Boron for Better Teeth, Bones, Thyroid and Parathyroid

“It has been suggested that boron is to the parathyroids what iodine is to the thyroid gland.”

~ Content Source

Boron is a mineral or trace element that is found in food and the environment. It has an atomic weight of 10.81 and symbol B. 

Boron is a tough element, very hard, second only to carbon (diamond).

Boron is an essential nutrient for all green plants and is present in all plants and unprocessed foods.

Boron compounds such as borax (sodium tetraborate, Na2B4O7.10H2O) have been known and used by ancient cultures for thousands of years. Borax is a white powder consisting of soft colourless crystals that dissolve easily in water. The name ‘borax’ is derived from the Arabic buraq, meaning white. 

Boron is an indispensable element in NIB (Neodymium-Iron-Boron) magnets, invented in the early 1980s, which are used in computers, mobile (cell) phones etc.

Health Effects of Boron

Borax and boric acid have basically the same health effects with good antiseptic, antifungal and antiviral properties, but only mild antibacterial action.

Boron is essential for the integrity and function of cell walls and for the way signals are transmitted across membranes. It is distributed throughout the body with the highest concentration in the parathyroid glands followed by bones and dental enamel. It is essential for healthy bone and joint function, regulating the absorption and metabolism of calcium, magnesium and phosphorus through its influence on the parathyroid glands. It has been suggested that boron is to the parathyroids what iodine is to the thyroid gland.

The parathyroid glands are small endocrine glands in the neck that produce parathyroid hormone. Humans usually have four parathyroid glands which are located on the rear surface of the thyroid gland. The parathyroid glands control the amount of calcium in the blood and within the bones. The main function is to maintain the body’s calcium levels within a very narrow range, so that the nervous and muscular systems can function properly. Parathyroid hormone controls calcium and phosphate homeostasis, as well as bone physiology.

Boron deficiency causes the parathyroid glands to become overactive, releasing too much parathyroid hormone which raises the blood levels of calcium by releasing calcium from bones and teeth. This then leads to arthritis, osteoporosis and tooth decay.

Boron also affects the metabolism of steroid hormones, and especially the metabolism of sex hormones. It increases low testosterone levels in men and oestrogen levels in menopausal women. It also has a role in converting vitamin D to its active form, thus increasing calcium uptake and deposition into bone. It is also said to improve thinking skills and muscular coordination.

Dietary Sources of Boron

Boron occurs in various forms in fruits (especially dried), vegetables, legumes and nuts. The actual amount varies, linked to the soil content of boron. The amount of boron is rather low, so that it is relatively easy to develop deficiency of boron. Foods with the highest content of boron (from www.algaecal.com/boron) include:

   
Food Boron (mg/100g)
   
Almond 2.82
Apricots (dried) 2.11
Avocado 2.06
Beans (red kidney) 1.40
Brazil Nuts 1.72
Cashew Nuts 1.15
Chick Peas 0.71
Dates 1.08
Hazel Nuts 2.77
Lentils 0.74
Prunes 1.18
Raisins 4.51
Walnut 1.63

Boron and Bone Health

Boron plays an important part in supporting healthy bones since it is involved with calcium and magnesium metabolism and vitamin D.

In a study of postmenopausal women, a boron-deficient diet was consumed for 119 days, followed by 48 days of boron supplementation. On the boron-depleted diet (0.25mg boron/day), the participants demonstrated increased urinary loss of both calcium and magnesium. On the boron-supplemented diet (3mg boron/day) however, they showed less urinary excretion of calcium and magnesium, as well as increased levels of two hormones associated with healthy bone mass.

From this study, adequate boron intake is essential to preserve the body’s stores of bone-building calcium and magnesium.

The researchers also studied the women during periods of both adequate magnesium intake and magnesium deficiency. Boron helped to preserve the essential stores of calcium and magnesium in the body. While the magnesium-depleted diet was associated with an increased loss of calcium in the urine, boron supplementation significantly reduced urinary loss of both calcium and magnesium. The researchers observed that boron deprivation produced changes similar to those seen in osteoporosis, and adequate boron status helped prevent calcium loss and bone demineralisation in postmenopausal women.

(Nielsen, F.H et al. Journal of Federation of American Societies for Experimental Biology (FASEB-J) 1987 Nov:1(5):394-7)

Thus boron has important applications in helping women preserve bone mass and in preventing osteoporosis following menopause.

Boron may help to alleviate the detrimental effects of vitamin D deficiency on calcium metabolism. Vitamin D is crucial to bone health because it helps to support calcium absorption.

People in an environment that is boron rich and who consume boron-rich foods have been shown to have less joint disorders. It is suggested that deficiencies of boron could contribute to the development of osteoarthritis.

Dosage of Boron

Ideally, boron should be obtained from the foods listed above.

If taken as a supplement, 3mg-6 mg of boron daily is recommended for bone health. A higher dose, up to 9mg per day, is suggested in the management of osteoarthritis. Commercial supplies generally come in 3 mg capsules (eg those from iherb.com).

Boron is often combined with a calcium supplement.

The following is an economical way of obtaining a therapeutic source of boron:

Dissolve a teaspoonful of borax (5-6 grams) in one litre of water. This is your stock solution. A standard dose is one teaspoonful (5ml) of stock solution. This contains 25-30mg of borax and provides about 3mg of boron. Take one dose daily with drink or food.

Up to 10mg of boron daily is considered safe. Toxic effects appear at an intake of about 100mg. My personal regimen contains about 165mg of boron per day with no toxic effects. However I did build up to that slowly over a 6 month period.

*Copyright 2012: The Huntly Centre.

Disclaimer: All material in the huntlycentre.com.au website is provided for informational or educational purposes only. Consult a health professional regarding the applicability of any opinions or recommendations expressed herein, with respect to your symptoms or medical condition.

~Further Reading – Nothing Boring About Boron

Mood, Personality, and Behavior Changes During Treatment with Statins: A Case Series

~Content Source – PDF: Mood, Personality, and Behavior Changes During Treatment with Statins

ABSTRACT

Psychiatric adverse drug reactions (ADRs) have been reported with statin use, but the literature regarding statin-associated mood/behavioral changes remains limited. We sought to elicit information germane to natural history and characteristics of central nervous system/behavioral changes in apparent connection with statin and/or cholesterol-lowering drug use, and delineate mechanisms that may bear on an association. Participants (and/or proxies) self-referred with behavioral and/or mood changes in apparent association with statins completed a survey eliciting cholesterol-lowering drug history, character and impact of behavioral/mood effect, time-course of onset and recovery in relation to drug use/modification, co-occurrence of recognized statin-associated ADRs, and factors relevant to ADR causality determination. Naranjo presumptive ADR causality criteria were assessed. Participants (n = 12) reported mood/behavior change that commenced following statin initiation and persisted or progressed with continued use. Reported problems included violent ideation, irritability, depression, and suicide. Problems resolved with drug discontinuation and recurred with rechallenge where attempted. Eight met presumptive criteria for “probable” or “definite” causality; others had additional factors not considered in Naranjo criteria that bear on casual likelihood. (1) Simvastatin 80 mg was followed in 5 days by irritability/depression culminating in suicide in a man in his 40s (Naranjo criteria: possible causality). (2) Simvastatin 10 mg was followed within 2 weeks by depression in a woman in her 50s (probable causality). (3) Atorvastatin 20 mg was followed in ~1 month by depression and irritability/aggression in a male in his 50s (probable causality). (4) Atorvastatin 10 mg was followed in several months by aggression/irritability and depression culminating in suicide in a man in his 40s (possible causality). (5) Fenofibrate + rosuvastatin (unknown dose), later combined with atorvastatin were followed in 1 month by aggression/irritability in a male in his 30s (probable causality). (6) Lovastatin (unknown dose and time-course to reaction) was followed by depression, dyscontrol of bipolar disorder, and suicide attempts in a male in his 40s (possible causality). (7) Atorvastatin 20 mg was followed within 2 weeks by cognitive compromise, and nightmares, depression, and anxiety culminating in suicide in a man in his teens (definite causality). (8) Simvastatin 10 mg was followed (time-course not recalled) by depression, aggression/irritability culminating in suicide in a man in his 60s (possible causality). (9) Simvastatin 20 mg then atorvastatin 10 mg were followed (time-course not provided) by irritability/aggression in a man in his 60s (definite causality). (10) Atorvastatin 10 then 20 then 40 mg were followed shortly after the dose increase by violent ideation and anxiety in a man in his 30s (probable causality). (11) Atorvastatin 20 mg and then simvastatin 20 mg were followed in 2 weeks by aggression/irritability in a man in his 50s (definite causality). (12) Lovastatin, rosuvastatin, atorvastatin, and simvastatin at varying doses were followed as quickly as 1 day by aggression, irritability, and violent ideation in a man in his 40s (definite causality). Most had risk factors for statin ADRs, and co-occurrence of other, recognized statin ADRs. ADRs had implications for marriages, careers, and safety of self and others. These observations support the potential for adverse mood and behavioral change in some individuals with statin use, extend the limited literature on such effects, and provide impetus for further investigation into these presumptive ADRs. Potential mechanisms are reviewed, including hypothesized mechanisms related to oxidative stress and bioenergetics.

KEY POINTS

Psychiatric adverse effects, altering mood, personality, and behavior, sometimes arise in patients receiving statins.

Statin psychiatric effects can include irritability/aggression, anxiety or depressed mood, violent ideation, sleep problems including nightmares, and possibly suicide attempt and completion.

INTRODUCTION

Most adverse drug reaction (ADR) reporting focuses on non-behavioral health risks to the medication-taking individual; however, attention is increasingly given to drug-induced behavioral and mood changes that may affect self or others. Drugs and medications with behavioral concerns include alcohol (best recognized) [], but also varenicline [], loratadine [], mefloquine [], tramadol [], isotretinoin [], tricyclics [], benzodiazepines [], and selective serotonin reuptake inhibitors (SSRIs) [], among others []. Emerging evidence suggests such problems may occasionally arise with cholesterol-lowering drugs []. These drugs are widely prescribed and most prominently include statins (3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors), which held the place of best-selling class of prescription drugs in the world and include the best-selling prescription drug in history [].

Neuropsychiatric ADRs of statins, including suicide and aggression, have been reported in pharmacovigilance databases [] and in adverse event reports and series []. Moreover, adverse behaviors have been reported in settings of low cholesterol []; and of lower omega-3 fatty acid levels (the omega-3 to omega-6 ratio is reportedly reduced with statins) []. Both naturally low cholesterol and randomized assignment to cholesterol reduction in the pre-statin era have been reported to be linked to increased violent deaths [], though statin randomization has not []. Recent randomized controlled trial (RCT) evidence indicating that statins can have bidirectional effects on aggression may be germane here: different mediating factors, including increased sleep problems and perhaps reduced testosterone, appear to drive effects in differing directions, and bidirectional effects on oxidative stress may also be speculated to do so. Nonetheless, the literature relating mood and behavioral changes to cholesterol-lowering drugs, and depicting the character and potential implications of adverse psychiatric effects with statins, remains relatively sparse []. Here we present 12 cases of mood and behavioral change apparently associated with lipid-lowering agents.

METHODS

A total of 12 subjects and/or their family members (if the subject was deceased) who reportedly experienced mood and behavioral changes while receiving one or more statin, as identified by the subject and/or by family members, contacted our study group and provided survey information. Written informed consent was obtained from each participant (or proxy for deceased subjects) for inclusion of their case in this case series. These 12 represent a convenience sample, chosen because the neuropsychiatric problem was the primary complaint, because the nature or severity appeared to warrant representation in the literature, because the participant or proxy was amenable to inclusion (with proper de-identification), and because the aggregate number, 12, was small enough to allow inclusion of some individual detail, yet sufficient to illustrate a suite of potential issues.

Elicited information included demographic characteristics, drug(s) used (statin and concomitant medications), dose(s), time-course of mood and behavior change relative to drug use (onset, duration, recovery), character of symptoms, and open-ended narrative of the impact of behavior, mood, and/or personality changes. We inquired whether a modification to the treatment regimen occurred—such as changes in dose, drug discontinuation, and drug rechallenge—and the impact on symptoms. Recognized risk factors for statin ADRs, and development of other recognized statin ADRs, were also elicited. Information for each case is presented in tabular form.

