Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.
Low thyroid: What to do?

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.

Comments (25) -

  • P

    2/8/2009 5:24:00 PM |

    How about acupuncture and chinese medicine? Anecdotally, they will be able to help you through monitored use of chinese herbs and acupuncture.

  • Anna

    2/8/2009 5:49:00 PM |

    I'd also like to add that if one can't get good thyroid care inside an HMO network or "universal" healthcare system, it can be money well spent to go "outside" the system  for private care.  Granted, paying for non-reimbursable care isn't cheap and one has to do a lot of investigating to make sure one isn't paying for more of the same inadequate care (or worse care).  But I think too many people who can afford to pay for private care suffer needlessly by doggedly sticking to inadequate care because alternatives cause a financial dent.  But in the long run, if one can find good care even though there is added expense, it can save a tremendous amount of suffering, as well as saving money.

    When I was seeing a thyroid doc out of my HMO network, I was still able to get my lab work done by the HMO approved lab  and covered by my HMO insurance (the lab faxed the results to the out-of state doc without question), though the results did go into the computerized file at my HMO network, so was visible to any HMO doc.  And my HMO insurance Rx plan covered the conventional meds prescribed by the out-of-network doc without question (but not the compounded Rx).  Yes, it cost me a few hundred dollars a year to see the doc once year, a few telephone consults, and the non-covered compounded Rx, but it well worth it.  I was finally feeling and functioning better.

    And when I went back to my HMO eventually (mostly because of travel scheduling difficulties in seeing the out-of-state doc), I was in a better position to make a case for similar care with the HMO endo (I told him flat out I'd had trouble getting good thyroid care from primary care physicians in the HMO and so went "private" for a couple years, but wanted to find someone local in the HMO for convenience) .  He doesn't do compounded Rx, and typically prescribes only Synthroid, but he accepted that I prefered T3 with the T4 (and he "accepted" the "odd" way I adjust my T4 dose with different amounts of 50 mcg Levoxyl on different days to get an overall weekly dose that works - the 50 mcg tablet has no dyes added and he accepted that I preferred Levoxyl over Synthroid).  So for the first time with the HMO system, I feel my thyroid care is more of a team effort that includes my input, instead of being at the mercy of whatever is dished out to me.  And if the situation changes, I will promptly go outside the HMO again.

  • Nameless

    2/8/2009 6:27:00 PM |

    I would also suggest using the Armour site to look for prescriber's.  Their site has a little 'doctor finder' feature.

    It doesn't mean they'll necessarily treat you, but they tend to be more open-minded that doctors who prescribe Synthroid only.

    Most doctors won't use body temperature as a guide, by the way. And most won't treat Hashimoto's unless your TSH is >5. I know it's wrong, but that's how it is.

    Supplementing iodine may be helpful, unless you do have Hashimoto's, then it could make it worse (so you know). But you won't know you have Hashimoto's until you get your thyroid antibodies tested.

    A couple of other suggestions:

    Ask your doctor for Free T3/T4 AND thyroid antibodies. If your TSH >3 and your anitbodies are high, it really improves your odds of getting treatment. Many doctors ignore antibodies, but some do pay attention to them.

    If your TSH or antibodies are high at all, ask your doctor for a thyroid ultrasound. If the ultrasound is abnormal at all, it improves your odds of getting treatment too.

    Just going to a doctor with a TSH of 1.5-2.0 and normal T3/T4, it'd probably be close to impossible to get treatment. It really helps if you have the antibodies or ultrasound or something else to show the doctor.

  • Anonymous

    2/9/2009 6:33:00 AM |

    No person should break the law.

    However, there might be people within the arctic circle who don't have easy access to a physician who is willing to prescribe natural thyroid, including armour thyroid.

    What to do in a situation like that?

    One solution:  Find a site on the internet that provides for ordering and shipping thyroid, including Armour Thyroid, without a prescription.  There is at least one site that can be found via google that will do this.

    Warning:  There are significant dangers in supplementing thyroid without being under a doctors care.

  • Dr. William Davis

    2/9/2009 12:50:00 PM |

    Thanks, Anna.

