How Much Iodine Should We Prescribe?

Joseph Pizzorno, ND, Editor in Chief

While some clinicians/educators recommend daily iodine dosages of 10+ mg, others assert anything more than 300 µg/d risks toxicity. I am not aware of any other nutrient for which the integrative medicine community has such divergent views on dosage and safety! While helping design a multivitamin and mineral supplement, I found myself in the middle of experts whom I greatly admire and trust insistently giving me surprisingly divergent recommendations. Sounds like time to dive into the research. Using iodine as the search term for PubMed yields almost 100,000 articles.

Iodine Consumption Has Decreased Dramatically in North America

The research is clear that iodine consumption in North America has decreased substantially in the past 30 years. Iodine deficiency, once thought only a problem of the past and in developing countries (where it is typically over 50%), has now become endemic in the United States and Canada. This is due to a dramatic drop in the consumption of foods rich in iodine, decreased consumption of iodized salt, and changes in food processing that result in lower levels of residual iodine in foods.

According to the 2001-2002 National Health and Nutrition Survey (NHANES), iodine intake, measured via 24-hour urine test, has dropped from median levels of 320 µg/L during 1971-1974 to 165 µg/L in 2001-2002—a drop of 50%. , Recent research assessing iodine levels in the breast milk of lactating mothers in Boston found that only 47% contained sufficient amounts of iodine to meet infantrequirements. A recent study looking at NHANES data from 2007 to 2008 found that about 29% had a urinary excretion of <100 µg/L, indicative of deficiency, with 9% having a urinary iodine of <50 µg/L, indicative of moderate to severe deficiency. This is all made worse by an increasing exposure to iodine uptake inhibitors—perchlorate, nitrate, and thiocyanate—in the food supply. These trends clearly indicate an increasing risk for iodine deficiency.

Although mostly known as a required nutrient for thyroid hormone production, iodine and iodide are now known to be involved in diverse physiological processes. Only about 30% of the body’s iodine actually resides is in the thyroid tissue and hormones. The body concentrates iodide in the liver, salivary glands, breast tissue, gastric mucosa, and choroid plexus of the brain.

This growing deficiency may have resulted not only in an increase in thyroid dysfunction but also in fibrocystic breast disease, breast cancer and other malignancies, obesity, attention deficit hyperactivity disorder, psychiatric disorders, and fibromyalgia.

For an excellent, comprehensive review see the two-part iodine article by Lara Pizzorno, MA, LMT, at

I tested 200 adults in a corporate wellness program I have mentioned in previous editorials and found over 70% were deficient in iodine according to the thyroglobulin (Tg) test discussed below.

Assessment of Iodine Status

There are basically five ways to determine iodine status. Each test has advantages and disadvantages as summarized in the table below.

Table. Strengths and Weaknesses of Methods to Assess Iodine Status
Test Strength Weakness Notes
Spot urine Sensitive indicator of recent iodine intake Highly variable from day to day Not valid to assess iodine intake in individuals
24-h urine Sensitive indicator of recent iodine intake Does not measure thyroid function Considered the gold standard
Thyroglobulin Iodine intake over wks to mos; thyroid function Also elevated in thyroid damage and thyroid cancer Appears a functional measure of actual rather than just iodine intake
Thyroid stimulating hormone Useful indicator of iodine in the newborn Limited usefulness in other age groups The standard for thyroid activity
Thyroid enlargement (ie, goiter) Long-term deficiency (months to years); thyroid function Changes very slowly with iodine status; palpation has poor sensitivity Ultrasound detects enlargement far sooner and more accurately than palpation

Tg is found only in the thyroid. It is a precursor in the synthesis of thyroid hormone and has no presently known physiological role outside the thyroid. Its production is stimulated by thyroid-stimulating hormone (TSH) and a small amount leaks into the blood. Tg is present in the serum of all healthy individuals. In the absence of thyroid damage, the serum level of Tg is proportional to thyroid cell mass and TSH levels. Thus, serum Tg is elevated in iodine-deficiency due to TSH hyperstimulation and thyroid hyperplasia, which result in increased leakage into the blood stream. Serum Tg concentration of >10 µg/L is considered indicative of iodine deficiency. Tg levels correlate well with 24-hour urinary iodine. However, the reason Tg is of particular interest is that it seems to be measure of an individual’s actual iodine need rather than only a comparison to average iodine requirements. Of course, conditions causing inflammation of the thyroid gland will invalidate the results, as will an elevated anti-thyroid antibody (ATA).

