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.
Iodine update

Iodine update

As the iodine experience grows, I've made several unique observations.

Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.)

Among the phenomena I've observed:

1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development.

2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.

3) Reversal of small goiters also occurs over about 6 months.

4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months.

5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet.

6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures.

7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L.


Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females.

All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.

Comments (30) -

  • GOJI BERRY

    7/4/2010 10:45:21 AM |

    Its really very much helpful.

  • google

    7/4/2010 12:41:31 PM |

    Initially by eating iodine-rich seaweeds daily, and then by taking 12.5 mg of Iodoral daily, my required T4 dose has decreased dramatically: from 165 ug per day to 100 ug per day so far. None of my doctors have every seen anyone reduce their T4 dose like this.

    It may not be the case that dramatic TSH increase on 12.5 mg or more of Iodoral is a sign of iodine toxicity. The docs with the most experience with mg level iodine supplementation (Abraham, Brownstein, Flechas) seem to agree that sometimes TSH will rise a lot, temporarily, but generally without hypothyroidism. They  believe this is a  functional adaption to the correction of iodine deficiency--i.e., TSH appropriately upregulating various aspects of iodine and thyroid hormone metabolism, including the iodine symporter system. Quite a few people have supplemented with doses of 100 mg per day or more with apparently no signs of iodine toxicity.

    See Dr. David Brownstein's book, "Iodine: Why You Need It, Why You Can't Live Without It," and the articles by Dr. Guy Abraham, the pioneer of modern iodine orthosupplementation, at http://www.optimox.com/pics/Iodine/opt_Research_I.shtml.

  • Anonymous

    7/4/2010 1:17:30 PM |

    Should iodine be taken with something (i.e. oil, etc) to help with absorption?

    -- Boris

  • Lori Miller

    7/4/2010 3:36:45 PM |

    Is iodine stored in fat or fluids? In other words, can a person eat a bunch of iodine-rich seaweed once or twice a week, or should it be eaten every day if you're going that route?

  • Dr. William Davis

    7/4/2010 10:46:22 PM |

    HI, Google--

    Read it. Know his stuff.

    I think he's got a lot of great lessons to teach us. But not in this case. This was a clear-cut instance of extreme TSH elevation with prolonged iodine. This was not the phenomenon that David Brownstein describes  of modest TSH increase in the face of early iodine supplementation, an effect I see every day with great frequency.

  • Anonymous

    7/5/2010 1:17:30 AM |

    Dr Davis

    Regarding your post "This was a clear-cut instance of extreme TSH elevation with prolonged iodine"

    Can you please explain more in layman's term?

    So iodine meds supplementation should not be whole year round?

    But iodine foods can be eaten everyday?

  • Garry

    7/5/2010 1:19:20 AM |

    Are there cases of patients being "allergic" to iodine?  I'm thinking of those who have reacted to some form of seafood in the past and now might be reluctant to try iodine supplementation.

  • Samantha

    7/5/2010 1:15:39 PM |

    What do you think about iodine and hashimotos´s? Should they supplement too? Regular medical advice seems to dissuade.

  • WilliamS

    7/5/2010 2:15:30 PM |

    Hi Dr. Davis,

    I'm curious if your patients with high TSH levels also showed clinical signs of hypothyroidism. I ask because I've read all the work I can find from the three docs most experienced with iodine supplementation (Abraham, Brownstein, and Flechas) and I don't recall any of them reporting any cases of iodine-induced clinical hypothyroidism—elevated TSH, yes, but clinical illness, no. And they use much higher iodine does than you do, in some cases ten to twenty times higher, for years.

    I'm also curious if you are aware of any plausible mechanism for iodine-induced hypothryroidism at the doses you are using. Other than than the mythical Wolf-Chaikoff effect (see http://www.optimox.com/pics/Iodine/IOD-04/IOD_04.html), I'm not aware of any.

    Since, as with Vitamin D, iodine deficiency appears to be extremely widespread and perhaps just as dangerous, clarifying any potential for toxicity that might discourage supplementation seems worthwhile.

    Thanks.

  • Anonymous

    7/5/2010 7:38:05 PM |

    What advantage does kelp have over something like potassium iodide?

    Although kelp is natural, it also tends to collect lead, etc. from the environment, which may not be so healthy.

  • Dr. William Davis

    7/5/2010 8:33:27 PM |

    Hi, Garry--

    My understanding of the iodine allergy issue is that, not being a protein, there is no such thing as genuine iodine allergy.

    There is something called "anaphylactoid reactions" to iodine-containing x-ray dye, which is not iodine allergy, but a reaction to the osmolality of the solution.