  • Anonymous

    2/9/2009 6:13:00 PM |

    Regarding the thyroid issues Dr. Davis has been commenting on lately, and wondering why it seems so prevalent, have you considered the possibility that diet is playing a role.

    And when I say diet, it's probably not in the way you think --

    Carbohydrate restriction can lower thyroid hormone output, especially conversion of T4 to T3. Those who practice caloric restriction tend to have lower levels of T3 too.

    If Dr. Davis is seeing somewhat low, but still in 'normal' range T3/T4, with perhaps sluggish T3 levels, in patients AFTER they change to a no wheat, low carb diet, perhaps that is the reason why? Or perhaps that's why Dr. Davis' own thyroid had somewhat sluggish numbers?

    But if people all have high thyroid antibodies too, or all have crummy thyroid levels while eating tons of carbs, that wouldn't be a reason then.

    Just throwing that out there to think about.

  • Don

    2/9/2009 6:49:00 PM |

    for those who are willing to do the research and check their tsh levels then ordering online is an option. start with a low dose 15 to 30 grains and then ck your tsh. Increase dose to normnal tsh levels.  There are multiple sites for armour and synthoid that do not require a prescription. When you take this road to self medication you must realize you are toally responsible for your actions and well being. Be sure you know what you are doing
    Don

  • Anna

    2/9/2009 8:14:00 PM |

    Lately I've been giving a lot of thought to the LC packaged foods that many people turn to when they first embark on a LC diet, such as low carb breads, crackers, etc.  For me, it was LC pita bread a few years ago, before I essentially went grain-free.  These products, in addition to usually having a lot of soy in them, also have added wheat gluten, to reduce the starch and boost the protein content.  Low carb they are, and generally will help with the BG control and overall weight reduction or maintenance.

    Both gluten-containing and soy foods are relatively new foods to the human diet (only consumed since the age of agriculture) and modern industrial processing bypasses many of the steps that earlier humans took to render them safer to consume.  Soy can be a powerful thyroid inhibitor (goitrogen)  and gluten can trigger an auto-immune response in susceptible people (genetic predisposition to gluten sensitivity is much more common than previously thought, though how widespread is subject to debate).  There does seem to be a strong connection to autoimmune thyroid conditions and issues with gluten.

    So people who eat a lot of soy and gluten-enhanced LC foods might be literally be shooting themselves in the thyroid, especially those who overconsume  consume them (dieters don't ever become overzealous, do they?  Smile), instead of foods that are naturally low carb and/or have a longer history in the human diet.

  • Anonymous

    2/9/2009 8:18:00 PM |

    I think ordering prescription medication over the internet from a less than reputable pharmacy, without a prescription, is a real bad idea. And if they don't require a prescription, that pretty much automatically makes them less than reputable.

    And don't assume thyroid medications are completely benign. They can have side effects too.
    And especially in patients with heart disease. You have to be titrated slowly and need to be under a doctor's care.

  • Lou

    2/10/2009 8:28:00 AM |

    DIY Armour/NTH treatments can be troublesome. If you are suffering from adrenal fatigue, starting immediately on thyroid replacement can cause heart palpitations and other symptoms of physical and mental anxiety. If you have low cortisol and DHEA (they invariably go together), you will probably need to take a low-dose steroid and/or DHEA replacement for a month before beginning thyroid. It is best to get these things tested first, even if you have to do it on your own. I think the Stop The Thyroid Madness author has put together some lab test packages for people to get the right things tested. And when you're taking the replacement steroids and hormones, you need to keep monitoring your levels every month at first, then every three-four months once you stabilise.

    Google for the "Top Thyroid Docs" list by Mary Shomon for sympathetic doctor suggestions/review.

  • Lou

    2/10/2009 8:33:00 AM |

    I forgot to add, the thyroid books by Dr Broda Barnes are good reading, easy to understand if you're a layman too. He had one on incidence of heart disease in patients with corrected thyroid function which is very interesting. I don't recall he mentioned wheat, but he certainly believed that we should eat good old saturated fats like butter, lard, coconut, etc, to support good health and thyroid.

