Jogging does NOT cause heart disease


Periodically, I'll come across a knuckleheaded report like this one from Minneapolis:

Marathon Man’s Heart Damaged by Running?


Of course, the obligatory story about how a cardiologist came to the rescue and "saved his life" with a stent follows. In other words, a stent purportedly saved the life of this vigorous man with no symptoms and high capacity for exercise.

Does vigorous exercise, whether it's marathon running, long-distance biking, or triathlons, cause coronary disease? Should all vigorous athletes run to their doctor to see if they, too, need their lives to be "saved."

Let me tell you what's really going on here. People with the genetic pattern lipoprotein(a), or Lp(a), tend to be slender, intelligent and athletic. For genetic reasons, these people gravitate towards endurance sports like long-distance running. Lp(a) is a high-risk factor for coronary disease. It is the abnormality present in the majority of slender, healthy people who are shocked when they receive a high heart scan score or have a heart attack or receive a stent. (I call Lp(a) "the most aggressive known coronary risk factor that nobody's heard about.")

The association between endurance exercise and heart disease is just that: an association. It does not mean that exercise is causal. Having seen coronary plaque detected with heart scans in many runners, virtually all of whom demonstrated increased Lp(a), I believe that Lp(a) is causal.

Unfortunately, the man in the Minneapolis story, now that his life is "saved," will likely be advised to take a statin drug and follow a low-fat diet . . . you know, the diet that increases Lp(a).

Warning: Your pharmacist may be hazardous to your health

Pharmacists can be very helpful resources when it comes to questions about prescription drugs.

The operant word here is drugs.

What they are most definitely not expert on are nutritional supplements. In fact, a day doesn't pass by without having to dispell one falsehood or another conveyed to a patient about a nutritional supplement by a pharmacist.

Among the more common falsehoods told to patients by pharmacists:

"You have to take Niaspan. Sloniacin doesn't work."

Patent nonsense. A few years back, I was the largest prescriber of Niaspan in Wisconsin. Although I am embarassed to admit it, I also spoke for the company, educating fellow physicians on the value of niacin for correction of lipid disorders.

Then I shifted to Sloniacin due to cost--it costs 1/20th the cost of prescription Niaspan. I examined the pharmacokinetic data (pattern of release in the body), the published literature (e.g., the famous HATS Trial), and have used Sloniacin over 1000 times in patients. In my experience, there is no difference: no difference in efficacy, no difference in safety, no difference in side-effects. There is a BIG difference in price.

Unfortunately, most pharmacists get their information on niacin from the Niaspan representative.


"You shouldn't be taking vitamin D supplements. I have prescription vitamin D here."

What the pharmacist means is that you should replace your vitamin D3, or cholecalciferol--the form recognized as vitamin D by the human body--with the plant form of vitamin D, vitamin D2 or ergocalciferol.

Since when is a plant form of a hormone (vitamin D is a potent hormone, not a vitamin; it was misnamed) better than the human form?

I've previously talked about this issue in a blog post called Vitamin D for the pharmaceutically challenged.

The notion that D2 is somehow superior to the real thing, D3, is absurd. I use D3 only in my practice and have checked blood levels thousands of times. As long as the D3 comes as a gelcap, drops, or powder in a capsule, it works great, yielding predictable and substantial increases in blood levels of 25-hydroxy vitamin D. If it comes as prescription D2 (or over-the-counter D2), I have seen many failures: no increase in blood levels of vitamin D or meager increases.

Prescription status is no guarantee of effectiveness.


"Why do you need iodine? You already get enough from food."

The NHANES data over the last 25 years argue otherwise: Iodine deficiency is growing, particularly as people are avoiding iodized salt and the iodine content of processed foods is diminishing. The explosion in goiters in my office also suggest this is no longer a settled issue.

On the positive side, it is exceptionally easy to remedy with an inexpensive iodine supplement. That is, until the pharmacist intervenes and injects his bit of nutritional mis-information.