Iodine (I2) vs Iodide (I-)

Part of the controversy in the integrative and conventional medicine communities is the interchangeable use of the terms iodide and iodine in the research literature as well as in books, lectures, etc, with iodine being the default term. These are different molecules with different physiological effects, organ absorption, and toxicity. Molecular iodine (I2) is not the same as ionic iodine (I-) that is found in potassium iodide. Of particular significance is that I2 is preferentially absorbed by fatty tissue, such as the breasts, compared to iodide that is preferentially taken up by the thyroid. Further complicating the issue is that some of the ingested I2 is converted to I- in the intestines.

The term iodine used below typically means iodide (even though most research studies do not differentiate) unless otherwise specified.

What is the Maximum Safe Dosage?

Key to determining the optimal dosage is to first determine the safe dosage: As Hippocrates says, “First, do no harm.” For adults, the World Health Organization has proposed that an iodine intake of 500 µg/d poses no excessive risk, and the European Food Safety Agency and the US Institute of Medicine have recommended 600 µg/d and 1100 µg/d, respectively, as the tolerable upper limit for iodine.

Most of the available toxicity data is from monitoring the effects of administration of iodine to iodine-deficient populations. Increasing iodine intakes in such populations is almost always accompanied by a clear rise in the incidence of hyperthyroidism (and sometimes hypothyroidism), the magnitude depending on the amount of iodine administered and the severity of the preexisting iodine deficiency. In general, those at high risk of developing iodineinduced hyperthyroidism have preexisting multinodular thyroid disease. Fortunately, it appears these initial hyperthyroidism reactions are not sustained, and most eventually return to normal function, even while patients continue to take the iodine supplements. The big challenge in determining maximum safe dosages is due to the studies of supplementation in deficient populations being what have been primarily used for determining safe dosages.

Several mechanisms are involved in the maintenance of normalthyroid hormone secretion, even when iodine intake exceeds physiologic needs by as much as a factor of 100. The sodium-iodide symporter (NIS) is a protein encoded by the SLC5A5 gene and is responsible for the transmembrane transport of iodine. Its level of activity contributes most to limiting thyroid dysfunction in the presence of excessive iodine exposure. Faced with an iodine excess, NIS decreases the transport of iodide into the thyroid cells, the ratelimiting step of hormone synthesis. However, this response takes several days to develop. The Wolff-Chaikoff effect is an autoregulatory phenomenon that inhibits organification (oxidation of iodide) in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream in response to a high or sudden increase in iodine levels. The Wolff-Chaikoff effect requires a high intracellular concentration of iodide. The block does not last long because eventually the sodiumiodide membrane transport system slows down, which allows intracellular iodide to decrease. In some susceptible individuals (eg, patients receiving radioiodine treatment of Graves’ disease or those with autoimmune thyroiditis), the sodium-iodide membrane transport system fails to shut down, the intracellular concentration of iodide remains high, and chronic hypothyroidism ensues.

Iodine excess may also cause hyperthyroidism. This happens in persons with goiters that have developed after long-standing iodine deficiency. These goiters may contain nodules carrying a mutation that confers a “constitutive” activation of the TSH receptor. This means loss of pituitary control with resultant nodule overproduction of thyroid hormone and thus iodine-induced hyperthyroidism upon supplementation. These autonomous nodules usually gradually disappear from the population after iodine deficiency has been properly corrected but not in everyone. More recent studies suggest that chronic high-iodine intake furthers classic thyroid autoimmunity (hypothyroidism and thyroiditis) and that iodine-induced hyperthyroidism may also have an autoimmune pathogenesis. However, not all research supports this assertion. One study looking at urinary iodine levels in several Japanese cities found no correlation with the incidence of thyroid antibodies.

Some have asserted that multi milligram dosages of iodine are safe because 10+ mg/d is the typical consumption in Japan. I was not able to confirm this. One study shows 1.2 mg/d of iodine due to the ingestion of seaweed in Japan, while a more recent study of dietary records, food surveys, urine iodine analysis (both spot and 24-hour samples) and seaweed iodine content estimated Japan daily intake of 1.0 to 3.0 mg. The thyroid antibody study above found daily iodine consumption of 1.5 mg of iodine in one of the cities.