Cases were assessed for adherence to presumptive causality criteria using the published Naranjo drug ADR causality classification. This employs a point system of positive and negative causality points to estimate the probability of an ADR, with a score ≥9 deemed to indicate “definite” ADR causality, 5–8 “probable”, 1–4 “possible”, and ≤0 “doubtful” []. For all participants, adverse event causality was at least “possible”, since psychiatric and behavioral reactions to statins or cholesterol reduction bear biological plausibility and prior reports. “Probable” causality was limited to those who experienced occurrence following drug initiation, had the drug discontinued, and improved following drug discontinuation. “Definite” causality assignments were limited to those who, in addition to recovery with discontinuation, were rechallenged with the drug, and experienced symptom recurrence.

RESULTS

Information on drug, drug dose, reported mood and behavioral effect, factors supporting a causal connection, other statin symptoms, family history of psychiatric problems associated with statin use, and presence of risk factors for statin adverse effects are listed in Table 1. Cases commonly involved more than one psychiatric element (Table 2). An expanded description of each case is provided (Table 3). Marked change in mood and/or behavior was commonly noted, in some instances leading to tragic consequences. In some cases, proximal mood or behavioral changes arising with cholesterol-lowering agents led to the addition of psychiatric medications, and a role for these psychotropic medications in behavioral sequelae cannot be excluded. Behavioral/mood findings often accompanied muscle, cognitive, or other better recognized statin adverse effects []. Some participants had family members who also had experienced psychiatric adverse effects attributed to statins. Several participants exhibited compelling on-off-on reproducibility of findings.

Based on Naranjo presumptive criteria for ADR causality, eight cases qualified as bearing a “probable” or “definite” causality designation. The four cases designated “possible” are included because of factors not considered in Naranjo criteria that bear on likelihood of a causal connection. (As was said for a drug bearing a similar spectrum of behavioral adverse behaviors, “the clear temporal relationship, lack of prior history of this behavior, and unusual nature of these events strengthens the accumulating scientific evidence” []). Each patient exhibited persistent absence of the symptom prior to administration of the statin, followed by persistent presence while receiving the statin (days to years). One possible exception was a man with bipolar disorder; however, he had manifested years of stability and good control since initiation of lithium until statin initiation, which resulted in loss of psychiatric stability persisting for the years he was receiving statins until his death. Prospects for a causal connection were buttressed by an adverse behavioral change while receiving statins in a first-degree relative who also experienced dechallenge–rechallenge support (family history and genetics are risk factors for statin problems) []. A total of 75 % of cases were accompanied by other symptoms with a confirmed relation to statin use, including muscle symptoms [], cognitive problems [], and dermatologic reactions []. Additionally, 50 % of cases had factors previously shown to be linked to an elevated risk of statin ADRs, such as thyroid conditions [].

Discussion

Summary

Behavioral and psychiatric changes in the cases presented range from violent nightmares to aggression, mood/personality change, violent or homicidal ideation (in some instances culminating in suicide), each in apparent association with statin use. The temporal association between the drug initiation and mood and behavior change, and again between drug discontinuation and resolution of symptoms where this occurred, suggests a causal connection in a number of these cases. Notable mood and behavioral changes for all patients or introduction of serious psychiatric events began after drug initiation. The latency profile is consistent with that for other statin ADRs that share common mechanisms [], and bear RCT support []. Symptoms persisted or progressed with continued use in all cases. Those able to discontinue the drug experienced resolution of symptoms. For those in whom rechallenge was possible, symptoms recurred. The presence of ADRs and risk factors with a confirmed relation to statin ADRs is consistent with common pathophysiological factors, hypothesized to underlie many statin adverse effects, extending to behavioral effects []. (12 cases are included; for those interested in knowledge of other cases of this kind, a 13th case, involving a physician with behavioral changes while receiving statins and leading to professional review, is planned for inclusion in a separate manuscript on statin adverse effects in physicians).

Explanation of Findings; Comparison/Contrast with Other Findings in Literature

Though a relation of statins to instances of behavior alteration may seem counterintuitive, it fits with a body of existing literature. Observationally, lower cholesterol has been linked to greater violence (including aggression, suicide, homicide, violence) in many studies, including prospective longitudinal studies []. Behavioral consequences of lipid-lowering medications have been reported for non-statin treatments, including fibrates [] (implicated in case 5), with support extending to meta-analyses of RCTs showing significantly increased violent death []. RCT meta-analysis in the statin era did not support an increase in violent death on average (indeed the point estimate was lower, though not significantly) []. RCT patient selection may be one factor: excess violent deaths on pre-statin lipid drugs were preferentially evident in those with risk factors for violence—e.g., alcohol, psychiatric history, and non-compliance []. Of note, there was no evidence of more patients with these characteristics in the cholesterol-lowering group, but the excess of events emphasized these patients. Psychiatric histories, alcohol/substance use, and low conscientiousness are risk factors for lower compliance, so may lead to exclusion with compliance run-ins, but are also risk factors for adverse behaviors, so vulnerable individuals might be preferentially excluded []. Relative exclusion may affect detection of risk in two ways. First, the same fractional (relative) risk change will lead to a greater number affected, and more power to show a change, in those at higher risk (a doubling of nothing is still nothing) []. Second, the fractional risk change itself may be greater in a behaviorally vulnerable subset (effect modification): illustrating this point, the odds ratios risk of psychiatric events with mefloquine use was reported to be 3.8 among those without a psychiatric history, versus apparently double that (8.0) in those with a psychiatric history [].

Other factors may also explain this. Randomized trial evidence examining statin effects on aggression provides potential insights: statins (vs. placebo) promoted both average significant increases and reduction in aggression, in different groups []. Typical effects in men (particularly in men who were both younger and less aggressive at baseline) were toward reduced aggression [], with older age and female sex shifting the distribution. Simvastatin has been shown to both significantly lower testosterone [] and worsen sleep problems on average []. (It may also promote sleep apnea in some []). For men receiving simvastatin, the magnitude of each of these effects significantly predicted the change in aggression, in opposite directions []. Sleep problems and sleep apnea are elsewhere linked to irritability [], as well as aggression and violence []. Lower testosterone in some settings is linked to lower aggression and violence [].

Other mechanisms may be theorized. Low central serotonin has been linked to low cholesterol and to aggression []. However, whole blood serotonin (which correlates inversely to central serotonin) did not predict aggression in mediation analysis within a randomized trial []. We also hypothesize that effects on aggression, and perhaps mood problems on statins, may be linked to oxidative stress [] and inter-related mitochondrial dysfunction (which has been linked to temper disorders) []. The explanation accords with our finding that behavioral adverse effects commonly co-occur with better known statin adverse effects, with the documented relation of better known statin adverse effects to oxidative stress and mitochondrial dysfunction [], and with the documented connection of mitochondrial dysfunction to a range of psychiatric problems [].

Other hypothetical mechanisms of potential relevance, such as the role of cholesterol in synapse formation or membrane function, and myelin production have been reviewed elsewhere [], but in contrast to mechanisms cited above, triangulating evidence for a role is currently lacking.

The explanation accords with our finding that behavioral adverse effects commonly co-occur with better known statin adverse effects, for which a relation to oxidative stress and mitochondrial dysfunction has been elucidated []. Mitochondrial dysfunction has a documented connection to a range of psychiatric problems [], and may also contribute to behavioral change with statin-induced oxidative damage.

More lipophilic statins have better brain penetration [], though all statins have some ability to cross the blood–brain barrier []. Whether this is important for central effects of the kinds described is unknown, since peripheral effects can have central consequences—and since prooxidant effects of statins, which are linked to the occurrence of statin adverse effects [], also raise blood–brain barrier penetrability []. Each of the patients in our report experienced problems while receiving at least one of simvastatin, atorvastatin, or lovastatin, which are lipophilic statins. However, most involved atorvastatin and simvastatin, which have also historically been the most frequently prescribed statins. This, and the lack of a defined base population in which statin prescribing rates are known, obviates our ability to comment on whether lipophilicity is relevant to these effects.

Limitations

This study has the limitations inherent to all case series: data are observational, which constrains causal inference. However, a profound change in state while receiving a drug, particularly with dechallenge–rechallenge support, strengthens the case for causality. There is no defined base population or control group, precluding calculation of rates and risk ratios, and occurrence of adverse neuropsychiatric effects in these cases, even if presumed causal, has no inherent implications for usual effects of statins on the outcomes reported—nor do usual effects have necessary implications to individual ones. Rather, this case series underscores that statins may in specific individuals promote adverse behavioral, mood, and personality changes, irrespective of whether behavioral (or mood) effects are on average favorable, adverse, or neutral. Even reporting rates relative to other ADRs may be a challenge to gauge meaningfully for neuropsychiatric problems, because these may be particularly sensitive, and may go unreported. In an analysis of emails abstracting statin ADRs mentioned spontaneously, mood or personality problems were spontaneously related as part of the ADR complex in a minority, but in a survey directly asking about each of a list of symptoms the participant attributed to statins, among those self-selected for having at least one such symptom, a majority cited a neuropsychiatric effect. (However, in the latter, there is no gauge of severity; and physical problems can themselves contribute to some level of psychic distress).

Some of our participants had underlying conditions (such as a psychiatric disorder) that can themselves lead to an adverse outcome; however, as above, the odds ratios for risk of psychiatric events due to a drug can be magnified in the presence of a psychiatric history []. Consistent with this, most of the excess cases of violent death arising in the active treatment, cholesterol-lowering arms in a pre-statin-era analysis of randomized trials had other risk factors for violent death []; since those risk factors themselves were not shown to be increased in the active treatment group, this underscores that individuals with such issues may represent a vulnerable subgroup (as with mefloquine). As a further analogy, an analysis of rhabdomyolysis cases in the San Diego area showed that typical instances involved the confluence of more than one risk factor—consistent again with an increase in the odds of an event “due to” each agent, in the presence of the other []. In our cases, factors such as the temporal relation to statin use, and concurrence of other statin-compatible ADRs increases the prospects for causality with statins.

Data rely on self-report. However, patient self-reports of ADRs can be a valuable and reliable tool [], and—if heeded—may hasten recognition of important ADRs []; such benefits have led to standardized implementation of patient reporting for EU-based pharmacovigilance databases []. Self-selection of participants is inherent to studies with volunteer patients; however, for studying those with ADRs, whether or not they reflect typical effects, observed effects are important.

Conclusions

Though statins are widely tolerated, they may be among the growing list of prescription agents that, in some participants, may increase the risk of serious psychiatric events and/or behavioral changes. In the cases cited here, these adverse experiences posed risks to the safety of self and others—sometimes, tragically, adversely affecting marriages and careers, or culminating in death. The possibility of such ADRs, even if rare, should be recognized by physicians who prescribe cholesterol-lowering drugs, such that if personality or behavior changes arise, the drug can be included in considerations of etiology and treatment. This series extends the modest literature on behavior and psychiatric changes apparently associated with cholesterol-lowering treatment. These findings further the evidence that cholesterol-lowering drugs should be added to the list of agents that bear consideration when new irritability, or aggressive or violent behavioral changes arise.

J.Crow’s Lugol’s Iodine Solution: Amazon Review on Dosage

Lugol’s Iodine Dosage Calculator – www.dropulator.com

HERE ARE THE EXACT USAGE INSTRUCTIONS THAT “WERE NOT” INCLUDED WITH THE BOTTLE OR INSIDE BOX- I HOPE THE MANUFACTURER INCLUDES THIS WITH ALL PURCHASES-USED IN EXCESS CAN CAUSE SERIOUS HEALTH PROBLEMS AND POTENTIAL LAW SUIT WITHOUT DIRECTIONS FOR USAGE .

INTERNALLY – For gas, bloating, indigestion, stomach problems, food or salmonella poisoning, use 6 drops in 1/2 glass of water, 2 or 3 times a day, for a few days. Take after meals and at bedtime. For severe cases, it can be increased to 12 drops. You’ll feel results shortly. For anxiety/mood swings, etc., or for a more relaxed and peaceful state, take 6 drops in water once or twice during the day. In general, 6 drops can usually end it all for a mild case of salmonella poisoning. Though very safe, use only when needed.

THYROID PROBLEM – Many problems, in general, can be attributed to iodine deficiency. 75 years ago, Lugol’s iodine was commonly used by doctors. 2/3 of a teaspoon (60 drops) was the standard dose for thyroid disease. You can start with 6 to 12 drops a day in water for about one week and you will notice improvement. Then it is advisable to consult with your doctor.

IODINE DEFICIENCY – Take about 2, 3 or 4 drops in water daily for about a month. Can be increased to 6 drops daily if needed. After you’ve replenished iodine, then take twice a week.