    There also seems to be allergy to iodine-modified proteins that can occur in fish and shellfish. Most of these people, in my experience, can safely take an iodine supplement. After all, most of these people use iodized salt.

    Very rarely, for reasons I do not understand, there seems to be a genuine allergy to iodinated compounds. I have met one or two people like this.

  • rmarie

    7/5/2010 8:36:35 PM |

    I have been taking an iodine supplement in liquid form called 'Iosol' off and on for years. It has been around a long time yet I have never seen it mentioned in any blogs. It is said to be water soluable, that is if the body doesn't need it it is excreted...so it's fairly safe to take. Here are two links for more info.

    The company that makes it http://www.tpcsdirect.com/

    and a good description on Byron Richard's site:
    http://www.wellnessresources.com/products/iosol_iodine.php

    Are you familiar with it Dr. Davis? Or anyone else?

  • William Trumbower

    7/5/2010 10:43:47 PM |

    I use Iosol quite frequently in my practice.  Particularly if the patient is on thyroid medication, as too high a dose can trigger hyperthyroid symptoms.  Some people will get acne on higher dose of I, probably due to excretion of other Halogens such as Bromine from the tissues.  I never use the 12.5mg dose to start.  My usual routine is Iosol 1drop daily increasing to 4 drops over 4-6 weeks (1drop=180mcg) and then switch to TriIodine capsules 6.25mg daily (available at our local health food store).  The only drawback to Iosol is that it does not contain Iodide as does Iodoral or TriIodine.  The other benefit to Iodine is the reduction in fibrocystic breast change and probably  breast cancer and prostate cancer.   I have only been doing Iodine for the past year, so I can't comment on cancer prevention results, but one of my pts. who was getting mammograms/MRI scans every 6 months for dense breast tissue with a terrible family history of Ca, has been on triIodine for 6 mon.  The radiologist asked to see her ID as her films did not look like they did 6 mon ago!   I also recommend VitD and correction of progesterone deficiency (estrogen dominence) to decrease breast cancer risk.

  • Anonymous

    7/5/2010 10:49:33 PM |

    Dr. Davis,

    Am I too presumptuous to assume that part of America's obesity crisis is due to our inefficient metabolisms caused, in part, by an iodine deficiency?

  • Catherine

    7/6/2010 1:17:02 AM |

    Anyone with a high Reverse T3 problem needs to be careful with iodine.  There are quite a few reports coming in on the thyroid forums that it increases RT3.  Apparently, if you have a problem converting T4 into RT3 instead of T3, it will sometimes encourage the RT3 conversion. Would love to hear any feedback/experiences from docs or thyroid patients on this.
    Warm regards, Catherine
    (I think we have 3 or 4 different Catherines posting here!)

  • MissPkm

    7/6/2010 1:21:07 PM |

    Great post, I am taking kelp at this point and you are so right - the energy I get from it is amazing! I am still very confused about the T3, T4, and TSH - what is normal, what is preferred and so on. What should I look for when I have a test done? If possible can anyone direct me to a easy to read basics on thyroid health and kelp/iodine supplement that describes the test results? I would like to go to the doctor to have some new tests done but if I can't understand the results then what good do they do?! Don't even know for sure that my doctor would be able to explain it to me...

  • Anonymous

    7/6/2010 2:04:03 PM |

    My two main concerns would be Hashimotos and potential pre-cancerous cells... both of which may be aggravated by iodine supplementation.  Do you make a point to rule both of these out before beginning supplements?

  • julianne

    7/7/2010 12:58:00 AM |

    I have Auto-immune thryroid disease, and have elevated anti-bodies, TSH,normal T4 and T3.
    I started taking a highish dose of iodine and my thryoid started enlarging and TSH shot up. As soon as I decreased the dose to RDI the enlargement stopped - in fact it's a little smaller.

    Can you explain more about your recommendations for AITD (Hashimotos)
    I am taking omega 3, vit D selenium, iodine, zinc, magnesium and doing strict paleo especially strict no gluten as I know there is a connection. I am not overweight, and have only mild thyroid symptoms sometimes.

  • Anonymous

    7/7/2010 4:11:00 AM |

    Hi
    I've been reading you're thyroid articles so I went out and bought a thermometer.
    Seems my temperature throught the day varies from 35.5C to 36.8C. (just measured today)
    That would sounds like possible hypothyroidism accoridng to your other articles.
    But reading arround I've seen lower body temperatures are typical when on calories restriction diets which I kinda do. And also that lower levels of T3 when under calorie restriction diet is one of the possible benefits of it.
    Anyway I'll go out and get some blood tests to get more information about my thyroid.
    But would like to know if you have data on body temperature of people on calorie restricted diets with healty thyroid.