I'm not bashing pharmacists. In fact, Track Your Plaque's own Dr. BG has a pharmacy background, and she is an absolute genius with nutritonal supplements. But she is a rare exception to the rule: Most pharmacists know virtually nothing about nutritional supplements. You might as well ask your hairdresser.

"Healthy" people are the most iodine deficient

Ironically, the healthiest people are the most likely to be deficient in iodine.

Why?

Healthy people tend to:

--Avoid iodized salt because of public health advice to limit sodium
--Use sea salt to obtain minerals like magnesium--but sea salt contains little iodine
--Limit meat--Carnivores obtain more iodine than vegetarians or vegans. In one study, up to 80% of vegans were iodine-deficient (Krajcovicova-Kudlackova M et al 2003).
--Exercise--Substantial amounts of iodine are lost through sweating. In a study of high school soccer players, 38.5% were severely iodine deficient, compared to 2% of sedentary students (Mao IF et al 2001).


That is indeed what I am seeing in my office, as well: The healthiest, most attentive to healthy eating, and most physically active are the ones showing up with small goiters (enlarged thyroid glands) and increased TSH and low free T4 levels.

Why am I checking thyroid and talking about iodine? Because even the smallest degree of thyroid dysfunction can double, triple, or quadruple your risk for cardiovascular events. See the posts Is normal TSH too high? and Thyroid perspective update.

What kind of iodine do you take?

The results of the latest Heart Scan Blog poll are in.

204 respondents answered the question:


Do you take an iodine supplement?

The responses:

Yes, I take Iodoral, Lugol's, or SSKI
26 (12%)

Yes, I take potassium or sodium iodide
19 (9%)

Yes, I take kelp tablets or powder
64 (31%)

No, I rely on generous use of iodized salt
23 (11%)

No, I don't supplement iodine at all
66 (32%)

Isn't iodine something you put on cuts and scratches?
6 (2%)


I am heartened by the number of respondents taking iodine in some form. After all, iodine is an essential trace mineral. Without it and health suffers, often dramatically.

However, I am concerned by the percentage of people who don't supplement iodine at all: 32%. Interestingly, this is approximately the proportion of people who come to my office who also do not supplement iodine who are now showing goiters, or enlarged thyroid glands due to iodine deficiency. Goiters lead to hypothyroidism (low thyroid hormone levels), followed by hyperactive nodules, not to mention undesirable effects like weight gain, fatigue, hair loss, constipation, intolerance to cold, higher LDL cholesterol and triglycerides, and heart disease.

11% of respondents report using lots of iodized salt. This may or may not be sufficient to provide enough iodine to prevent goiter and allow normal thyroid function. The success of this strategy depends to a great extent on how often salt is purchased. Salt that sits on the shelf for more than a month is devoid of iodine, given iodine's volatility.

I am also favorably impressed by the number of people who take "serious" iodine supplements like Lugol's solution, Iodoral, or SSKI. Of course, people who read The Heart Scan Blog tend to be an unusually informed, healthy population. The 12% of people in the poll who take these forms of iodine does clearly not mean that 12% of the general population also takes them. But 12% is more than I would have predicted.

On the Track Your Plaque website, we are awaiting an interview with iodine expert, Dr. Lyn Patrick. I'm hoping for some juicy insights.

And you thought gasoline was expensive

In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.



Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Lipoprotein(a): 205 nmol/L



The atherogenicity, or plaque-causing potential, of this pattern was reflected in Ed's heart scan score of 2133.

You can readily see that, of this combination, only HDL cholesterol would be adequately identified through conventional lipid testing. Small LDL and lipoprotein(a) need to be specifically measured via lipoprotein testing.

And, contrary to the drug industry's "statin drugs for everybody" motto, this pattern, while improved with statin therapy, is not shut off.