MOUTHWASH AND CLEANSER – Great as a mouthwash/mouth cleanser against bacteria, fungus, mucus, virus, coated tongue, etc. Use 3 to 6 drops in glass of water, gargle, do not drink, spit out in glass and observe what comes out. Your mouth will feel refreshed and great.

HOPE THIS HELPS CURRENT AND FUTURE CUSTOMERS

Selenium and Iodine

~Content Source

The Interaction of Selenium and Iodine

Selenium and iodine interact with each other in one key area: thyroid hormone. Because this hormone plays a key role in metabolism and development, it is important to have an optimal level of it. Let’s find out more about how the two minerals impact thyroid health.

Thyroid Health

The thyroid contains one of the higher concentrations of selenium per gram than other tissues, making sufficient levels important for thyroid health. This is likely due to several selenoproteins being involved in thyroid health, including glutathione peroxidase, thioredoxin reductases, and the three deiodinase enzymes.

On a physiological level, it makes sense why these two minerals are essential for thyroid health. Thyroid hormone is made of a compound of iodine and tyrosyl residues in thyroglobulin, which are coupled together to create T3 and T4. T4 is converted into the active form, T3, when the deiodinase enzyme, which is a selenoprotein, removes one of the iodine compounds. Type I and II deiodinase enzymes are stimulated by TSH to convert more of the active form of the thyroid hormone. The other selenoproteins help to protect against the generation of H2O2, which in excessive levels can lead to oxidative damage.

Therefore, for a healthy functioning thyroid, you must have sufficient levels of both of these minerals. With both of these minerals, it is key to keep the right balance; too much can be just as disastrous as too little. Both situations can contribute to dysfunction in thyroid hormone production, as well as thyroid autoimmune disorders. Additionally, there must be a balance between the two minerals. An excess of one might contribute to or exacerbate a deficiency in the other.

The recommended daily value and tolerable upper limit, both of which are listed above, are helpful guides to plan your optimal consumption of both minerals. You can measure your individual status of iodine and selenium using a urine test, and you can measure your selenium status through a blood test, to determine if you are at risk of a deficiency or excessive intake. One study found evidence to support the WHO’s recommendation for urinary iodine between 100 to 200 mug/l for thyroid health. Another study found a reduced risk for thyroid disease with serum selenium levels between 69 and 90.99 ug/L compared to the bottom and top quintiles. Discuss your test results and any symptoms you might have with your doctor or health practitioner to determine if you require a different intake level to meet your individual needs.

Some studies have found that supplementing with selenium can help with and might even reverse thyroid problems, including autoimmune thyroid. In one study, researchers looked at the effect of supplementing with 83 mcg selenomethionine per day for a period of four months in 192 participants, of which there were 96 supplemented and 96 control patients. Out of all participants, 33 or 17.2 percent restored normal thyroid activity. Those who were supplemented had a higher success rate, with 31.3 percent of treated patients restoring euthyroid compared to just 3.1 percent.

In another study reviewing patients with goiter in Pakistan, researchers reviewed the impact of selenium status and its impact on iodine deficiency. Compared to the controls, both males and females with goiter had a lower serum level of selenium and a higher urinary selenium. These patients also had lower levels of iodine compared to age-matched controls. The researchers concluded that the selenium levels might help to determine the severity of the hypothyroidism experienced by those deficient in iodine, but that more research was needed.

In a study on rats reviewing the impact of independent and simultaneous zinc, selenium, iodine deficiency on thyroid activity, the serums levels of both total T4 and free T4 were significantly lower and the TSH was higher in all groups that were iodine deficient. Serum T3 levels were lower in selenium and iodine, selenium and zinc, and zinc only deficient groups. Additionally, the groups that were deficient in just selenium or selenium and zinc had lower levels of thyroid glutathione peroxidase activity. However, when there was also a concurrent iodine deficiency, this enzyme had a greater activity than the controls.

Healthy Development

Sufficient levels of both iodine and selenium are essential for the healthy development of fetuses and young children, in part due to their importance to the creation of thyroid hormone. The thyroid hormone plays a key role in brain development in the womb. In the initial trimester, the fetus relies on thyroid hormone from the mother. Although the fetus starts to create its own hormone in the second trimester, even at birth, roughly 20 to 40 percent of T4 in cord blood is from the mother.

In one study reviewing data from the Generation R Study, the researchers compared the level of maternal thyroid hormones and the risk of verbal and non-verbal cognitive function and executive function in the children. The researchers did not find a connection between TSH and free T4 with any impact on language function, except for high levels of free T4 did predict a lower risk of having a delay in expressive language at 2.5 years old. However, having mild hypothyroxinaemia (a condition where TSH levels are within range but free T4 levels are low) prior to 18 weeks of gestation was correlated with having expressive language delay at 1.5 and 2.5 years of age (an OR risk of 1.44). Severe hypothyroxinaemia had an even greater risk, with an OR of 1.8. There was also a higher risk of delay in nonverbal cognitive function.  

Maternal hypothyroxinemia might also contribute to the development of ADHD in the child. In one population-based cohort study, the researchers found that children born to mothers with hypothyroxinemia had higher ADHD scores at 8 years old compared to children not exposed to it, even after adjusting for confounders. There was no association with subclinical hypothyroxinemia.  

Because of the importance of iodine to thyroid hormone production, severe iodine deficiency can cause developmental problems in the fetus, especially to the brain, and contributes to brain damage and cretinism. Even mild iodine deficiency might contribute to some cognitive dysfunction. In a longitudinal follow-up of an Australian cohort at 9 years old, the children who were born to mothers who had mild iodine deficiency (urinary levels under 150 ug/L), performed worse in spelling, grammar, and English-literacy compared to those who were not. There was a 10 percent reduction in spelling performance, 7.6 percent reduction in grammar, and 5.7 percent reduction in English literacy. Even after adjusting for certain other factors, the association remained. The cohort included children born prior to the implementation of an iodine fortification, so they experienced iodine insufficiency during gestation but not during early childhood. 

Although most studies pointing to this issue look at iodine deficiency, some studies have started to also look at the impact of selenium levels in the neurodevelopment of children. Sufficient selenium levels during pregnancy are also important to proper development of the child. In one prospective cohort study, there was a positive association between the level of selenium during the first trimester of pregnancy and the motor skills and language skills of the child at one year old. Another study also found a positive association between maternal levels of selenium and the development in their children at 1.5 years old. This was most evident in language comprehension and psychomotor development, especially in girls. 

How to Get Sufficient Levels of Selenium and Iodine 

Food Sources of Selenium 

Food sources are always a great place to start to ensure you have sufficient levels of selenium and iodine. There are several selenium-rich foods, especially if they come from soils that are rich in selenium. The richest sources of selenium from greatest to least include:  

– Brazil nuts (2,549.6 ug for 1 cup of whole Brazil nuts)
– Turkey breast
– Eggs
– Rockfish
– Tuna
– Sunflower seeds
– Sardines
– Mollusks 

Food Sources of Iodine:  

Although many people only think about iodized salt for their iodine, you can find it in other food sources. Fish and dairy products are some of the richest sources of iodine. For those who are vegetarian or vegan, or otherwise avoid these foods, seaweed is also a rich source of iodine, with some varieties having almost 2,000 percent of the daily recommended value. Fruits and vegetables also have some iodine, especially if they are grown in areas that have iodine-rich soil. If you do rely on iodized table salt, it is important to be careful that the salt levels do not increase your sodium levels too much.  

Supplements: What You Need to Know 

Supplements can be a great source of selenium and iodine if you are at risk of a deficiency and cannot consume sufficient levels through your food, especially if you live in an area deficient of these minerals in the soil. As discussed above, if you do choose to supplement, care should be taken to not end up with excessive amounts of selenium or iodine. With both, some of the same problems that occur with deficiency occur with excess levels. When determining whether you need to supplement with iodine, do not forget to accurately calculate how much you get through your salt if you choose iodized salt. 

Pregnant women, and those who plan to become pregnant, should discuss with their doctor whether they are at risk of an iodine and/or selenium deficiency, as well as a thyroid problem, to reduce the risk of problems with cognitive development.  

Selenium plays many key roles in the body, but one key role is its synergistic relationship with iodine to ensure thyroid health. If you live in an area with low levels of either mineral in the soil, or you are otherwise at risk of a deficiency, then talk with your doctor, nutritionist, or another medical professional about ways to increase your consumption and/or supplement so you benefit from the health benefits discussed above. 

How Much Iodine Do I Need?

By Dr. Mercola – How Iodine Deficiency May Affect Your Child’s Brain Function and IQ <–Content Source

In this fascinating video, taped at last year’s Restorative Medicine Conference in Portland, Oregon, Dr. Jorge Flechas, MD discusses the importance of total body iodine sufficiency, and how lack of iodine might severely affect your child’s brain and intellectual prowess. Iodine is an essential trace element required for the synthesis of hormones, and the lack of it can also cause or contribute to the development of:

  • Hypothyroidism
  • Goiter
  • Mental retardation
  • Cretinism (severely stunted physical and mental growth and deafness due to untreated congenital hypothyroidism)
  • Certain forms of cancer

Iodine is used by your thyroid gland to help regulate metabolism and development of both your skeleton and brain, among other things. But how much iodine do you need, really? There’s quite a bit of contention on this issue.

Some, like Dr. Flechas insists severe iodine deficiency is rampant, while others claim this is not the case at all, and that taking higher doses of iodine can be harmful. I don’t proclaim to have the answer to this question… There’s no doubt you need iodine. But it’s difficult to say precisely how much.

I suspect the dosages recommended by Dr. Flechas, Dr. Brownstein, and others, may be too high, so I would encourage you to do your own research, and adopt a sensible, middle-of-the-road approach when it comes to iodine.

I also want to clarify the difference between Iodine and Iodide. Iodine is the molecule that is taken up by cells in the body. However, Iodine is a gas and is not very available in food and supplements. Instead, it is the iodide form that is more stable and can be consumed. In the body, Iodide converted into Iodine which is the active form.

Why Is Hypothyroidism More Prevalent in Women than Men?

There is simply no question that optimizing your iodine levels is essential for thyroid health. Hypothyroidism disproportionately affects women at a rate of about 9 to 1 in the US. The reason for this is that the female hormone estrogen inhibits the absorption of iodine.

According to Dr. Flechas, hypothyroidism is associated with up to 80-90 percent free estrogen levels, compared to the normal value of 40-60 percent free estrogen. Hyperthyroidism is associated with only 20 percent free estrogen levels, and low iodine intake can lead to a hyperestrogenic state. In his lecture, Dr. Flechas explains the interplaying dynamics of estrogen, thyroid hormones, and iodine at greater depth, so for more information, please set aside 40 minutes to watch the video above.

Your Body Needs Iodine for More than Just Your Thyroid

Dr. Flechas presents a number of interesting facts about iodine that is not widely known. For example, did you know that thyroid hormones are created not just in your thyroid, but also in a woman’s ovaries (thyroid T2), and in the white blood cells of your bone marrow? Furthermore, iodine is not only required for proper function of your thyroid. Other tissues that absorb and use large amounts of iodine include:

~ Breasts | Salivary Glands | Pancreas | Cerebral Spinal Fluid | Skin | Stomach | Brain | Thymus ~

Salivary glands = inability to produce saliva, producing dry mouth Iodine deficiency, or insufficiency, in any of these tissues will lead to dysfunction of that tissue. Hence the following symptoms could provide clues that you’re not getting enough iodine in your diet. For example, iodine deficiency in:

  • Skin = dry skin, and lack of sweating. Three to four weeks of iodine supplementation will typically reverse this symptom, allowing your body to sweat normally again
  • Brain = reduced alertness, and lowered IQ
  • Muscles = nodules, scar tissue, pain, fibrosis, fibromyalgia

How Much Iodine Does Your Body Need?

According to Dr. Flechas, researchers have determined that the average dietary intake of iodine for Japanese women is 13.8 milligrams (mg) per day. He recommends 12.5 mg/day, especially for his pregnant patients to optimize their child’s intelligence. He shares a couple of success stories in his lecture, where iodine supplementation at higher doses resulted in children with remarkably advanced intelligence.