  • Trinkwasser

    2/10/2009 1:19:00 PM |

    Anecdotally along with the iodine I've heard a brazil nut per day suggested for the selenium. Where I live is not selenium deficient, thanks to the end of the Ice Age glaciation: this is reputed to be one reason for the longevity here. Next time I catch a doctor I'll ask if there's much thyroid disease here (they will diagnose and treat here, my TSH was 0.99 so something is working!)

  • Anonymous

    2/10/2009 1:40:00 PM |

    That iodine dose may still be too low. Remember the RDA was set at a level just to prevent goiter, not for optimal health. Check out www.breastcancerchoices.org.
    Healthy Japanese get 12.5mg (12500 mcg) of iodine per day. Probably we are all low in iodine and bromine competes for binding sites. Bromine is ubiquitous in our chemically laden environment and is used as a dough conditioner by commercial bakeries---they used to use iodine. The thyroid gets the bulk of our low iodine but it turns out that iodine is also concentrated in our gonads, adrenals and especially the breasts. Our epidemic of breast cancer and fibrocystic disease may be due to iodine deficiency.

  • Saint Patrick

    2/10/2009 5:46:00 PM |

    If you cannot get this treatment on HMO, then you should look at going private. Believe me, it is not something that you can ignore

  • Eichler

    2/10/2009 7:52:00 PM |

    Dr. Davis,

    I realize that you aren't in the business of diagnosing ailments or conditions via the internet, but I've recently experienced some hypothyroidism symptoms (low body temp. average of 96.7, fatigue, weight gain, hair loss, etc..) that my Doctor insists are unrelated to the disease.  In addition, he has also just put me on a combination of Crestor and Trilipix for an abnormally high triglyceride reading, despite this reading being a one-time fluke.

    My labs are as follows:
    TSH:       2.761
    Thyroxine (T4): 6.4

    He was not interested in doing any more thyroid testing beyond these two.

    Lipids:
    Total Cholesterol: 165
    Triglycerides:     415
    HDL:               22
    LDL:               N/A

    After a week on the Crestor (10mg) / Trilipx (135mg) combo, I was stricken with muscle aches and pains, tinnitus, popping ears, dizziness and a foggy out-of-it feeling.  After two weeks and finding your site, I discontinued the use of the two cholesterol medications against the Doctor's advice.  I've since starting taking an Omega 3-6-9 supplement three times daily along with my daily multi-vitamin.  I also take diazide/HCTZ for slightly elevated BP (130/96) and have recently begun following a strick low-carb diet and exercise routine.

    Again, I don't expect a diagnosis from you, but would appreciate if if you could voice your thoughts on the viability of me continuing to find a doctor willing to be more open minded to thyroid issues as well as pursuing more natural remedies to lipid issues.  

    Thanks for providing such a valuable resource for those of us who are getting fed up with the flawed standard of care that is currently being forced on so many people.



    My labs show the following.

  • Dr. William Davis

    2/10/2009 9:13:00 PM |

    I agree on the iodine dose question.

    The difficulty comes in trying to generate conversation through the blog for people who may or may not, for instance, have underlying Hashimoto's thyroiditis or thyroid nodules, in which case taking higher doses of iodine can trigger extreme excesses of thyroid hormone.

  • Anonymous

    2/10/2009 10:14:00 PM |

    I had been on Sythyroid for a few years but no one had ever mentioned or tested for Hashimoto's. Still feeling horrible, I found a holistic MD, and was diagnosed with Hashimoto's and started on Armour.
    Do I still have Hashimoto's or is it quiet now that I am taking a different hormone?
    The holistic said it would "kill" my thyroid and move on to another area, like adrenals.
    I did have a positive ANA for many years and tested for Lupus, RA, etc. many times. Then routine testing showed my ANA had returned to normal values.  
    Any ideas because my current endo. sure isn't forthcoming with any and doesn't/hasn't tested for antibodies.  He feels I am just hypothyroid.
    I appreciate all your information!