  • Jim

    7/7/2010 12:36:19 PM |

    @Julianne,

    There's a newly posted series about iodine and AITD over at The Healthy Skeptic.

    The first of the three is at http://thehealthyskeptic.org/the-most-important-thing-you-may-not-know-about-hypothyroidism

  • Daniel

    7/7/2010 5:54:15 PM |

    Your post contains opposite advice to that given in this blog post at healthyskeptic:

    http://thehealthyskeptic.org/iodine-for-hypothyroidism-like-gasoline-on-a-fire

  • J. Huggins

    7/7/2010 6:01:11 PM |

    William Trumbower recommended using Trilodine capsules after a few weeks of Iosol for people who are presently on thyroid medication. I am presently taking Synthroid and have been for many years now. I have tried to find the Trilodine but with no success.  Is there another name or product that will do the same thing, or could you advise me as where I can purchase it?

  • Maniek

    7/9/2010 5:13:48 PM |

    http://curezone.com/upload/_I_J_Forums/Iodine/Maniek/flechas_questions_answers_2006_lynn.doc

    http://curezone.com/upload/_I_J_Forums/Iodine/Maniek/Iodine_New_Member.doc

    Rread frends Smile

  • WilliamS

    7/10/2010 12:47:31 AM |

    I came across an account of Dr. Flechas's views on iodine-induced hyperthyroidism (he's one of the docs most experienced with iodine supplementation). Apparently it does happen on occasion, but it's not necessarily a reason to discontinue iodine. The source for this is:

    http://curezone.com/upload/_I_J_Forums/Iodine/Maniek/flechas_questions_answers_2006_lynn.doc



    What happens to thyroid hormone production in the presence of iodine supplementation?

    Iodine supplementations should be prescribed only when iodine testing indicates iodine deficiency. Iodine testing kits can be ordered from my office (828 684 3233) by individuals or by medical practitioners.

    Traditional medical literature indicates that patients who have thyroid nodules or thyroid goiter may have the potential to develop hyperthyroidism when supplementing with iodine. Hence, before commencing iodine supplementation, it would be advantageous for a person to have their primary care doctor order a thyroid ultrasound to rule out the possibility of pre-existing goiter or thyroid nodules.
    The primary care doctor should also order thyroid lab work (to be used as a baseline) before prescribing iodine therapy and this lab work should be repeated and followed at regular intervals during the patient's iodine therapy.

    For iodine therapy patients not also on thyroid hormone replacement therapy, adjustments to the iodine therapy should be made if signs of hyperthyroidism should occur.

    Should signs of hyperthyroidism occur in patients who are taking thyroid hormone replacement therapy as well as taking iodine supplementation, the physician should first recommend an adjustment in the thyroid hormone therapy rather than in the iodine supplementation.

    This adjustment in therapy is recommended because iodine is required not only by the thyroid but is required for the proper functioning of many other tissues.

    The presence of pre-existing thyroid nodules or goiter does not preclude the patient from iodine supplementation therapy. In fact, in the extensive research with iodine therapy done in my office, I have seen many case of pre-existing thyroid nodules and goiter shrink in the presence of iodine therapy.

    Hyperthyroid patients. Graves disease patients and other with autoimmune disease take iodine also but use lithium and copper among other minerals (he didn't say) to decrease the overproduction of thyroid hormones. Iodine isn't reduced because it's the neutralizer of the thyroid.  Patients in a thyroid storm with high heartbeats are given iodine to calm it down as normal medical practice.


    Goiters. In some patients with goiters the iodine will stimulate it to produce more thyroid hormone and the patient will suddenly look hyperthyroid with elevated T4 and losing weight. As the goiter shrinks this normalizes. 


    http://www.helpmythyroid.com/iodine.htm

  • WilliamS

    7/10/2010 12:48:03 AM |

    I came across an account of Dr. Flechas's views on iodine-induced hyperthyroidism (he's one of the docs most experienced with iodine supplementation). Apparently it does happen on occasion, but it's not necessarily a reason to discontinue iodine. The source for this is:

    http://curezone.com/upload/_I_J_Forums/Iodine/Maniek/flechas_questions_answers_2006_lynn.doc



    What happens to thyroid hormone production in the presence of iodine supplementation?

    Iodine supplementations should be prescribed only when iodine testing indicates iodine deficiency. Iodine testing kits can be ordered from my office (828 684 3233) by individuals or by medical practitioners.