Another study showed that even high dosages of iodide are not necessarily toxic. Due to a compounding error, a selenium-plusiodine supplementation study in New Zealand mistakenly gave participants (older people with average age of 73) >50 mg of iodine as iodate per day for 8 weeks. Thyroid hormones, selenium status, and median urinary iodine concentration were compared at weeks 0 and 8 and 4 weeks postsupplementation. Ten of 43 participants exposed to excess iodate showed elevated TSH (hypothyroidism) at week 8. In all but two, TSH had returned to normal by week 12 (ie, 4 weeks after supplementation ceased). In three participants, TSH decreased to <0.10 mIU/L (hyperthyroidism) at week 8, remaining low at week 12. In other words, about one in four study participants reacted to these extremely high dosages with either hypothyroidism or hyperthyroidism. As iodine deficiency has reemerged in New Zealand, I suspect that many of those who reacted had an undiagnosed nodular goiter.

Also, I can’t help but wonder if those who experience toxicity at modest dosages (other than those with nodular thyroids) are deficient in important balancing nutrients such as vitamin E and selenium.

The benefit of deficiency correction certainly outweighs the harm, yet there is clearly risk of harm in susceptible individuals. Finally, note that these toxicity studies are all of the iodide form.

What Is the Optimal Dosage?

There is no doubt that iodine deficiency causes serious health problems worldwide, especially for fetuses and children. Unfortunately, finding research on the optimum intake of iodine—in the absence of thyroid disease—for all health benefits appears nonexistent in the published peer-reviewed research. There are a few studies using high dosages of I2 for specific clinical purposes. Examples include fibrocystic breast disease and cancer.

One study looked at the use of I2 in daily dosages of 0, 1.5 mg, 3.0 mg, and 6.0 mg for 6 months in euthyroid women with fibrocystic breast disease unresponsive to local heat or nonprescription analgesics. Statistically significant, dose-dependent improvement, according to physician and patient rating, was found at the 3.0-mg and 6.0-mg dosages, but not in placebo or the 1.5-mg dosage. No dose-related increase in any adverse event was observed. A very interesting early study found that while 70% of women with fibrocystic breast disease responded to sodium iodide (in the form of Lugol’s iodine, which in this study was 95% iodide and 5% iodine), adverse thyroid dysfunction was high (4.0%) with another 3% developing iodism (increased lacrimation and salivation rhinitis weakness and skin). These developments resulted in the researchers deciding to try other forms of iodine. Switching to I2 (0.08-0.09 mg/kg body weight) resulted in comparable improvement with fewer—but not zero—adverse events, including 0.1% hyperthyroidism, 0.3% hypothyroidism, and 0.1% iodism. The main adverse event was a transient increase in pain in 5.7% of the participants, which the researchers attributed to structural remodeling of the breast.

While the clinical research is minimal, there is considerable cell line and animal research on the antiproliferative effects of I2. Iodine inhibits cancer cell growth as well as inducing apoptosis in cancerous and precancerous cells and in some models is even cytotoxic to several cancer cell lines. Interestingly, some studies have found that I2—but not iodide—caused apoptosis in several thyroid and breast cancer cell lines.

In a large study using lactating and nonlactating rats with and without carcinogen-induced mammary gland cancer, researchers administered high dosages of radioactive and nonradioactive iodine and iodide and then looked at gene expression, tissue concentration, thyroid activity, and cancercidal effects. The dose of I2 or potassium iodide was quite high: 0.05% of drinking water for 3 weeks (the equivalent of 500 mg/d in a human). The results were quite interesting. As expected, the high dose of potassium iodide initially significantly impaired thyroid hormone secretion followed by decreased NIS iodine transport with hormone levels returning close to normal after a few days. In contrast, I2 did not cause a drop in thyroid hormone levels (the thyroid’s adaptation to high I2 levels is apparently more effective than for iodide) and had higher update in the mammary gland, especially cancer tissues. In a later study, the same research team elicited the mechanisms of action and showed that these higher levels of I2 are antiproliferative and cytotoxic to various human cancer cell lines.

Similar promising research on the antiproliferative and apoptotic effects of various forms of iodine for prostate cancer in animals and human cell lines is now emerging.

Conclusion and Recommendations

One of the challenges of prescribing iodine is the lack of differentiation of iodine and iodide in the research and conversations. The research makes clear that their physiological effects, clinical application, dosages, and toxicology are very different.