Specific correction of each abnormality is required. For instance, niacin addresses all three: increases HDL, reduces small LDL, and (usually) reduces lipoprotein(a). A standard low-fat diet makes this pattern worse by reducing HDL, increasing small LDL, and (usually) increasing lipoprotein(a).
All posts by william-davis

Dr. Michael Eades on the Paleolithic diet

Dr. Michael Eades has posted an absolutely spectacular commentary on the Paleolithic diet concept:

Rapid health improvements with a Paleolithic diet

The post was prompted by publication of a study that tried to recreate a Paleolithic-like diet experience over a brief study period:

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.

Dr. Eades discussion is wonderfully insightful and comprehensive and there's little to say to improve on his discussion.

I'd make one small point: From what I see in my experience, the improvements in lipid patterns seen in the brief period of this study are very likely to have been primarily due to the removal of wheat. Followers of this blog know that wheat elimination is among the most powerful cholesterol-reducing strategies available.

What vitamin D form?

In response to questions regarding why don't vitamin D tablets work, here are my observations.

When I first started correcting vitamin D levels around 3 1/2 years ago, people would begin with starting 25-hydroxy vitamin D blood levels of around 20 ng/ml.

Taking, say, 6000 units vitamin D as tablets over 3 months yielded blood levels of 24-30 ng/ml. Taking 6000 units in an oil-based form, and blood levels would commonly be 60-70 ng/ml.

In other words, tablets are very poorly absorbed. I also saw very erratic absorption with tablets, with tremendous variation in blood levels.

I witnessed this effect many times. I finally began telling patients to avoid the tablets altogether. It's simply not worth it. Taking dose X of tablets, you cannot predict what the blood level of vitamin D will be.

Now, you can sometimes make the tablets get absorbed by either taking with a teaspoon of oil (e.g., olive, flaxseed) or taking with an oil-rich meal. However, I am uncertain just how consistent the absorption is under these circumstances, not having done this enough times to know.

Oil-filled gelcaps are no more expensive than tablets (or perhaps a dollar more). Health food store employees and pharmacists don't know this. I have had many patients come to the office claiming they changed to tablets because that's all their health food store or pharmacy carried and the person behind the counter assured them it was the same. Blood level of vitamin D to confirm: right back down to the starting level or near it--little or no absorption.

The only way to know whether a preparation is absorbed is to check a blood level. But, in my experience, having checked vitamin D blood levels thousands of times, gelcaps never fail; tablets fail over 80% of the time.

Vitamin D for the pharmaceutically challenged

Most Heart Scan Blog readers already know:

Your doctor has been brainwashed by the pharmaceutical industry.

Your doctor more than likely has spent the better part of his or her career in the Guantanamo Bay of healthcare, water-boarded by seductive sales representatives, enticed with promises of fame and riches, threatened with ostracism from the clubby internal halls of healthcare if--gasp!--he or she didn't subscribe to the "rule" that only drugs are good, anything else is bad.

The same FDA-approval-is-necessary-to-be-good brand of nonsense is gaining popularity among my colleagues who, having caught some mention (on the Today Show, Oprah, or similar source of medical information), hope to join the vitamin D hoopla.

People will proudly declare that they are taking a high dose of vitamin D: 50,000 units once per week.

No. They are taking a barely useful form: D2, ergocalciferol.

Studies examining the reliability of the D2 form differ:

There's the Heaney study suggesting that D2 is less effective than D3:
Vitamin D2 is much less effective than vitamin D3 in humans

Then there's the Holick study showing they are equivalent:
Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D.

My experience is more in line with the Heaney study: Little or no real effect with D2.

One particularly illustrative case I witnessed was a woman who was mistakenly prescribed D2 at 50,000 units per day. She told me that she'd been taking it for a year. I fully expected to see clear-cut signs of toxicity (e.g., high blood calcium levels). Curiously, she showed no signs of toxicity. Nor did she show any vitamin D at all in her blood: 25-hydroxy D level of zero--literally zero.

I've witnessed similar phenomena several times: plenty of vitamin D2 . . . very little vitamin D in the blood.

All in all, I suppose that D2 is better than No-D at all. But you are far better off joining the ranks of the pharmaceutically challenged and go with the stuff that really works: D3.