Hypothyroidism, which is one of the first ailments to develop in response to iodine deficiency, is indeed particularly troublesome during pregnancy. One 1999 study found that thyroid deficiency during pregnancy can lower your child’s IQ by about seven points. The researchers noted that for the first 12 weeks of pregnancy, before the unborn child’s thyroid becomes active, the mother is the sole source of thyroid hormones. Studies suggest that these hormones play an important role in brain development. Overall, compared with other children, the offspring of thyroid-deficient mothers had impaired school performance and lower scores on tests of attention, language, and visual-motor performance.

But pregnant women aren’t the only ones who need to be concerned with the iodine content of their diet. According to Dr. Flechas, your thyroid alone needs about 6 mg of iodine per day; the breasts of a 110-pound woman will need about 5 mg/day (larger women or women with larger breasts need more); and other body tissues, such as your adrenals, thymus, ovaries, hypothalamus, and pituitary gland, need about 2 mg/day.

Here are a few more interesting facts:

  • In total, the human body can hold 1,500 mg of iodine
  • Your thyroid can hold a maximum of 50 mg of iodine
  • 20 percent of the iodine in your body is held in your skin (if your skin is depleted of iodine, you will not be able to sweat)
  • 32 percent of your body’s iodine stores are in your muscles (if muscles are depleted, pain and other fibromyalgia symptoms can develop)

Although he makes a compelling argument, I am not yet convinced that such large amounts may be necessary. Dr. Brownstein and others would label this as iodinophobia, but I believe caution may be appropriate here before swallowing mg amounts of iodine on a regular basis. Personally, I am not yet convinced and do not take such high doses in supplemental form.

The US RDA May Be Insufficient for Many

It is important to realize that the current US daily recommended allowance (RDA) for iodine are not in milligram doses but in micrograms:

  • 150 micrograms (mcg) per day for adult men and women
  • 220 mcg for pregnant women
  • 290 mcg for lactating/breastfeeding women

However, this RDA was set with the intention to prevent goiter only. Dr. Flechas makes a compelling argument for it being completely insufficient for overall physical health and prevention of diseases such as thyroid disease, fibromyalgia, and cancer. Iodine actually induces apoptosis, meaning it causes cancer cells to self destruct. Dr. Flechas is adamant that absence of iodine in a cell is what causes cancer, and statistics tend to support this view. In his lecture, he shows the results of a number of NHANES surveys.

For example, between 1971 and 2000, the average iodine levels declined by 50 percent in the US. During that same time, cancers specifically associated with iodine deficiency—such as cancer of the breast, prostate, endometrium, and ovaries—increased.  He also points out that the RDA completely ignores the presence of increasing amounts of goitrogens in the environment. The following halides compete for the same receptors used in your thyroid gland and elsewhere to capture iodine, so if you’re exposed to too many of these, your thyroid hormone production can be severely disrupted, resulting in a low thyroid state:

  • Bromide / bromine (Bromide can be found in several forms. Methyl bromide is a pesticide used mainly on strawberries, found predominantly in the California areas. Brominated vegetable oil (BVO) is added to citrus drinks to help suspend the flavoring in the liquid. Potassium bromate is a dough conditioner found in commercial bakery products and some flours)
  • Chlorine
  • Fluoride

Could High-Dose Iodine Be Dangerous?

As I mentioned at the beginning, while Dr. Flechas provides very compelling arguments for using doses as high as 12.5 milligrams (mg) per day, which is a far cry from the RDA of 150 micrograms (mcg), I’m hesitant to make such a recommendation. I think the jury is still out, and we need more research to determine the health effects of too much iodine.

As reported by Reuters at the beginning of this year1, a recently published study has cast some doubts on high-dose iodine supplementation. The study, published December 28, 2011 in the American Journal of Clinical Nutrition, randomly assigned one of 12 different dosages of iodine (ranging from 0 to 2,000 mcg/day) to healthy adults for four weeks.

When diet was factored in, those taking 400 mcg/day were receiving a total of about 800 mcg of iodine per day.

At doses at and above 400 mcg of supplemented iodine per day, some of the study participants developed subclinical hypothyroidism, which appeared to be dose dependent. At 400 mcg/day, five percent developed subclinical hypothyroidism; at the highest dose—2,000 mcg/day—47 percent of participants were thus affected. Subclinical hypothyroidism refers to a reduction in thyroid hormone levels that is not sufficient to produce obvious symptoms of hypothyroidism (such as fatigue, dry skin, depression or weight gain, just to mention a few common tell-tale signs).

So, these findings suggest it might not be wise to get more than about 800 mcg of iodine per day, and supplementing with as much as 12-13 mg (12,000-13,000 mcg’s) could potentially have some adverse health effects.

The Great Iodine Debate

~ Content Source

Iodine is critical to human health. It forms the basis of thyroid hormones and plays many other roles in human biochemistry. While the thyroid gland contains the body’s highest concentration of iodine, the salivary glands, brain, cerebrospinal fluid, gastric mucosea, breasts, ovaries and a part of the eye also concentrate iodine. In the brain, iodine is found in the choroid plexus, the area on the ventricles of the brain where cerebrospinal fluid (CSF) is produced, and in the substantia nigra, an area associated with Parkinson’s disease.


Iodine is essential to normal growth and development. Iodine deficiency in utero and during growth can result in cretinism, a condition of severely stunted physical and mental growth due to prolonged nutritional deficiency of iodine or from untreated congenital deficiency of thyroid hormones (hypothyroidism). The condition is characterized by short stature, delayed bone maturation and puberty, infertility, neurological impairment and cognitive impairment ranging from mild to severe. Iodine deficiency also causes goiter, the gradual enlargement of the thyroid gland. Both conditions have led to public health campaigns of iodine administration in many countries. The addition of iodine compounds to table salt or water represents the first attempt to provide nutrient supplementation via “fortification” of common foods.

Iodine in Public Health Campaigns

In the past, endemic cretinism due to iodine deficiency was especially common in areas of southern Europe around the Alps. It was described by ancient Roman writers and often depicted by medieval artists. The earliest Alpine mountain climbers sometimes came upon whole villages of cretins. In the late eighteenth and early nineteenth centuries, several travellers and physicians described alpine cretinism from a medical perspective, often attributing the cause to “stagnant air” in mountain valleys or “bad water.”

More mildly affected inland areas of Europe and North America in the nineteenth century were referred to as “goiter belts.” The degree of iodine deficiency was milder and manifested primarily as thyroid enlargement rather than severe mental and physical impairment. In Switzerland, where the soil is poor in iodine, cases of cretinism were abundant and even considered hereditary. As the variety of food sources dramatically increased in Europe and North America and the populations became less completely dependent on locally grown food, the prevalence of endemic goiter diminished.

Only in the early twentieth century did scientists discover the relationship of cretinism with lack of iodine and thyroid deficiency. The addition of iodine to salt or drinking water is credited with the reduction or elimination of cretinism and goiter, although cretinism still remains a serious problem in many rural sections of China.

In coastal areas, the action of ocean waves makes iodine gas. Once airborne, iodine combines with water or air and enters the soil. Plant and animal foods grown on soil containing iodine will take up iodine so that it becomes available in the food. It can also be absorbed through the skin from air in seacoast areas, which may explain why many report improved health after a visit to an oceanside resort, and why individuals with severe allergies to iodine risk a reaction if they venture too close to the sea.

Iodine and Breast Health

Japanese women have very low rates of breast cancer and consume high levels of iodine. This observation has led to the theory that high iodine levels in the Japanese diet, rich in seaweed and seafood, provide protection against breast cancer and other diseases of the breast. Proponents of this theory note that today one in seven American women (almost 15 percent) will develop breast cancer during her lifetime. Thirty years ago, when iodine consumption was twice as high as it is now (480 mcg per day) one in twenty women developed breast cancer. Thirty years ago, consumption of iodized salt was higher than it is today; in addition a form of iodine was used as a dough conditioner in making bread, and each slice of bread contained 0.14 mg of iodine. In 1980, bread makers started using bromide as a conditioner instead, which competes with iodine for absorption into the thyroid gland and other tissues in the body. Iodine was also more widely used in the dairy industry as a teat cleaner thirty years ago than it is now. According to this argument, 15 percent of the U.S. adult female population suffers from moderate to severe iodine deficiency.1

The correlation of iodine deficiency with breast cancer is strengthened by reports in the scientific literature. Women with a history of breast cancer are almost three times more likely to develop thyroid cancer than women with no such history, and there is a geographic correlation between the incidence of goiter and breast cancer.2 Demographic studies show that a high intake of iodine is associated with a low incidence of breast cancer, and a low intake with a high incidence of breast cancer.3

Animal studies show that iodine prevents breast cancer, arguing for a causal association in these epidemiological findings. The carcinogens nitrosomethylurea and DMBA cause breast cancer in more than 70 percent of female rats. Those given iodine, especially in its molecular form as I2, have a statistically significant decrease in the incidence of cancer.4 Other evidence adding biologic plausibility to the hypothesis that iodine prevents breast cancer includes the finding that the ductal cells in the breast, the ones most likely to become cancerous, are equipped with an iodine pump (the sodium iodine symporter, the same one that the thyroid gland has) to soak up this element.5

Similar findings apply to fibrocystic disease of the breast. In animal studies, female rats fed an iodine-free diet develop fibrocystic changes in their breasts, and iodine in its elemental form (I2) cures it.6

As far back as 1966, Russian researchers showed that iodine effectively relieves signs and symptoms of fibrocystic breast disease. Seventy-one percent of 167 women suffering from fibrocystic disease experienced a beneficial healing effect when treated with 50 mg potassium iodide during the intermenstrual period.7

A 1993 Canadian study likewise found that iodine relieves signs and symptoms of fibrocystic breast disease in 70 percent of patients. This report is a composite of three clinical studies, two case series done in Canada of 696 women treated with various types of iodine, and one in Seattle. The Seattle study was a randomized, double-blind, placebo-controlled trial of 56 women designed to compare 3-5 mg of elemental iodine (I2) to a placebo (an aqueous mixture of brown vegetable dye with quinine). Investigators followed the women for six months and tracked subjective and objective changes in their fibrocystic disease.8

An analysis of the Seattle study showed that iodine had a highly statistically significant beneficial effect on fibrocystic disease. Iodine reduced breat tenderness, nodularity, fibrosis, turgidity and number of macrocysts compared to controls. This 36-page report9 was submitted to the Food and Drug Administration (FDA) in 1995, seeking the agency’s approval to carry out a larger randomized controlled clinical trial on iodine for treating fibrocystic breast disease. FDA declined to approve the study, because “iodine is a natural substance, not a drug.” But the FDA has now decided to approve a similar trial sponsored by Symbollon Pharmaceuticals.

Other Benefits

Iodine may be helpful in treating other cancers because it induces apoptosis, programmed cell death. Apoptosis is essential to growth and development (fingers form in the fetus by apoptosis of the tissue between them) and for destroying cells that represent a threat to the integrity of the organism, like cancer cells and cells infected with viruses. In one experiment, human lung cancer cells with genes spliced into them that enhance iodine uptake and utilization underwent apoptosis and shrank when given iodine, both when grown in vitro outside the body and implanted in mice.10 Some practitioners predict a wider use for iodine in treating cancer.

Iodine may have other benefits – for which more study is needed. Evidence indicates that increased iodine consumption replaces and therefore helps detox other halogens, such as fluoride and bromide, and even toxic metals like lead, aluminum and mercury.11 One theory is that liberal amounts of iodine in the diet can protect against the harmful effects of fluoridated water.12 Iodine supports the immune system and protects against abnormal growth of bacteria in the stomach.13

In addition to the thyroid and mammary glands, other tissues possess an iodine pump (the sodium-iodine symporter) which allows iodine concentration. Thus, it is logical to conclude that iodine plays an important role in these organs—the stomach mucosa, salivary glands, ovaries, thymus gland, skin, brain, joints, arteries and bone.

A History of Iodine Therapy

Iodine was discovered in 1811 and shortly thereafter entered the materia medica. It was used in large amounts until the mid-1900s for treating various dermatologic conditions, chronic lung disease, fungal infestations, tertiary syphilis and even arteriosclerosis.14 The Nobel laureate Dr. Albert Szent Györgi (1893-1986), the physician who discovered vitamin C, wrote: “When I was a medical student, iodine in the form of KI [potassium iodide] was the universal medicine. Nobody knew what it did, but it did something and did something good. We students used to sum up the situation in this little rhyme:

If ye don’t know where, what, and why Prescribe ye then K and I.”15

According to the 11th edition of the Encyclopedia Britannica, published in 1911, the pharmacological action of compounds containing potassium iodide, “is as obscure as their effects in certain diseased conditions are consistently brilliant. Our ignorance of their mode of action is cloaked by the term deobstruent, which implies that they possess the power of driving out impurities from the blood and tissues. Most notably is this the case with the poisonous products of syphilis. In its tertiary stage—and also earlier—this disease yields in the most rapid and unmistakable fashion to iodides, so much so that the administration of these salts is at present the best means of determining whether, for instance, a cranial tumor be syphilitic or not.” (Perhaps what the iodides did was remove toxic mercury from the bodies of syphilitics who had been treated with mercury-based medicines!)