Unequivocally, iodine deficiency is a common, worldwide problem. The daily intake of iodine/iodide for normal thyroid activity appears to be 200 µg to 300 µg. However, this is not necessarily the optimal level for other health benefits. If your patient has multinodular thyroid disease, the safe dosage is lower until the supplementation has allowed normalization of the thyroid. This will likely take many months, and those with goitrous nodules will require very careful titration of their iodine intake and may always be susceptible to iodine toxicity at even modest dosages.

In the absence of thyroid disease, the maximum safe dosage of iodide appears to be at least 1.0 mg/d. The maximum safe dosage of I2 is unclear but definitely higher.

Is there benefit in using higher dosages of I2? Definitely for women with disorders such as fibrocystic disease as well can breast cancer. High-dose I2 may also be indicated in women at high risk of breast cancer. The antiproliferative and cytotoxic effects of I2 for several common human cancer cell lines are intriguing and suggest prophylactic use of iodine for patients at high risk of cancer.

If you are going to prescribe high dosages of I2, I strongly recommend regularly monitoring Tg, TSH, thyroid hormone, and thyroid antibody levels.

Bottom line, high-dosage iodide will cause toxicity in a significant portion (about 25%) of the population. High-dosage I2 is likely safe for most, but definitely not all, patients.

Thanks to the Brain Trust

I’d like to thank my unofficial brain trust—leaders in nutritional medicine whom I contact when I am stuck on something or need another perspective—for their outstanding help on this challenging editorial: my coauthor on six(!) books, Michael Murray, ND,Peter D’Adamo, NDand editorial board members of Integrative Medicine: A Clinician’s Journal Alan Gaby, MD, Jeffrey Bland, PhD and Jonathan Wright, MD. Each provided expert guidance and commentary on this editorial. Excerpted below are some of their thoughts:

Jeffrey Bland, PhD. This is a very well-written editorial. My most sincere congratulations for taking on an important issue and doing a tremendous job navigating through the confusion. I have only one comment on the third to the last paragraph thatstarts “Is there benefit in using higher dosages of I2? Definitely for women with disorders such as fibrocystic disease as well can breast cancer. High-dose I2 may also be indicated in women at high risk of breast cancer.” Are you sure that you want to be so strong in your conclusion that “definitely” women with fibrocystic disease as well as breast cancer be treated with high dose iodine/iodide? The strength of this statement doesn’t seem consistent with the weight of the evidence that you describe earlier in your editorial.

Peter D’Adamo, ND. I have no idea what the best nutritional daily dose of iodine is. I also do not know how much noni juice my patients should drink nor whether calcium supplements will strengthen my patient’s bones or kill them via a massive heart attack. That is due to the fact that insufficient information—vicissitude—is our inevitable companion when we attempt to set standards for micronutrient dosage beyond the remediation of deficiency. It forces us to face the larger problem with only the simplest of word games: For example, in which situations are the descriptive terms sufficient sufficient, satisfactory satisfactory, proper proper, or optimum optimum?

In the case of iodine, the state-space (the sum total of all variables, functions and parameters) for even one multiorgan component, the sodium-iodide symporter (NIS) is enormous; complex extracellular stoichometrics; distribution in tissues other than thyroid; glycosylation dynamics in health and disease, etc. Any and all of these will suffice to thwart attempts to define optimal iodine standards. It might be possible to accumulate enough data (at least theoretically) to develop purely deterministic guidelines, but to me this appears unrealistic, impractical, and unlikely to be effectively predictive.

So what does that leave us with? I believe that we best consider a solution that approaches this dilemma heuristically, using old fashioned rules-of-thumb. A potential heuristic for use in these circumstances is actually among the simplest: informed trial and error.

“Informed” in that data are either already extant or can be developed to define the metabolic demands in specific situations: for example, the iodine requirements of a patient who is currently breast-feeding. These can then be assembled into the projected needs of a more complex scenario (female, high familial risk of breast cancer, currently breast-feeding, vegan dieter).