  • Nameless

    2/11/2009 5:20:00 AM |

    To test for Hashimoto's you need your TPO and TGAB antibodies tested. If they are above normal range, you probably have it. The definitive diagnosis is via a biopsy, but without a nodule that isn't usually done. An ultrasound is another diagnostic tool -- if your thyroid looks enlarged, nodular or all lumpy, along with antibodies, it's pretty safe to say you have Hashimoto's.

    I have never read, or heard of, Hashimoto's 'attacking' other organs after your thyroid is burnt out. That theory seems a bit out there to me.

    Antibodies can fluctuate, and with thyroid hormones usually become lower over time.  Inflammation tends to be reduces with hormones too.

  • Trinkwasser

    2/11/2009 4:13:00 PM |

    OK I caught one of our GPs yesterday, the selenium in the soil connection appears to be a non-starter. Her experience was that she found hypothyroid "quite often" predominantly in post-menopausal women and with incidence increasing with age. It's impossible to compare numbers with other areas since they actively look for the condition here and don't elsewhere. Also we have a lot of local longevity so more patients with systems wearing out purely through ageing.

  • Anna

    2/14/2009 12:27:00 AM |

    I always wonder about something I hear frequently - the issue of "soil mineral depletion".  Not that it isn't possible, but how significant is this and how widespread?  People don't generally eat "locally" produced food anymore; food supplies are distributed from all over the globe now, though agriculture is quite intense in some places, like the Central Valley of California, or cornfield in Iowa.  Wouldn't the shipping of food products all over sort of "average out" the minerals like iodine and selenium?  Or are  all the major agricultural regions of the world growing with depleted soil propped up with little more than NPK replacement?  

    I'm actually more into local, seasonal organic food than worldwide food.  LIving near the coast, presumably there is adequate iodine in the soil, but here I am, hypothyroid anyway.  Just wondering...

  • Trinkwasser

    2/15/2009 3:47:00 PM |

    Hard to tell about the soil mineral depletion thing, there are major regional variations which can show in animal diseases and require supplementation, salt licks etc. as well as human disease clusters. Deficiencies can show before "deficiency diseases"

    I trialled several different supplements but none of them made any discernible difference, probably a widely varying diet helps, plus fish, and local farmers who use high levels of organic manure and feed the soil as a whole rather than (increasingly expensive) stuff out of a bag and treat the soil as a sterile growing medium. Grass-fed rather than grain-fed meat, and game, probably helps too in picking up trace elements

    The downside of World Trade may be that while you get more trace elements from crops from different regions you are probably also getting more pesticides some of which are banned in the West

  • roaminghermit

    2/20/2009 8:35:00 PM |

    I've been doing so great after taking 1 1/2 gr nature-Throid brand of thyroid since october 08 and stopping all statins. Taking the Now D-3 at 5,000 per softgel. Now if I can just get back in the forums again....LOL   Dennis  still no 4th heart attack since 12/04

  • Laura

    3/14/2009 6:44:00 PM |

    I wish my family doctor was open to new things. I asked him about Armour thyroid he said that he has hundreds of patients on Synthroid with no problems and I don't want to start a new prescription without my family doctor knowing about it. I'm on 75mcg of Synthroid and would really like to try Armour thyroid...might have to wait until he retires (could be soon) before I see if I can get Armour..

  • Jessica

    5/8/2009 1:23:00 AM |

    Dr. Brownstein (Family physician, holistic doc in Michigan) in his book, "Iodine, Why You need it, Why You can't live without it" makes an interesting case for temporarily increased TSH (5-30mU/L higher) after correcting iodine deficiency.

    In addition to just stimulating thyroid hormone production, TSH also increases the production of the iodine transport cells (NIS). Without more NIS available, iodine couldn't enter the cells and be utilized. Therefore, increased TSH makes sense during the initial phase of iodine correction.

    As one increases their iodine consumption, they could experience this increase in TSH for as long as several months. As long as the T3 and T4 levels are normal, then the TSH elevation probably isn't a sign of hypothyroidism.

    If you haven't yet read this book, it's worth the 2 hours it took me to get through it.

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