was confirmed with conventional testing in the hospital, including a heart catheterization.

Elizabeth ended up in emergency surgery--very unusual, by the way, for valve surgery of the sort she had--but died in the first few hours after her procedure. Her heart had simply been too damaged from her heart attacks, and the extraordinary stress of surgery that included two valves was too much. She died on the ventilator.

Coronary disease is a very serious matter. When I see cases like Elizabeth, it boosts my commitment to tell everyone that heart disease--when identified early enough--is a controllable, preventable, even reversible process. For poor Elizabeth, she was much too far down the path of severe, irreversible disease that control or reversal was simply not an option. She was in imminent danger of dying even upon arrival.

It's exciting yet sometimes frightening to know what you have in your hands: The means to control this monster called coronary disease. Use it wisely. But don't lose sight of what it can do it you permit it to grow, fester, and explode.

How many ways can you disguise sugar?

I came across this shockingly silly report on AOL, who obtained their info courtesy Health Magazine:

The Best New Healthy Foods for Busy People
from Health


The foods on their list:

Kettle Brand Bakes Hickory Honey BBQ--the healthy claim is based on the lack of trans-fatty acids and low-fat.










Post Healthy Classics Raisin Bran Cereal Bars, Cranberry--Likewise, low-fat, sweet, and addictive means healthy to these people.




Amy’s Mediterranean Pizza With Cornmeal Crust --Please!!



Horizon Organic Colby Cheese Sticks --Because it's made by cattle without use of growth hormone or antibiotics, they declare this healthy. I guess we can ignore the saturated fat content and high total fat content.

100% Whole Grain Chips Ahoy! Cookies --You mean we can add the bran back to wheat products and make it healthy?!


This kind of mass-market marketing trickery leaves me incredulous. Don't believe it for a moment. This is typical of the food industry: Take one aspect of nutrition that is truly healthy, such as high-fiber, or low-fat, or organic. Then add undesirable, unhealthy ingredients. The current fad is to add lots of sugar and or sugar-equivalents (usually flour and other wheat products). Because there's one healthy ingredient, they'll call the end-product healthy, too.

If you want to see what health looks like if you indulge in "healthy" products like this, just look up and down the grocery aisles at your neighborhood grocery store. You're likely to see the results: Gross obesity, diabetes, and arthritis.

You won't, of course, see the huge acceleration of growth in coronary plaque, but it's there, ticking away.

To remind us what ideal body weight is: Watch an old movie!

Jack was skeptical. At 273 lbs, 5 ft 11 inches, he felt that he was "just right".

"I feel fine. I don't see why you think I should lose weight," he declared. "In fact, when I lost 25 lbs a couple of years ago, everyone said I was too skinny!"

I showed Jack why: He had an HDL of 35 mg/dl, small LDL (over 90% of all LDL particles), an elevated blood sugar of 123 mg/dl (diabetes is officially 126 mg/dl or greater), high blood pressure, and increased inflammation (C-reactive protein). These were all manifestations that his body weight was too much for it to handle.




So I told Jack that we've all forgotten what ideal weight should look like. Our perception of "normal" has been so utterly and dramatically distorted by the appearance of our friends, family, co-workers, and other people around us that we've all lost a sense of what a desirable weight for health should be.




So I suggested to Jack that, if he wanted to rememember what ideal weight is and what people are supposed to look like, just watch old movies.

Old movies, like the 1942 production of Casablanca, or the 1952 production of Singin' in the Rain, show the body build that was prevalent in those days. Look at Humphrey Bogart or Gene Kelly--men with average builds, weighing 140-160 lbs--that's how humans were meant to look.

A report this morning on the Today Show showed the "after" photos of several people following bariatric (weight reduction) surgery. The "after" pictures, from the perspective of ideal weight and ideal health, remain hugely overweight.

We need to readjust our perceptions of weight. The average woman in the U.S. now weighs 172 lbs(!!!). Don't confuse average with desirable.

Diabetes is a choice you make

Tim had heart disease identified as a young man. He had his first heart attack followed by a quadruple bypass surgery at age 38. Recurrent anginal chest pain and another small heart attack led to several stents over three procedures in the first four years after bypass.

Tim finally came to us, interested in improving his prevention program. You name it, he had it: small LDL, low HDL (28 mg/dl), lipoprotein(a), etc. The problem was that Tim was also clearly pre-diabetic. At 5 ft 10 inches, he weighed 272 lbs--easily 80 or more pounds overweight.

Tim was willing to make the medication and nutritional supplement changes to gain control over his seeminglly relentless disease. He even turned up his exercise program and lost 28 lbs in the beginning. But as time passed and no symptoms recurred, he became lax.

Tim regained all the weight he'd lost and some more. Now Tim was diabetic.

"I don't get it. I eat good foods that shouldn't raise my insulin. I almost never eat sweets."

I stressed to Tim that diabetes and pre-diabetes, while provoked acutely by sugar-equivalent foods (wheat products, breads, breakfast cereals, crackers, etc.), is caused chronically by excess weight. If Tim wants to regain control over his heart disease, he needed to lost the weight.

Unlike, say, leukemia, an unfortunate disease that has little to do with lifestyle choices, diabetes is a choice you make over 90% of the time. In other words, if you become diabetic (adult variety, not children's variety) as an adult, that's because you've chosen to follow that path. You've neglected physical activity, or indulged in too many calories or poor food choices, or simply allowed weight to balloon out of control.

But diabetes is also a path most people can choose not to take. And it is a painfully common choice: Nearly two-thirds of the adults in my office have patterns of pre-diabetes or diabetes when I first meet them.

Let me stress this: For the vast majority of adults, diabetes is a choice, not an inevitability.

I'll call the doctor when I feel bad!

Max just had his heart scan. He sat down with the x-ray technologist at the work console while she pointed out the white areas in his coronary arteries that represented plaque.

"It looks like you're going to have a fairly high score," the technologist commented. "The final report will be available after one of our cardiologists reviews your images."

Max shrugged. "Well, I don't feel anything. I'm always running around with work, with my kids, stuff like that. That's better than any stress test. I guess I'll worry about it if it starts to bother me."


You'd be surprised how common this view remains: If it's not bothering you, then just forget about it. It's easy to do, since you have no symptoms, nothing to impair your physical activities. But what are the potential consequences of ignoring your heart scan? Here's a few:

--Prevention and plaque reversal efforts are most effective the earlier you start. From a heart scan score viewpoint, the lower your starting score, the easier it is to gain control over it. More people will succeed in reducing their score when the starting score is lower.

--The role of prevention of heart disease instantly crystallizes when you know your score. Your LDL cholesterol of 142 mg/dl or HDL of 41 mg/dl no longer seem like just numbers of borderline signficance. Instead, they become useful tools to gain control over plaque. They cast your numbers in a new and clear light.

--Knowing your heart scan score today gives you a basis for comparison in future. Your score of, say 250, today, can be 220 in one year. Without your preventive efforts, it will be 30% higher: 325. That's a big difference!

--Sudden death or heart attack--can occur in up to 35-40% of people with hidden heart disease--without warning.

Don't even bother getting a heart scan if you're going to ignore it. I've said it before and I'll say it again: A heart scan is the most important health test you can get--but only if you do something about it.
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.