    Traditional medical literature indicates that patients who have thyroid nodules or thyroid goiter may have the potential to develop hyperthyroidism when supplementing with iodine. Hence, before commencing iodine supplementation, it would be advantageous for a person to have their primary care doctor order a thyroid ultrasound to rule out the possibility of pre-existing goiter or thyroid nodules.
    The primary care doctor should also order thyroid lab work (to be used as a baseline) before prescribing iodine therapy and this lab work should be repeated and followed at regular intervals during the patient's iodine therapy.

    For iodine therapy patients not also on thyroid hormone replacement therapy, adjustments to the iodine therapy should be made if signs of hyperthyroidism should occur.

    Should signs of hyperthyroidism occur in patients who are taking thyroid hormone replacement therapy as well as taking iodine supplementation, the physician should first recommend an adjustment in the thyroid hormone therapy rather than in the iodine supplementation.

    This adjustment in therapy is recommended because iodine is required not only by the thyroid but is required for the proper functioning of many other tissues.

    The presence of pre-existing thyroid nodules or goiter does not preclude the patient from iodine supplementation therapy. In fact, in the extensive research with iodine therapy done in my office, I have seen many case of pre-existing thyroid nodules and goiter shrink in the presence of iodine therapy.

    Hyperthyroid patients. Graves disease patients and other with autoimmune disease take iodine also but use lithium and copper among other minerals (he didn't say) to decrease the overproduction of thyroid hormones. Iodine isn't reduced because it's the neutralizer of the thyroid.  Patients in a thyroid storm with high heartbeats are given iodine to calm it down as normal medical practice.


    Goiters. In some patients with goiters the iodine will stimulate it to produce more thyroid hormone and the patient will suddenly look hyperthyroid with elevated T4 and losing weight. As the goiter shrinks this normalizes. 


    http://www.helpmythyroid.com/iodine.htm

  • Anonymous

    7/10/2010 12:48:29 AM |

    I came across an account of Dr. Flechas's views on iodine-induced hyperthyroidism (he's one of the docs most experienced with iodine supplementation). Apparently it does happen on occasion, but it's not necessarily a reason to discontinue iodine. The source for this is:

    http://curezone.com/upload/_I_J_Forums/Iodine/Maniek/flechas_questions_answers_2006_lynn.doc



    What happens to thyroid hormone production in the presence of iodine supplementation?

    Iodine supplementations should be prescribed only when iodine testing indicates iodine deficiency. Iodine testing kits can be ordered from my office (828 684 3233) by individuals or by medical practitioners.

    Traditional medical literature indicates that patients who have thyroid nodules or thyroid goiter may have the potential to develop hyperthyroidism when supplementing with iodine. Hence, before commencing iodine supplementation, it would be advantageous for a person to have their primary care doctor order a thyroid ultrasound to rule out the possibility of pre-existing goiter or thyroid nodules.
    The primary care doctor should also order thyroid lab work (to be used as a baseline) before prescribing iodine therapy and this lab work should be repeated and followed at regular intervals during the patient's iodine therapy.

    For iodine therapy patients not also on thyroid hormone replacement therapy, adjustments to the iodine therapy should be made if signs of hyperthyroidism should occur.

    Should signs of hyperthyroidism occur in patients who are taking thyroid hormone replacement therapy as well as taking iodine supplementation, the physician should first recommend an adjustment in the thyroid hormone therapy rather than in the iodine supplementation.

    This adjustment in therapy is recommended because iodine is required not only by the thyroid but is required for the proper functioning of many other tissues.

    The presence of pre-existing thyroid nodules or goiter does not preclude the patient from iodine supplementation therapy. In fact, in the extensive research with iodine therapy done in my office, I have seen many case of pre-existing thyroid nodules and goiter shrink in the presence of iodine therapy.

    Hyperthyroid patients. Graves disease patients and other with autoimmune disease take iodine also but use lithium and copper among other minerals (he didn't say) to decrease the overproduction of thyroid hormones. Iodine isn't reduced because it's the neutralizer of the thyroid.  Patients in a thyroid storm with high heartbeats are given iodine to calm it down as normal medical practice.


    Goiters. In some patients with goiters the iodine will stimulate it to produce more thyroid hormone and the patient will suddenly look hyperthyroid with elevated T4 and losing weight. As the goiter shrinks this normalizes. 


    http://www.helpmythyroid.com/iodine.htm

  • WilliamS

    7/10/2010 12:55:25 AM |

    Sorry for the multiple identical posts regarding Dr. Flechas. Google (Blogger) kept giving an error that made it seem the posts hadn't been published.

  • mtflight

    9/16/2010 6:20:25 PM |

    I second the healthy skeptic post.  In the presence of TPO auto antibodies (Hashimoto's), it could backfire as the autoimmune attack may worsen.

    I've read that autoimmune thyroid disease is more common in iodine sufficient areas, which correlates too.

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