D3, or cholecalciferol, yields confident increases in blood levels. It is inexpensive, safe, and an exact copy of the human form of vitamin D. (Of course, gelcap or drops only, NEVER tablets.)

There is absolute NO reason to take vitamin D2, the form that sometimes works, sometimes doesn't, the facsimile plant form issued by the drug industry.

Why don't stents prevent heart attack?



No study has ever documented that stents prevent future heart attack. But, in day-to-day practice, stents are frequently implanted for just this reason.

A little clarification. Stents do prevent heart attack--if the heart attack is already underway, either as an "acute myocardial infarction" or "unstable angina."

In other words, a plaque in a coronary artery can rupture just like a little volcano. Rather than spewing lava, the underlying plaque contents--fibrous tissue, inflammatory cells, cholesterol crystals, fatty material, debris--are exposed to flowing blood and trigger spasm of the artery and blood clot formation. A ruptured plaque is typically found in people who go to the emergency room with severe chest pain or have difficulty breathing.

A heart catheterization is performed, a severe (e.g., 90-100%--completely closed) is found. A stent in this situation is of clear-cut benefit.

What is not clearly beneficial is someone with no symptoms, symptoms only with physical activity that has been present for at least several months, or someone with a high heart scan score and no symptoms. In these circumstances, stent implantation does not reduce risk for future heart attack.

Why?



Take a look at this angiogram of a right coronary artery. You can seen plaque all along the artery (represented by areas that appear pinched off. There are at least 4 visible.)

Putting one 15 millimeter stent in the artery will only affect the area of artery stented. (Stents vary in length, but typically are 12-18 millimeters in length.) The right coronary artery is about 10 times or more this length. There are also two other arteries of similar length. A stent at one location will do nothing to affect the potential for rupture in any of the other plaque-laden areas.

Say a stent is implanted in the "worst" blockage in this right coronary artery, the plaque located at around 9 o'clock. What about all the other plaques? They can still rupture.

Why not put in many stents, say, 4 or 5, and stent all the visible plaques?

Two reasons: 1) Plaque you can't even see on an angiogram can still rupture, and 2) it is very costly (easily $30,000 at the very least), 3) incurs greater procedural risk, and 4) messes up the artery for future procedures, since a steel-lined artery that develops more disease in future will be more difficult to re-implant stents, bypass, or perform other procedural manipulations.

The point: Putting in stents does not reduce potential for plaque rupture in the entire artery.

What can prevent plaque rupture? That's the whole point of following an effective prevention program: prevent plaque rupture.

(Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

Top image courtesy National Heart, Lung, and Blood Institute.

Low thyroid: What to do?

I've gotten a number of requests for solutions on how to solve the low thyroid issue if either 1) your doctor refuses to discuss the issue or denies it is present, or 2) there are government mandates against thyroid correction unless certain (outdated) targets are met.

Oh, boy.

While I'm not encouraging anyone to break the laws or regulations of their country (and it's impossible to generalize, with readers of this blog originating from over 30 countries), here are some simple steps to consider that might help you in your quest to correct hypothyroidism:

--Measure your body temperature--First thing in the morning either while lying in bed or go to the bathroom and measure your oral temp. Record it and, if it is consistently lower than 97.0 degrees (Fahrenheit), show it to your doctor. This may help persuade him/her.(You can still be hypothyroid with higher temperatures, but if low temperatures are present, it is simply more persuasive evidence in favor of treatment).

--Supplement with iodine 150 mcg per day to be sure you are not iodine deficient. This is becoming more common in the U.S. as people avoid iodized salt. It is quite common outside the U.S. An easy, inexpensive preparation is kelp tablets.

--Show your doctor a recent crucial study: The HUNT Study that suggests that cardiovascular mortality begins to increase at a TSH of only 1.5 or greater, not the 5.5 mIU usually used by laboratories and doctors.

--Ask people around you whether they are aware of a health practitioner who might be willing to work with you, or at least have an open mind (sadly, an uncommon commodity).