“Trial and error” in that once implemented, the dosage heuristic navigates the search-space (AKA, the patient) according some broad-based fitness algorithm. In this case, perhaps the combination of a primary biomarker such as thyroglobulin; a secondary biomarker of some nonthyroid sort but known to be influenced by the iodine variable, such as freedom from breast pain; and even tertiary parameters, biomarkers aberrant in that patient but thought to be unrelated to the first two, such as an elevated breath hydrogen or a low hematocrit. Over repeated iterations, the dosimetry heuristic is adjusted as per its feedback (any improvement in the fitness score it returns.) This feedback itself constitutes an additional enriched source of data for potential wider use.

Some readers may feel that I’ve merely described the best practices of any competent bedside physician, whilst those with a background in informatics might notice that I’m suggesting that the role of “evolutionary algorithm” be added to the job description of the practicing nutritional physician. Both opinions would probably be correct.

Alan Gaby, MD. My understanding is that thyroglobulin is useful for epidemiological studies but is not a reliable indicator of iodine status for individuals. While thyroglobulin does correlate with urinary iodine, correlations are not useful in the clinical setting unless they are close to 1.0. Furthermore, urinary iodine itself is not considered a useful indicator of iodine status, except among populations.

Elevated TSH in the United States is usually due to autoimmune thyroiditis and usually has nothing to do with iodine status. In an iodine-sufficient hypothyroid patient, iodine supplementation can make the hypothyroidism worse. Therefore, giving a hypothyroid patient more iodine on the basis of an elevated thyroglobulin level could be harmful.

(Editor response: perhaps a better use is to measure Tg, dose with iodine, and then remeasure Tg. If Tg goes down, the patient was low in iodine, but if it goes up, patient is receiving excessive iodine.) The emphasis is on “perhaps.” I see no reason to waste people’s money on a lab test of questionable value, particularly when relying on the results could be harmful. A 7-day diet history is probably the best indicator of iodine status.

Michael Murray, ND. In answering the question “What is the proper dosage of iodine?,” the major determinant should first be based upon the physiological need of iodine. Based upon iodine balance studies, it would be hard to justify dosages greater than 150 µg to the general population, certainly no greater than 300 µg. Regarding some of the comments in the editorial regarding the “endemic“ of iodine deficiency, it seems these statements refer to only specific subsets of the general population. According to the most recent NHANES data (see reference 4), the median urinary iodine concentrations for the general US population in 2005-2006 and 2007-2008 were 164 ug/L (95% confidence interval [CI] 154-174) and 164 ug/L (95% CI 154-173), respectively. The populations at risk for less than 125 ug/L included pregnant women and non-Hispanic black survey participants. So, to say that iodine deficiency is an endemic is certainly not substantiated especially since the conclusion of the study used in the editorial to reference an endemic of iodine deficiency concluded with “these findings affirm the stabilization of UI concentration and adequate iodine nutrition in the general US population since 2000.”

Also, in regards to the mention of the high percentage of “iodine deficient“ determined in the corporate wellness program as determined by thyroglobulin status, I have a couple of additional comments: (1) Is thyroglobulin a suitable indicator of iodine status in population-based assessments? and (2) What were the demographics and geography of the subject population? In other words, were there high percentages of Native Americans and non-Hispanic blacks? Were the participants in the interior part of North America or along the coast? Did they belong to some other population group that have been identified as being at greater risk for iodine deficiency or elevations of thyroglobulin despite normal iodine status (eg, was there a highpercentage of people indigenous to the Arctic, etc.)?

So, as far as what is the proper dosage of iodine for physiological need, it seems that 150 µg is sufficient and certainly no greater than 300 µg. In addition, basing optimal dosage on toxicity data does not seem appropriate. Just because iodine may be relatively nontoxic at supraphysiologic does not mean that it provides any additional health benefit. Furthermore, it may create more subtle disruption of physiology below a toxic effect.

Now, the other question that needs to be addressed is “What are the pharmacological or therapeutic dosage levels of iodine?” The answer to this question requires a discussion of the different molecular forms and review of the clinical data as expressed in the editorial. However, the clinical data are extremely preliminary, short term, and incomplete. So, in my opinion, no clear conclusions can be made at this time. For me the takeaway recommendation is to encourage increased dietary intake of foods naturally high in iodine while supplementing no more than 300 µg daily.