Sarah Pope, our Tampa/St. Petersburg chapter leader, reports that her father, a pediatrician, routinely gave Lugol’s solution (a combination of iodine and potassium iodide) to treat congestion in the lungs and sinuses. The theory was that the iodide drops would thin the mucus and make coughing more productive. The dose was five drops in water, continued for several days. In his professional experience, the remedy cleared congestion and, in the case of asthmatics, dilated the bronchial tubes and assisted breathing. This author received the same remedy as a child—the taste of iodine brings back memories of being sick and in bed, and receiving the drops in orange juice.

The decline in the use of iodine in medicine began in 1948 when researchers Wolff and Chaikoff published a landmark paper on the thyroid effects of increasing amounts of potassium iodide, injected into rats. The authors stated: “Organic binding of iodine within the glands can be almost completely blocked by raising the level of plasma inorganic iodine (PII) above a certain critical level, which for the rat amounts to about 20 to 35 percent.”16 This effect became known as the Wolff-Chaikoff (W-C) effect. According to the conventional view, high levels of intracellular iodide suppress the transcription of thyroid peroxidase (TPO) enzyme, along with NADPH oxidase, leading to a reduction in the synthesis of thyroid hormone, thyroxin.17 As proof of the W-C effect, the textbooks point to the fact that large amounts of potassium iodide can remedy hyperthyroidism. Another apparent confirmation is the thyroid-suppressing effect of several iodine-containing drugs, of which the most famous is amiodarone, which can cause both under- and overactivity of the thyroid. In a trial that compared amiodarone with other medications for the treatment of atrial fibrillation, biochemical hypothyroidism (as defined by a TSH level of 4.5-10 mU/L) occurred in 25.8 percent of the amiodarone-treated group as opposed to 6.6 percent of the control group (taking placebo or sotalol). Overt hypothyroidism (defined as TSH greater than 10 mU/L) occurred at 5.0 percent compared to 0.3 percent.18

Over time, these observations led to a decline in the use of iodine in medicine. While health officials came to a general agreement that iodine deficiency caused, in increasing order of severity, goiter and hypothyroidism, mental retardation and cretinism, authorities in the U.S. and Europe agreed upon a low Reference Daily Intake (RDI), formerly called the Recommended Dietary Allowance (RDA), of 100-150 mcg per day. This amount will prevent goiters and other overt signs of deficiency but may not be adequate to prevent other conditions of iodine deficiency, and is much lower that the amounts formerly given routinely to patients.

Critics of the W-C effect note that the standard dose of potassium iodide was 1 gram until the mid-1900s, which contains 770 mg of iodine, over five thousand times more than the RDI. For many years physicians used potassium iodide in doses starting at 1.5 to 3 gm and up to more than 10 grams a day, on and off, to treat bronchial asthma and chronic obstructive pulmonary disease, apparently with good results and few side effects. Even today, dermatologists treat certain skin conditions, including fungal eruptions, beginning with an iodine dose of 900 mg a day, followed by weekly increases up to 6 grams a day as tolerated.

But the general use of iodine and iodine compounds in medicine has waned, as has its use as an additive in the food supply. Today’s medical establishment is wary of iodine as are public health officials. Thyroidologists cite the W-C effect and warn that TSH (thyroid stimulating hormone) blood levels can rise with an iodine intake of one milligram or more.

In a 2000 review paper on use of iodine as a water disinfectant, author Joe Hollowell notes that studies indicate marked individual sensitivity to iodine; the most vulnerable to adverse effects are those with underlying thyroid disease and previous low iodine intake. Problems from consumption of iodized water—including both hypothyroidism and hyperthyroidism—usually resolve after consumption is discontinued. A safe dose is 1-2 mg per day, and most can tolerate much higher amounts without problems.19

The Challenge

A challenge towards the reigning attitudes to iodine compounds came in 1997, when Dr. Guy Abraham, a former professor of obstetrics and gynecology at UCLA, mounted what he calls the Iodine Project. He had his company, Optimox Corporation, make Iodoral, the tablet form of Lugol’s solution (which combines iodine and potassium iodide), and he engaged two family practice physicians, Dr. Jorge Flechas (in 2000) in North Carolina and Dr. David Brownstein (in 2003) in Michigan to carry out clinical studies with high doses of the iodine compound.20 The project’s hypothesis is that maintaining whole body sufficiency of iodine requires 12.5 mg a day, an amount similar to what the Japanese consume and over eighty times the RDI of 150 mcg. The conventional view is that the body contains 25-50 mg of iodine, of which 70-80 percent resides in the thyroid gland. Dr. Abraham concluded that whole body sufficiency exists when a person excretes 90 percent of the iodine ingested. He devised an iodine-loading test where one takes 50 mg iodine/potassium iodide and measures the amount excreted in the urine over the next twenty-four hours. He found that the vast majority of people retain a substantial amount of the 50 mg dose. Many require 50 mg per day for several months before they will excrete 90 percent of it. His studies indicate that, given a sufficient amount, the body will retain much more iodine than originally thought, 1,500 mg, with only 3 percent of that amount held in the thyroid gland.

According to Abraham, more than 4,000 patients in this project take iodine in daily doses ranging from 12.5 to 50 mg, and in those with diabetes, up to 100 mg a day. According to these physicians, iodine at these doses does indeed reverse fibrocystic disease; allows diabetic patients to use less insulin and hypothyroid patients to use less thyroid medication; resolves symptoms of fibromyalgia; and stops migraine headaches. They report that the side effects of iodine, including hypo- or hyperthyroidism, allergies, swelling of the salivary glands and thyroid, occur in less than 5 percent.21 Urine tests confirm that iodine at these doses removes the toxic halogens fluoride and bromide from the body.22

They believe that iodism, an unpleasant brassy taste, runny nose, and acne-like skin lesions, is caused by the bromide that iodine extracts from the tissues. Symptoms subside on a lower dose of iodine.

In 2005, Dr. Abraham published a long paper challenging the Wolff-Chaikoff effect. “The W-C effect is supposedly the inhibitory effect of peripheral inorganic iodide (PII) levels equal to or greater than 0.2 mg/L (10-6M) on the organification of iodide by the thyroid gland of rats, resulting supposedly in hypothyroidism and goiter. These rats never became hypothyroid and thyroid hormones were not measured in their plasma. Nevertheless, the W-C effect, which did not even occur in the rats, was extrapolated to humans. The correct interpretation of the results obtained in rats from the W-C experiments is: Iodide sufficiency of the thyroid gland was achieved when serum inorganic iodide levels reached 10-6M . . . . These law-abiding rats refused to become hypothyroid and instead followed their normal physiological response to the iodide load. They were unjustly accused of escaping from the W-C effect. Labeling these innocent rats as fugitives from the W-C effect was a great injustice against these rodents.

“To the disgrace and stupidity of the medical profession, U.S. physicians swallowed the W-C forgery uncritically, which resulted in a moratorium on the clinical use of inorganic, non-radioactive iodine in effective amounts. However, this moratorium did not include toxic organic iodine-containing drugs and radioiodide. The iodophobic mentality prevented further research on the requirement for inorganic, non-radioactive iodine by the whole human body, which turns out to be 100-400 times the very recently established RDA. . . Prior to World War II and the W-C publication, U.S. physicians used Lugol solution safely, effectively and extensively in both hypo- and hyperthyroidism.”23

Abraham cites a 1970 paper which evaluated the effect of Lugol’s solution, administered at five drops (30 mg iodine/iodide) three times a day in five thyrotoxic patients. Following a well-designed protocol, they reported, “It is concluded that the rapid decrease in T4 secretion induced by iodine is not the result of an acute sustained inhibition of T4 synthesis (the Wolff-Chaikoff effect), but rather results from an abrupt decrease in the fractional rate of thyroid T4 release.”24

Abraham thus argues that in hyperthyroidism, iodine/iodide in Lugol’s at a daily dose of 90 mg induced a physiological trend toward normalization of thyroid function, “a beneficial effect, not the fictitious W-C effect as proposed by Wolff and Chaikoff. It is amazing that the W-C effect, which is still mentioned in iodophobic publications, has never been confirmed in rats by other investigators and has never been demonstrated in any animal species.

“In 1948, there was already evidence that the W-C effect, if it was for real in rats (and it was not), did not occur in humans. The Lugol’s solution and saturated solution of potassium iodide (SSKI) were used extensively in medical practice for patients with asthma. The recommended daily amount was 1,000-2,000 mg. This amount was used in patients with asthma, chronic bronchitis, and emphysema for several years. Hypothyroidism and goiter were not common in this group of patients. Those amounts of iodine would have resulted in serum inorganic iodine levels 100 times higher than the serum inorganic iodide levels of 10-6M claimed by Wolff and Chaikoff to result in the W-C effect.”

According to Abraham, iodine in amounts considered “excessive” by endocrinologists today represent only 3 percent of the average daily intake of iodide by 60 million mainland Japanese, a population with a very low incidence of cancer overall, and in particular of the female reproductive organs.

According to Abraham, “Medical iodophobia resulted in the thyroid hormone thyroxine replacing iodine in iodine deficiency-induced simple goiter and hypothyroidism. Thyroxine has been the most prescribed drug in the U.S. for several years. So, the manufacturers of thyroxine benefited tremendously from this deception. It also resulted in the destruction of the thyroid gland by means of radioiodide in patients with hyperthyroidism caused by iodine deficiency, although this condition had previously been treated successfully with Lugol solution. The radioablation of the thyroid gland with radioiodide resulted in 90 percent of these patients becoming hypothyroid within the first year and eventually joining the ever-increasing thyroxine-consuming population. “Supplying thyroid hormones to iodine-deprived individuals masks the iodine deficiency and can result in zombie-like effect. The patients are capable of performing physical work but are not able to think and reason at maximum capacity. An even greater negative effect is realized if iodine deprivation is combined with goitrogen saturation, using the potent goitrogens bromide, fluoride and perchlorate in the food and water supply.

“Iodine is involved in many vital mental and physical functions, and yet whole body sufficiency for iodine has never been determined. Why? Medical textbooks discuss inorganic, non-radioactive iodine only in relation to the most severe deficiencies of this essential element: cretinism, hypothyroidism and endemic goiter. Based on an iodine/iodide loading test developed by the author to assess whole body sufficiency for iodine, the amounts of iodine needed for whole body sufficiency and optimal physical and mental health are 250-1,000 times higher that the amount of iodine needed to control cretinism, hypothyroidism and endemic goiter.”

Thus, according to Abraham and his colleagues, the Wolff-Chaikoff effect is of no clinical significance. An elevated TSH, when it occurs during treatment with Lugol’s solution, is “subclinical.” This means that no signs or symptoms of hypothyroidism accompany its rise. Some people taking milligram doses of iodine, usually more than 50 mg a day, develop mild swelling of the thyroid gland without symptoms. Abraham believes that the vast majority of people, 98 to 99 percent, can take iodine in doses ranging from 10 to 200 mg a day without any clinically adverse effects on thyroid function.

The Debate

With Abraham’s work, and its popularization by physicians such as Jorgas and Brownstein, many health-conscious individuals began taking Lugol’s solution regularly, even without medical supervision. A challenge to this practice came from Dr. Alan Gaby in an editorial published in the Townsend Letter for Doctors and Patients, August/September 2005.25

“Recently, a growing number of doctors have been using iodine supplements in fairly large doses in their practices,” wrote Gaby. “The treatment typically consists of 12 to 50 mg per day of a combination of iodine and iodide, which is 80 to 333 times the RDA of 150 mcg (0.15 mg) per day. Case reports suggest that iodine therapy can improve energy levels, overall well-being, sleep, digestive problems and headaches. People with hypothyroidism who experienced only partial improvement with thyroid hormone therapy are said to do better when they start taking iodine. In addition, fibrocystic breast disease responds well to iodine therapy, an observation that has been documented previously. The reported beneficial effects of iodine suggest that some people have a higher-than-normal requirement for this mineral, or that it favorably influences certain types of metabolic dysfunction.