Also, see thyroid advocate and prolific author, Mary Shomon's advice on how to find a doctor willing to work with you. Yes, they are out there, but you may have to ask a lot of friends and acquaintances, or meet and fire a lot of docs. It shouldn't be this way, but it is. It will change through public pressure and education, but not by next week.

Another helpful discussion from Mary Shomon: The TSH Normal Range: Why is there still controversy? You will read that even the endocrinologists (a peculiarly contentious group) seethingly debate what constitutes normal vs. low thyroid function.

Also, you might remind a resistant health practitioner that guidelines are guidelines--they are not laws that restrain anyone. They are simply meant to represent broad population guidelines that do not take your personal health situation into consideration.

Which statin drug is best?

I re-post a Heart Scan Blog post from one year ago, answering the question: Which statin drug is best?

I still get this question from patients in the office and online, nearly always prompted by a TV commercial. So let me re-express my thoughts from a year ago, which have not changed on this issue.


The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.

Dr. Nancy Sniderman, heart scans on Today Show

While shaving this morning, I caught the report by NBC medical expert, Dr. Nancy Sniderman, about her coronary plaque and CT coronary angiogram.




Those of you in the Track Your Plaque program or who follow The Heart Scan Blog know that we should tell Dr. Sniderman and her doctor that:

She has done virtually nothing that will stop an increasing heart scan score! In fact, Dr. Sniderman is now following the "prevention program" that is eerily reminiscent of Tim Russert's program! We all know how that turned out.

It is pure folly to believe that a combination of Lipitor, exercise, and a "healthy diet" (usually meaning a low-fat diet--yes, the diet that promotes heart disease) will stop the otherwise relentless increase in heart scan score.

Dr. Sniderman, please consider:

1) Having the real causes of your coronary plaque identified. (It is highly unlikely to be just LDL cholesterol, though the drug industry is thrilled that you believe this.)

2) Ask yourself (or, if your doctor knew what she was doing, ask her): Why do I have heart disease? LDL cholesterol is insufficient reason--virtually nobody I know has high LDL cholesterol as the sole cause. LDL cholesterol is, at most, one reason among many others, but is insufficient as a sole cause.

3) What is your vitamin D status? Crucial!

4) What is your thyroid status?

5) Fish oil--a must!

6) Do you have lipoprotein(a)? Small LDL?

Just addressing the items on the above checklist would put you on a far more confident path to stop your heart scan score from increasing.

If you were to repeat your heart scan score, my prediction: Your score will be higher by 18-24% per year.

My personal experience with low thyroid

Something happened to me around October-November of last year.

I usually feel great. Ordinarily, my struggles are sleeping and relaxing. As with most people, I have too many projects on my schedule, though I find my activities stimulating and fascinating.

I blasted through a very demanding November, trying to meet the needs of a book publisher. This involved sleeping only a few hours a night for several days on end, all after a full day of office practice and hospital duties.

But it was getting tougher. My concentration was becoming more fragmented. Getting things done was proving an elusive goal. Exercise became a real chore.

Although I usually force myself to go to sleep, I was starting to fall asleep before my usual bedtime, and I was sleeping longer than usual.

It's been a tough winter in Wisconsin. Let's face it: It's Wisconsin. But it's been tough even for this region, with weeks of temperatures consistently below 10 degrees. Even so, I was having a heck of a time keeping warm. Extra shirts, socks, soaking my hands in hot water--none of it worked and I was freezing.

So I had my thyroid values checked:

Free T3: 2.6 pg/ml (Ref 2.3-4.2)
Free T4: 1.20 ng/dl (Ref 0.89-1.76)
TSH: 1.528 uUI/ml (Ref 0.350-5.500)


Normal by virtually all standards. I measured my first morning oral temperature: 96.1, 96.3, 95.9. Hmmmm.

My experience coincided with the Track Your Plaque and Heart Scan Blog conversations about low thyroid being enormously underappreciated, with the newest data on thyroid disease suggesting that a TSH for ideal health is probably 1.5 mIU or less. (More about that: Is normal TSH too high? and Thyroid perspective update .