Jonathan Wright, MD. Having treated hundreds of women with fibrocystic breast disease since the 1970s with high-dose iodine (following the procedures taught by John Myers, MD) and having observed 100% of them eliminate all symptoms and dramatically shrink or eliminate their cysts, having monitored all of them for thyroid suppression, induction of hyperthyroidism, and/or autoimmune disease and having observed none, it appears to me that apparently widespread phobia concerning high-dose iodine (or iodide) if used in appropriate clinical situations and monitored carefully as necessary can result in suboptimal results for patients.Given our century’s prevalence of breast cancer, which threatens approximately half of all Americans, the breast cancer–preventing properties of iodine more than amply demonstrated by Bernard Eskin, MD, of the Drexel University College of Medicine, the relatively recent research showing that many breast cancer cell lines are actually killed by iodine and the widespread occurrence of unrecognized subclinical hypothyroidism, the recommendations for maximum safe daily dosages of iodide and iodide made by Dr Pizzorno are entirely justified and will do much more good than harm. In time, they may well be seen as conservative.

In This Issue

We are starting a new feature that I hope to include in most issues. I am quite sure this is going to be controversial—so your comments are welcome! While we work hard to make this journal a reliable science-based resource for the integrative medicine community, I think there is great value in also conveying more subjectively how clinicians think and how they actually practice. One way to do this is with case histories, another is to interview clinicians, and yet another is to help them to freely describe what they do and how they understand patients. Sometimes the result is not very scientific and, of course, there is always the bugaboo of the placebo effect seemingly validating virtually any theory or therapy. Nonetheless, there is a fundamental difference between carefully controlled and circumscribed clinical studiesand complex patients in real clinical practice. So, we are going to start publishing the thoughts and experiences of practicing integrative medicine doctors. These will not be submitted to peer review since I think there is value in learning what clinicians are really thinking and not what has been approved by others, no matter how expert. I want to be very clear that I do not necessarily agree with everything they will say. Nonetheless, these are all successful clinicians with some remarkable case histories. There is something to learn here. First is Wayne Steinke, ND, whose story of complete cure of a patient with well-documented advanced pancreatic cancer was so intriguing that the idea of this feature occurred to me.

Our interview is with Mehri D. Moore, MD, and my dear daughter Raven Bonnar-Pizzorno, MS, RD, of the Moore Center for Eating Disorders in Bellevue, Washington. No, this is not nepotism but rather a very interesting look at a success clinic helping people with serious, complex eating disorders through comprehensive, carefully integrated care.

We continue to receive some excellent submissions on nonpharmacological interventions. Majid Golabadi, MD; Habibollah Taban, MD; Mohammad Yaghoubi, MSc; and Ali Gholamrezaei, MD, provide us an intriguing pilot study on the use of hypnotherapy for opium addiction. As we all know, this is a very difficult condition to treat, so anything that helps reduce relapse without adverse events is welcome.

Michael Friedman, ND,and Joshua Baisley provide us a case study on the treatment of lymphoma with Pacific yew and pokeroot, two botanicals known to have anticancer, antiinflammatory, and immunostimulating properties. I think this most intriguing, especially considering long historic use of pokeroot for disorders of the immune system.

Steven C. Masley, MD, FAAFP, CNS, FACN; Lucas V. Masley; and C. Thomas Gualtieri, MD, provide us a disturbing look at the cognitive effects of mercury in seafood. While the omega-3 levels of deep-water fish are of huge benefit, their research shows that it is not enough to counter mercury if the levels are too high in the fish.

I find encouraging the growing research in integrative medicine. John Weeks summarizes in Industry Insights the International Research Congress on Integrative Medicine and Health (IRCIMH) in Portland which was attended by drew over 1000. Especially exciting is the outcomes research showing clinical efficacy and cost effectiveness. Ryan Bradley, ND, MPH reported that the use of naturopathic medicine, rather than a specific therapy or defined protocol, was effective in the treatment of diabetes. This is particularly significant since, as John states, “The beauty of this study is that it exemplified ‘real world research’ on the impact of a discipline (naturopathic medicine) on a population.” This is critically important as a key strength of integrative medicine is treating the unique person, not their disease, nor following a cookbook protocol.

Interesting that while my editorial on “Recognizing Our Heroes” for the Feb/Mar issue of IMCJ was in the printing process, Bill Benda, MD, was independently thinking along the same lines with his “The First Annual BackTalk Leadership Award,” which he presents this issue. As usual, his take on this is quite different from mine—which is why we make such good bookends! And thank you Bill for the very kind compliment.

(By the way, “Heroes” nominations are still open. Access the nomination form online:

Joseph Pizzorno, ND,Editor in Chief


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