“While iodine therapy shows promise, I am concerned that two concepts being put forth could lead to overzealous prescribing of this potentially toxic mineral. First is the notion that the optimal dietary iodine intake for humans is around 13.8 mg per day, which is about 90 times the RDA and more than 13 times the ‘safe upper limit’ of 1 mg per day established by the World Health Organization. Second is the claim that a newly developed iodine-load test can be used as a reliable tool to identify iodine deficiency.”

Gaby takes issue with the argument that the optimal human requirement is 13.8 mg per day, by noting that “the idea that Japanese people consume 13.8 mg of iodine per day appears to have arisen from a misinterpretation of a 1967 paper. In that paper, the average intake of seaweed in Japan was listed as 4.6 g (4,600 mg) per day, and seaweed was said to contain 0.3 percent iodine. The figure of 13.8 mg comes from multiplying 4,600 mg by 0.003. However, the 4.6 g of seaweed consumed per day was expressed as wet weight, whereas the 0.3 percent-iodine figure was based on dry weight. Since many vegetables contain at least 90 percent water, 13.8 mg per day is a significant overestimate of iodine intake. In studies that have specifically looked at iodine intake among Japanese people, the mean dietary intake (estimated from urinary iodine excretion) was in the range of 330 to 500 mcg per day, which is at least 2.5-fold lower than 13.8 mg per day.”

Regarding the other argument in support of a high iodine requirement, namely that it takes somewhere between 6 and 14 mg of oral iodine per day to keep the thyroid gland fully saturated with iodine, “. . . it is not clear that loading the thyroid gland or other tissues with all the iodine they can hold is necessarily a good thing. . . Our thyroid glands have developed a powerful mechanism to concentrate iodine, and some thyroid glands (or other tissues) might not function as well after a sudden 90-fold increase in the intake of this mineral. . . relatively small increases in dietary iodine intake have been reported to cause hypothyroidism or other thyroid abnormalities in some people.”

As for the observation that iodine supplementation “promotes the urinary excretion of potentially toxic halogens such as bromide and fluoride. While that effect might be beneficial for some people, it is not clear to what extent it would shift the risk-benefit ratio of megadose iodine therapy for the general population.”

Abraham and colleagues promote the use of the iodine-load test, in which the patient ingests 50 mg of a combination of iodine and iodide and the urine is collected for the next twenty-four hours. The patient is considered to be iodine-deficient if less than 90 percent of the administered dose is excreted in the urine, on the premise that a deficient person will retain iodine in the tissues, rather than excrete it in the urine. According to the literature of a laboratory that offers it, 92-98 percent of patients who have taken the iodine-load test were found to be deficient in iodine.

According to Gaby, “the validity of the test depends on the assumption that the average person can absorb at least 90 percent of a 50-mg dose. It may be that people are failing to excrete 90 percent of the iodine in the urine not because their tissues are soaking it up, but because a lot of the iodine is coming out in the feces. There is no reason to assume that a 50-mg dose of iodine, which is at least 250 times the typical daily intake, can be almost completely absorbed by the average person. While this issue has not apparently been studied in humans, cows fed supraphysiological doses of iodine (72 to 161 mg per day) excreted approximately 50 percent of the administered dose in the feces.”

Gaby expressed concerns about iodine toxicity: “Fairly modest increases in iodine intake have been reported to cause thyroid dysfunction, particularly hypothyroidism. In a study of 33 Japanese patients with hypothyroidism, the median serum TSH level decreased from 21.9 mU/L to 5.3 mU/L (indicating an improvement in the hypothyroidism), and one-third became euthyroid, when the patients stopped eating seaweed and other high-iodine foods for 1-2 months. In a survey of 3,300 children aged 6-12 years from five continents, thyroid glands were twice as large in children with high dietary iodine intake (about 750 mcg per day), compared with children with more normal iodine intake. While the significance of that finding is not clear, it suggests the possibility of iodine-induced goiter. In addition, there is epidemiological evidence that populations with ‘sufficient’ or ‘high normal’ dietary iodine intake have a higher prevalence of autoimmune thyroiditis, compared with populations with deficient iodine intake. In a study of children in a mountainous area of Greece with a high prevalence of goiter, public-health measures taken to eliminate iodine deficiency were followed by a three-fold increase in the prevalence of autoimmune thyroiditis. In addition, modest increases in dietary iodine have been suspected to cause hyperthyroidism in some people, an effect that is known to occur with larger doses of iodine.

“Other well-known side effects of excessive iodine intake include acne, headaches, allergic reactions, metallic taste in the mouth and parotid gland swelling. While the doses of iodine reported to cause those side effects have often been higher than those currently being recommended, some people appear to be especially sensitive to the adverse effects of iodine.” Gaby concludes: “The possibility that high-dose iodine/iodide can relieve certain common conditions is intriguing. Considering the positive anecdotal reports, an empirical trial of iodine/iodide therapy, based on the clinical picture, seems reasonable. The case has not been made, however, that the average person should markedly increase his or her iodine intake in an attempt to saturate the tissues with iodine. Nor has the case been made that the iodine-load test can provide reliable guidance regarding the need for iodine therapy. Thyroid function should be monitored in patients receiving more than 1 mg of iodine per day.”

Subsequent counter arguments by Drs Abraham and Brownstein and rebuttals by Dr. Gaby focused on the amount of iodine in the Japanese diet and the safety of ingesting large amounts. An important point made by Abraham and Brownstein is that the requirement for iodine depends on the goitrogen load. Bromine, now very prevelant in the food supply, is a goitrogen, and may increase our need for iodine. They also claim that many of the toxic effects reported in the literature were due to radioactive forms of iodine. Finally, they dispute the assertion that the values of iodine in seaweed consumed by the Japanese were computed in dry weight. “The average daily intake of iodine by mainland Japanese in 1963 was 13.8 mg, based on information supplied by the Japanese Ministry of Health, which used only dry weight in their calculations, confirmed by a phone interview of one of us (GEA) on June 21, 2005, with officials of this organization.”26

Abrahams and Brownstein also defended the urine test for iodine loading, noting studies showing that organic iodine is not excreted in the feces. They also cited their own clinical experience. “Our experience at the Center for Holistic Medicine has shown that patients with the lowest urinary iodide levels on the loading tests are often the most ill. Many of these patients with very low urine iodide levels following the loading test have severe illnesses such as breast cancer, thyroid cancer or autoimmune thyroid disorders. All of these conditions have been shown in the literature to be associated with iodine deficiency. Positive clinical results were seen in most of these patients after supplementation of orthoiodosupplementation within the range of 6.25-50 mg of iodine/iodide (1/2 to 4 tablets of Lugol in tablet form).”27

In response, Gaby noted that “all but one of the references I cited discussed the adverse effects of inorganic iodine” and that while Dr. Lugol did use high doses of his combination iodine/potassium iodide compound, “they were recommended primarily to treat infections (iodine is a broad-spectrum antimicrobial agent) and hyperthyroidism, not as routine nutritional support for the average person.” Finally, he notes a review article, published in 2000, in which the authors state that in the 1920s and 1930s, when potassium iodide (KI) was widely used, many patients died of KI-induced side effects, particularly pulmonary edema and associated heart failure.28

Conclusions

It is axiomatic that there are no uncomplicated issues in the field of diet and health – and the subject of iodine is no exception. What conclusions can we draw from these conflicting assertions about iodine, especially supplementation containing iodide?

Let’s start by looking at the RDI of 100-150 mcg iodine per day. Most would argue that this intake is too low. Yet it is in line with what Weston Price reports in primitive diets. In preliminary analyses, he found a range of 24-32 mcg daily for the northern American Indians and 131-175 daily for the Inuit.29 Apparently the Inuit of the far north do not eat seaweed.30Unfortunately, Price did not carry out more extensive measurements, especially among those he reported to eat seaweed—the Gaelic peoples of the Outer Hebrides and the Andean Indians of Peru.

It appears to be very difficult to estimate the iodine intake in diets that contain seaweed. Based on the reported values in seaweed, some have claimed levels of 12 mg (12,000 mcg) in Japanese diets,31 leading Abraham and Brownstein to propose that “only mainland Japanese consume adequate amounts of iodine and that 99 percent of the world population are deficient in inorganic, non-radioactive iodine; that is, they have not reached whole body sufficiency for that essential element.”32

However, a published analysis of iodine intake in Japan found a range of 45-1921 mcg per day,33 and Weston Price found healthy peoples consuming iodine amounts in the lower end of this range. Furthermore, without seaweed, it would be very difficult to exceed 1,000 mcg per day, based on values found in typical traditional foods (see chart, page 47). For example, one meal of cod, one meal of shellfish including the 20 grams of the hepatopancreas, and one meal of mussels, plus additional meat, vegetables and legumes would supply about 1,000 mcg iodine; diets based on meat, even organ meats, would supply considerably less.

The late distinguished researcher Emmanual Cheraskin and his colleagues conducted a survey of reported total number of clinical symptoms and signs (as judged from the Cornell Medical Index Health Questionnaire) and correlated the findings with average iodine consumption. An intake of approximately 1,000 mcg per day correlated with the lowest number of reported symptoms, that is, the highest level of health.34

Abraham and Brownstein argue that the human iodine requirement is 1,500 mcg per day (1.5 mg) which is difficult to achieve without using seaweed, iodized salt or supplementation. They argue that because of widespread bromide and fluoride toxicity, most people today require between 5 and 50 mg per day, amounts only possible with supplementation; they do note that such supplementation should only be taken under the supervision of a physician to monitor iodine status.35

We cannot ignore the many reports of improved health using various types of iodine supplementation—whether through tincture of iodine on the skin, the atomidine protocol recommended by Edgar Cayce or use of iodine/potassium iodide compounds as proposed by Drs. Abraham and Brownstein. Increased exposure to goitrogenic mercury, bromides and fluoride compounds, and soy products ubiquitous in the food supply, coupled with declining levels of thyroid-supporting nutrients such as selenium and vitamin A in modern diets, may explain why some people need much higher levels of iodine than those found in traditional diets. Dr. Brownstein is to be credited with alerting the public to the dangers of bromides increasingly used in processed foods, sodas, vegetable oils, breads and even replacing iodine in teat washes for dairy cows, as well as in thousands of consumer products.

The Abraham protocol does carry a risk of adverse reactions and should be carried out under the supervision of a physician with experience in using it. As these physicians point out, consuming iodine in milligram doses should be coupled with a complete nutritional program that includes adequate amounts of selenium and magnesium, and, they claim, omega-3 fatty acids, and with careful supervision of detoxing reactions. According to Dr. Brownstein, chloride increases renal clearance of bromide and the use of salt or ammonium chloride shortens the time required for bromide detoxification. He recommends oral administration of sodium chloride (6-10 gm per day) or intravenous sodium chloride for increasing the renal clearance of bromide.31

Dr. Gaby’s call for a careful study should not be ignored. Not every physician reports the sterling results described by doctors using the Abraham protocol, and some individuals—including this author—have experienced adverse reactions to Lugol’s solution. The study should include a control group and groups using other iodine therapies, such as tincture of iodine on the skin, the atomidine protocol or even oral supplementation with elemental iodine rather than the iodine/potassium iodine combination. Comparison of the iodine-load urine test with the blood test for iodine status in relation to various symptoms of thyroid deficiency is another area begging for further research. Studies involving even a small number of individuals would be helpful in providing further answers to the great iodine debate.


SIDEBARS

Food Sources of Iodine

PLANT FOODS: Any food grown near the sea is likely to contain iodine, but especially rich sources include asparagus, garlic, lima beans, mushrooms, strawberries, spinach, pineapple and leafy greens. Coconut products, which always grow near the ocean, are good sources of iodine. Blackstrap molasses also provides iodine.

SEAFOOD: Iodine levels vary widely in fish and shellfish, but all seafoods contain some iodine. In published reports, cod, haddock, whiting, oysters and mussels test high. The hepatopancreas (yellow “butter” or “mustard”) in lobster tested as an extremely rich source and it is likely that the hepatopancreas of other saltwater shellfish would contain high levels of iodine as well.

BUTTER: Butter from cows pastured on iodine-rich soil will contain iodine. Look for butter from farms located near the ocean, or that have used seaweed or fish meal as a soil amendment. The cows should also be fed sea salt. The combination of iodine with selenium and vitamin A in butter make this traditional fat an ideal food for the thyroid gland.