Could this simply be a case of medical student-oma in which every beginning medical student believes he has every disease he learns about?

Despite the apparently "normal" thyroid blood tests, I took the leap and started taking Armour thyroid, beginning at 1/2 grain (30 mg), increasing to 1 grain (60 mg) after the first week.

Within 10 days, I experienced:

--Dramatic restoration of the ability to concentrate
--A boost in mood. (In fact, the last few blog posts before I replaced thyroid reflect my deepening crabbiness.)
--Large increase in energy, now restored to old levels
--Need for less sleep
--I'm warm again! (It's still <20 degrees, but I get easily stay warm while indoors.)

I am absolutely, positively convinced of the power of thyroid. I am further convinced from the clinical data, patient experiences, and now my own personal experience, that low levels of hypothyroidism are being dramatically underappreciated and underdiagnosed.

I shudder to think of what my life would have been like 6 months or a year from now without correction of thyroid hormone.

Now, the tough question: Why the heck is this happening to so many people?

Speaking availability

Just a quick announcement:

If you would like to hear more about the concepts articulated in The Heart Scan Blog or in the Track Your Plaque program, I am available to speak to your group.

Among the possible topics:

Return to the Wild: Natural Nutritional Supplements That Supercharge Health
Why this apparent "need" for fish oil and other heart-healthy supplements? I discuss why some nutritional supplements make perfect sense when we are viewed in the context of primitive humans living modern lives, while other supplements do little.


Shrink Your Tummy . . .or, Why Your Dietitian is Fat!
Weight loss doesn't have to involve calorie counting, deprivation, or hunger pangs. But the conventional "rules" for weight loss and health have to be broken.

The Politically Incorrect Guide to Extraordinary Heart Health
Heart health is something that you can seize control over, something identifiable, correctable, and . . . reversible. Much of this can be achieved with little or no medication, nor procedures. I detail all the enormously empowering lessons learned through the Track Your Plaque program.


I can also present in-depth yet entertaining discussions on the power of vitamin D, natural cholesterol control, screening for heart disease, and similar topics covered in the blog.

To learn more, just e-mail us at contact@trackyourplaque, or call my office at 414-456-1123.

Learn how to eat from Survivorman


Look no farther than Discovery Channel to learn how humans were meant to eat.

The Survivorman show documents the (self-filmed) 7-day adventures of Les Stroud, who is dropped into various remote corners of the world to survive on little but ingenuity and will to live. Starting without food or water, the Survivorman scrapes and scrambles in the wilderness for essentials to survive in habitats as far ranging as the Ecuadorian rainforest to sub-arctic Labrador.

What does Survivorman have to do with your nutrition habits?

Everything. The lessons we can learn by watching this TV show are plenty.

Survivorman plays out the life we are supposed to be living: slaughtering wild game with simple handmade tools and his bare hands, identifying plants and berries that are safe to eat, trapping fish, scavenging the kill of other predators. He's even resorted to eating bugs and caterpillars, particularly following several days of unsuccessful hunting and scavenging.

What is notable from the Survivorman experience is what is absent: In the steppe, desert, tundra, or jungle, you will not find bread, fruit drinks, or Cheerios. You won't find farm-fattened, corn-fed livestock with meat marbled with fat.

Imagine the result of such an experience for us, drawn out over 6 months. Even an obese, diabetic, gluttonous, XXX dress size 350-lb woman would return a lean 105 lbs, size 0, non-diabetic, fully able to run miles in the wild tracking game.

Survivorman's quiet desperation of living in the wild, preoccupied with worries over where his next meal might be found, is a stark contrast to the bloated, shelves stacked floor-to-ceiling supermarkets, and our modern society's all-you-can-eat several times per day lifestyle.

Am I advocating selling the car and house and chucking modern society for the "safety" of the jungles of Borneo?

No, of course not. I am advocating taking a lesson from the clever experiment conducted by Mr. Stroud, a return-to-the-wild experience that should teach us something about how perverse our modern nutritional lives have become.