SEAWEED: Levels of iodine in seaweed vary widely according to species and how the seaweed is dried. One study found a huge range of 2-817 mcg iodine per 100 grams. Iodine content is reduced when seaweed is dried in the sun, and iodine may vaporize during cooking and humid storage conditions. Some Asian seaweed dishes contain in excess of 1,100 mcg iodine (Thyroid Oct 2004, 14(10):836-841). Seaweed contains lignans, phytoestrogens that can depress thyroid function. This may explain why thyroid problems (except for goiter) are common among the Japanese, even though they eat a lot of seaweed.

SALT: Five grams (one teaspoon) of unrefined sea salt, a conservative estimate of the amount typically consumed in a day, provides only about 3 mcg iodine; iodized salt provides over 1,500 mcg iodine per five grams. The FDA’s Tolerable Upper Intake Level (UL) for adults is 1,100 mcg per day; thus, it is possible to greatly exceed the UL by using iodized salt.

Mysteries of the Goiter Belts

The use of iodine supplementation in the goiter belts of the world—and these areas of endemic goiter and associated problems exist in a great many countries—represents one of the first public health initiatives involving treatment of the general population through the addition of a nutrient (in this case iodine) to water or food. “Mass prophylaxis” with iodine was pioneered by two countries, the U.S. and Switzerland. The first controlled experiment took place in the early 1920s in Akron, Ohio, where 5000 school girls took 0.2 g of sodium iodide daily in their drinking water for a period of ten days in the spring and autumn while an equal number of controls drank untreated water. Of those taking the iodide who began the experiment with a normal thyroid, none developed goiter, whereas 50 percent of the controls developed goiter. Following this study, several cities in the Great Lakes region started to add iodide to central water supplies and iodized salt entered the food supply. In Switzerland, many cantons introduced iodized salt, and those districts where it was used experienced a decline almost to zero in the incidence of goiter (http://whqlibdoc.who.int/monograph/WHO_MONO_44_(p443).pdf).

In spite of these successes, mass iodine supplementation programs met with much resistance, especially as side effects emerged. While the programs almost completely eliminated goiter, the prevalence of autoimmune thyroiditis increased in areas with iodated water or in those using iodized salt. For example, a threefold increase in autoimmune thyroiditis was noted once iodine deficiency was eliminated in an area of endemic goiter in northwestern Greece, an association confirmed in clinical settings. In one study, dietary restriction of iodine reversed hypothyroidism in twelve of twenty-two patients; seven of the patients with reversed hypothyroidism were re-fed iodine and became hypothyroid again (Anthony P Weetman, Autoimmune Diseases in Endocrinology, pp 50-51).

In addition, further epidemiological studies have cast doubt on the simple association of goiter with iodine deficiency. Recently British researchers compared the distribution of endemic goiter in England and Wales with the distribution of environmental iodine. Despite a very clear goiter belt through the west of England and Wales, they found no patterning in the environmental iodine distribution and concluded that the presence of endemic goiter is no indicator of how iodine is distributed in the environment or vice versa (Stewart AG and others. The Illusion of Environmental Iodine Deficiency. Environmental Geochemistry and Health25:165-170, 2003). Early observations of goiter belts in Switzerland recorded strange distribution patterns, with villages completely free of goiter next to villages where goiter and cretinism affected many people, and even the promoters of mass iodine supplementation have noted that iodine supplementation works best in conjunction with an improvement of general nutrition.

Like all things in nature, the relationship of iodine status to thyroid health is resistant to simplified explanations. Many other nutrients contribute to thyroid health besides iodine, and numerous environmental and industrial toxins can depress thyroid function. And the body’s ability to use iodine almost certainly has a genetic component. The moral: be wary of one-size-fits-all solutions and if you choose to supplement with iodine, be carefully observant of any side effects.

Forms of Iodine

IODINE (I2): Elemental iodine is available in a formulation called Thyactin by TriMedica, described as a “stabilized colloidal iodine preparation.”

IODIDE (I-): Elemental iodine is unstable so it usually combines with another element, such as potassium or sodium. Salt is iodized using potassium or sodium iodide. Potassium iodide (KI) is available in tablet form in doses ranging from 0.23 to 130 mg. Lugol’s solution contains 6.3 mg of molecular iodine/iodide per drop; Iodoral tablets contain 12.5 mg iodine/iodide each. Both Lugol’s solution and Iodoral are one-third molecular iodine (5%) and two-thirds potassium iodide (10%). Most formulations of tincture of iodine are a combination of iodine and sodium iodide. Supersaturated potassium iodide (SSKI) contains 19–50 mg of iodide per drop. SSKI tablets are recommended in case of nuclear accident, to protect the thyroid gland from radioactive iodine, but otherwise should be avoided.

IODATE: Iodine in combination with oxygen, such as potassium iodate (KIO3), is considered inferior to potassium iodide in terms of protection against radioactive iodine.

ENDOGENOUS ORGANIC IODINE COMPOUNDS: In food and in the body, iodine is usually bound with protein compounds. The main iodine-containing compounds in the body are the thyroid hormones thyroxine (T4, four iodine atoms joined to tyrosine) and triiodothyronine (T3, three iodine atoms joined to tyrosine).

SYNTHETIC ORGANIC IODINE COMPOUNDS: Drugs such as Amiodarone (an antiarrhythmic medication) contain iodine. The simplest organoiodine compound is iodomethane, used as a soil fumigant. More complex iodate compounds include nonylphenoxypolyethoxyethanol-iodine (C17H28I2O2) or Byacin, used as a germicide, as in teat washes.

DETOXIFIED IODINE: Sold as Atomidine, the manufacturing method is called a “modified detoxification process” which involves a stage in which electricity is run through the iodine in saline solution to produce a solution containing free iodine (see sidebar on Atomidine, page 43).

NASCENT IODINE: Similar to Atomidine, although requiring more electricity and a longer time to produce. The diatomic bond of the iodine molecule is broken and retains a high amount of electromagnetic energy. According to the manufacturer, “once in contact with fluids of the body, the charged atom of iodine starts a process of relaxation where it gradually loses energy over two to three hours.“

Iodine on the Skin

The application of iodine to the skin as a way of iodine supplementation has been a common practice for over one hundred years. In 1932, researchers from the College of Pharmacy at Rutgers University carried out experiments on dogs and rabbits. They determined that, in fact, free iodine does penetrate through unbroken skin, although about 88 percent of the iodine applied evaporates from the surface within three days. Colloidal iodine (I2 in aqueous solution) was found to evaporate more quickly than tincture of iodine (I2 in alcoholic solution), and tincture of iodine evaporated more rapidly than Lugol’s solution (iodine plus potassium iodide). The authors concluded: “. . . iodine which penetrates through the skin is removed only slowly from within this area into the body, thus forming an iodine depot in the skin for several days. In this prolonged retention of iodine within the skin, we see a favorable condition for a possible local prophylactic and therapeutic action.” More recent studies, these involving humans, indicate that application of iodine to the skin is not effective in preventing the uptake of radioactive iodine by the thyroid gland; however, it is a slow but effective way to provide iodine supplementation, increasing serum levels at about 10-40 percent compared to oral ingestion (Abrahams, GE. The bioavailability of iodine applied to the skin. www.optimox.com).

Holistic practitioners have also applied iodine to the skin as a way to assess whole body iodine status—the so-called skin iodine patch test. The published data throws doubt on the effectiveness of the iodine patch test as a diagnostic aid. Many factors play a role in the disappearance of the yellow color of iodine from the surface of the skin including ambient temperatures and atmospheric pressure—the iodine will disappear faster in Denver than it will in Los Angeles. And in some people the iodine is reduced to iodide by the skin, which will result in the disappearance of the yellow color because iodide is white. Nevertheless, many have reported that the iodine applied to the skin remains longer after following the practice for several weeks, indicating a kind of saturation effect.

Unfortunately, we have no clinical trials on the use of iodine on the skin, but holistic practitioners have reported good results. For example, from Geoffrey Morell, ND: “A female patient with nodules on the thyroid gland and scheduled to have it removed applied tincture of iodine to the skin for over sixty days, at which point the stain remained for twenty-four hours. Upon reporting to the hospital for the operation, she was told that the nodules had disappeared and the operation was no longer necessary. In another case, a woman saw her visible goiter disappear after many weeks using tincture of iodine on the skin.”

The inefficient uptake of iodine from the skin and slow release can be seen as an advantage for those wishing to safely improve their iodine status without medical supervision. This treatment does not seem to provoke a detoxification reaction that often occurs with oral ingestion of Lugol’s.

Iodine applied to the skin is an excellent treatment for pre-malignant lesions, dark moles, keloid scars and other oddities of the skin. According to Dr. David Derry, “. . . iodine’s ability to trigger natural cell death (apoptosis) makes it effective against all pre-cancerous skin lesions and likely many cancerous lesions. The local site is replaced with normal skin.” He recommends topical iodine for insect bites as well (iodine4health.com/special/measurement/derry_measurement.htm).

For skin application, use mild tincture of iodine or Lugol’s solution, both available on the Internet.

Atomidine

Atomidine is a stable compound of iodine in a saline solution “that liberates the element in an atomic or nascent state on contact with an excess of solvent, such as the fluids of the body.” The use of Atomidine was popularized by Edgar Cayce, the so-called Sleeping Prophet, who gave medical diagnoses and suggested treatments in a trance. He often recommended the use of Atomidine, produced by Schieffelin & Company in New York, which he referred to as “iodine with the poisons taken out,” for a variety of conditions including thyroid and other glandular problems, sore throat, gum problems and infection (www.iodinesource.com/Excerpts.asp). A typical treatment consisted of “one drop in half a glass of water each morning for five days before the morning meal, leave off ten days, and then take again” or “three to five drops in water morning and evening.” He also recommended Atomidine for use as a gargle, as a douche and in topical preparations. (One intriguing ointment recipe called for adding 10 drops tincture of Benzoin, 5 drops Atomidine and 3 drams powdered snuff to 1 ounce ‘Oil of Butterfat’.”)

A theme running through Cayce’s writings was the use of Atomidine as a gentle way of “cleansing or purifying the body,” alternating with days when Atomidine was not used. He issued the same precautions for foods containing iodine, especially seafood, which he said should be consumed occasionally but not everyday. In one reading he indicated that seaweed could be toxic because of its high iodine content.

A paper published in the 1930s to promote Atomidine, written by the Schieffelin & Company, is posted on the internet (www.mnwelldir.org/docs/history/atomidine.htm). According to the report, Atomidine should be diluted when taken “and never given after a starchy meal.” The paper cites many cases of improvement when Atomidine is given for gum problems, as an antiseptic after surgery, gastrointestinal problems, urinary tract infections, high blood pressure, goiter, malaria and tropical fevers, venereal disease, infections of eye, ear, nose and throat, bronchitis and asthma.

Iodine Loading Protocol

Developed by Drs. Guy Abraham and David Brownstein, the protocol involves giving 50 mg iodine/iodide per day as Iodorol® and monitoring the excretion of iodine in the urine. The high levels of iodine/iodide are necessary to replace bromine and fluorine (and also chlorine) that have built up in the tissues, due to years of toxic exposure.

The iodine/iodide loading test is based on the concept that the normally functioning human body has a mechanism to retain ingested iodine until whole body sufficiency for iodine is achieved. During supplementation with iodine, the body progressively adjusts the excretion of iodine to balance the intake. As the iodine content in the body increases, the percentage of the iodine retained decreases, showing up as an increased amount of iodide excreted in the 24-hour urine collection. When whole body sufficiency for iodine is achieved, the absorbed iodine/iodide is excreted as iodide in the urine.

In the U.S. population, the percent of iodine load excreted in the 24-hour urine collection prior to supplementation with iodorol averages 40 percent. After three months of supplementation with 50 mg iodine/iodide per day, (four tablets of Iodoral ) most non-obese subjects not exposed to excess goitrogens achieve whole body iodine sufficiency, arbitrarily defined as 90 percent or more of the iodine load excreted in the 24-hour urine collections.

In addition to monitoring iodine excretion, Brownstein and colleagues also monitor urinary excretion of bromide and fluoride, goitrogenic halogens that the iodide gradually replaces over the course of supplementation. To facilitate the excretion of bromine, Dr. Brownstein recommends a combination of vitamin C, unrefined salt and magnesium, including baths of Epsom salts and sea salt. The patient is advised to avoid all sources of bromine, including fire retardant in carpet, clothing and mattresses, and bromide-treated breads, baked goods and grains. Bromine and chlorine are used extensively in materials in automobiles of recent vintage—in the seats, armrests, door trim, shift knobs—so avoidance of riding in cars with the windows closed is important.

Dr. Brownstein reports numerous benefits from the protocol including reduced need for thyroid medications, reduced allergies, increased energy, reduced fibromyalgia, weight loss, clearing of ovarian cysts and reduction of hypothyroid symptoms such as brain fog. In his experience, side effects including metallic taste in mouth, sneezing, excess saliva and frontal sinus pressure occur in less than 5 percent of patients.

For ongoing thyroid protection, it is important to avoid sources of bromide, fluoride and chloride (including environmental perchlorates, often found in drinking water). That means drinking purified or filtered water instead of tap water, consuming organic food (conventional produce and grains are treated with bromide-, chloride- or fluoride-containing pesticides and fumigants), avoiding bromated breads and consuming plenty of unrefined sea salt along with an iodine-rich diet.

Sources: http://www.optimox.com/pics/Iodine/loadTest.htm#6http://iodine4health.comhttp://iodine4health.com/ortho/brownstein_ortho.htm.

Report from Germany

“Here in Germany we are suffering from an epidemic of autoimmune thyroid disease due to the government’s huge campaign to iodize our salt and water. The food industry uses iodized salt for all products. Animal feed and milk is iodized. The German government claims that the earth has no iodine and that natural foods do not contain enough iodine. Even food for fresh water fish is iodized.

“The German thyroid league admits that iodization has caused a rise in autoimmune diseases of the thyroid. About ten million Germans are affected. Doctors tell us about studies showing that these patients should not eat iodized food as it makes their disease worse. Thyroid illnesses are painful and hard to heal. The thyroid gland controls our body’s metabolism. Also, the eyes can be destroyed. The standard therapy is to remove or radiate the sick gland. Then the patient needs thyroid hormones to survive.

“The sad thing is that most people don’t even know that what they eat is iodized. In Germany iodized salt in packaged food has to be declared but iodine in salt in restaurants or in bread is not labeled.

“The German iodization program is not popular with the public at all. We had it during the Third Reich and it took quite a lot of government campaigning to bring back mass iodization, a public relations campaign to convince people that iodine is healthy and has no dangers at all. Government officials say that people can choose iodized or noniodized salt but no one mentions the hidden salt. In the Third Reich they called it “silent iodization,” to avoid any resistance.

“I have run a self help group for thyroid patients for years now and it is a very difficult situation for patients to not have enough food! It is even difficult to get all the information we need.

“We hear a lot of discussion about fluoride in the water but I am surprised that there is none about iodine. In Germany they sell salt with iodine and fluorine—both affect the metabolism and can damage the thyroid gland. Natural salt has the advantage of giving us minerals we need and in a way that our body can handle instead of the low quality chemistry added to food or water. I know that the healthy thyroid gland needs more than iodine. It also needs vitamins A and C, and many other minerals. A natural diet can offer more benefit for our heatlh and fewer dangers and side effects. The tragedy is that the WHO has started to ban natural foods. In India, Himalayan salt was banned and iodized salt then sold five times as much as natural salt. Poor people can’t afford the natural salt and so many didn’t have any salt at all anymore. The German media reported on protests in India and I don’t know whether natural salt is allowed again.

“Here in Germany, thousands of thyroid patients are signing a petition asking the Bundestag to change the law, and to require iodization labels on packages.”

-Ute Aurin

Reaction to Iodoral

“Three articles appeared recently in The Original Internist concerning clinical research with the use of iodine/iodide in megadoses. Our medical group, consisting of three MDs and one ND/Acupuncturist decided that we should try to find out whether any one of us was iodine-deficient. Our practice is in the Great Lakes region that was described as the ‘Goiter Belt’ by David Brownstein. We therefore followed Brownstein’s recommendation for the iodine/iodide loading test. Five individuals within our office took the test and, by the criteria outlined, we were all iodine-deficient.

“Three of us, two MDs and our Laboratory Director, then proceeded to take the 50 mg of Iodoral a day with the intention of repeating the iodine/iodide loading test after three months of treatment. After about six weeks of continuous treatment, I experienced dysphagia [difficulty swallowing], resulting in lower chest pain on swallowing both food and fluids. This was particularly marked with hot fluids, a totally new experience for me. I told the Laboratory Director that I was going to discontinue taking the Iodoral since I had concluded that it was the potential cause. To my surprise, she told me that she had experienced exactly the same symptom and had also discontinued the treatment. The other two MDs who took the treatment did not experience this symptom. Some four weeks after discontinuation of the Iodoral, we both continue to experience the same kind of dysphagia, although it is much milder. We can only conclude that we experienced some esophagitis though this has not been proved by further study.

“If this is indeed a toxic effect of the Iodoral, we concluded that it needed to be drawn to the attention of the CAM medical community. If the conclusions are correct, we should expect to hear that other ‘guinea pigs’ have experienced something similar. The question remains in our minds as to whether the test outlined by Brownstein is an accurate determination of chronic iodine deficiency. It may well be that iodine has a sensitive dose relationship like that which is so well known with selenium, for example, and with other minerals. The question, put so eloquently recently by Alan Gaby is whether we are embarking on a strategy that can be toxic for some while beneficial for those sick individuals reported by Brownstein and his co-author, Guy Abraham. Indeed, as Gaby questioned later, of the 4,000 patients treated by the Michigan Clinic, how many were carefully monitored in detail for potential side effects? Since gastroesophageal reflux (GER) is mentioned in a drug commercial as a common affliction, it might be that some patients who are being treated with high-dose iodine would never conclude that GER might be related to the iodine consumption. It might not be recognized as a side effect even by a physician, since it is so remote from any expected or predicted symptom.”

-Derrick Lonsdale MD, FAAP, FACN, Westlake, Ohio The Townsend Letter for Doctors and Patients, April 2006

Iodine-Steroidogenesis, Fat Burning and Muscle Building

~Content Source

Iodine is used by the thyroid to produce thyroid hormones, and is actually used by other tissue as well. Only 80% of iodine is found in the thyroid, whereas the other 20% are found in other tissue such as salivary glands, gastric mucosa, the choroid plexus (brain), ciliary body of the eye, lacrimal gland, thymus, skin, placenta, prostate, and pancreas…

Oceans are the main source, where soil contains very little. Foods that grow close to the sea contains more iodine, due to the sea winds that bring iodine to he soil. Seaweeds such as wakame, nori or mekabu, contains significant amounts of iodine.

The thyroid manufactures thyroid hormones in the gland from one molecule of the amino acid tyrosine and iodine—four iodine atoms per tyrosine molecule in the case of thyroxine (T4), and three iodine atoms in the case of triiodothyronine (T3).

99% of all thyroid hormones are bound to proteins, while only 1% is free in serum. 80% of T3 is deiodinated from T4, to be used by tissue. T4 crosses the blood brain barrier better than T3, so he brain requires more T4 as it can covert it to T3. A decrease in T4 result in an increase in thyroid stimulating hormone (TSH) which signals the thyroid to produce more thyroid hormones. TSH also increases the conversion of T4 to T3.

Major effects of thyroid hormones:

  • Regulates basal metabolic rate
  • Regulates nutrient metabolism (digestion, absorption, transport, insulin sensitivity etc…)
  • Regulates on ion transport/muscle contraction
  • Development, growth (height and muscle size), and steroidogenesis

Being more active and healthy, with a fast metabolism and high testosterone production demands more thyroid hormones, spesifically T3.

Many other nutrients are important for optimal thyroid function as well as the conversion of T4 to T3. Few of these nutrients include vitamin A, selenium, vitamin D, zinc, magnesium, vitamin B6, and more.

For e.g. a deficiency is zinc, selenium and iodine decreases TSH, T4 and T3.

About 120mcg of iodine is sufficient for thyroid hormone production. But it’s just the very bare minimum requirement, same as with the minimum vitamin D requirement to prevent rickets.

As toxins, halogens, inflammation, infection increase, so does the need for iodine and it’s cofactors.

Same goes for increased physical activity, steroidogenesis, metabolism all require more thyroid hormone to function more effectively.

Once the thyroid is saturated with iodine (which requires much more than just the RDA of 150mcg to saturate), it further detoxes, replaces and protects the thyroid from radioactive elements as well as toxic halogens which can interfere with thyroid hormone production, such as chlorine, fluoride, bromine and heavy metals such as mercury, lead, aluminium, copper etc.

Powerful antioxidant, anti-inflammatory, anti-viral, anti-septic and anti-cancer

Iodine is one of the best free radical scavengers and immune system supporters. It neutralizes and breaks down hydrogen peroxide to form water, preventing he formation of a hydroxyl radical. I2 exerts a 10- or 50-fold greater antioxidant action than ascorbic acid or KI (potassium iodide), respectively.

Iodine also suppresses the levels of pro-inflammatory messengers such as nitric oxide, prostaglandin-E2 (which increases estrogen as well), and pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6, and interleukin-1β), making iodine a very effective anti-inflammatory mineral.

Iodine has shown to exert powerful antiproliferative action (prevent the spread of cancerous and tumor) via PPARγ receptor activation. Iodine also protects healthy cells against apoptosis (cell death) and induce apoptosis on cancerous cells.

Iodine has also been used to treat asthma, parasites, syphilis, cancer, Graves’ disease, periodontal disease, and arteriosclerosis.

As iodine has been found in the mucous of the stomach, it protects against incoming toxins and also against abnormal growth of bacteria in the stomach, keeping the gut sterile, clean, healthy and protected. Iodine could thus also be a potent agent against the progression of leaky gut.

Seaweeds and other iodine rich plants have been used 4 century BC by Theophrastus, Aristotle’s pupil, to treat wounds, such as from sunburns, and its probably also been used before that by others for wounds/inflections.

Adaptogen and anti-cortisol

Animal studies have proven that iodine normalizes elevated adrenal corticosteroid hormone secretion related to stress, so it acts as an adaptogen.

Testosterone

Iodine reverses the effects of hypothyroidism on the testicles. Thyroid hormones increase testosterone synthesis, and inadequate T3 will lead to low testosterone and testosterone receptor sensitivity.

Iodine will protect the testes and testosterone from free radicals and oxidative stress, however, when there too way too much iodine in the testes, without enough cofactors, it can actually increase reactive oxygen species (free radicals) and lower testosterone via down regulation of varies enzymes.

Iodine also binds/interacts with nucleus/steroid receptors and helps to increase receptor sensitivity of T and DHT.

Iodine administration is also able to regenerate damaged Leydig cells (cells in testes where testosterone is made).

Not only does iodine protect the thyroid against toxins such as bromine, flouride, chlorine, etc, but also all other tissue including testes. If toxins and heavy metals are present in testes, proper testosterone synthesis can not occur.

Anti-estrogen

Iodine is potentially anti-estrogenic. As seen in this study, treatment with iodine and iodide increases the mRNA levels (increase the expression and activity) of Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1). These two enzymes are phase I estrogen metabolizing enzymes that oxidizes 17β-estradiol (which is carcinogenic) to 2-hydoxyestradiol (2-OH-E2) and 4-hydoxyestradiol (4-OH-E2), respectively. Higher activity of these enzymes lead to greater catabolism of estrogen and urinary excretion of the metabolites.

Iodine also decreases the levels of the estrogen responsive genes TFF1 and WISP2.

Iodine increases peroxidase activity, which is inversely related to estrogen receptor alpha (ER) concentration, thus restricting estrogen’s action. 2-5mg/day of iodine (I2) diminished translocation of the estrogen receptor alpha.

Iodine treatment increases the catabolism of estrogen and decreases estrogen receptors and estrogen responsiveness to receptors.

Furthermore, iodine saturates as well as inhibit the lipid peroxidation of polyunsaturated fatty acids, preventing its endocrine and metabolism disrupting actions to a great degree.

Extras and supplements

I advise to stay away from iodated salt and get your iodine from food sources and from supplements containing only organic iodine, not combined with inorganic iodine.

Weston Price reported that the intake of iodine was 131-175 mcg for the Inuit (about the level of the DRI) and 25-34 mcg for Canadian Indians (considered very low, although they did not exhibit thyroid problems). Traditional food of Japanese contains significant amounts of dietary iodine, and they possibly consume at least 7000 mcg of iodine daily from kombu alone with no suppressive effect on the thyroid.

Liquid iodine is clean iodine with a mix of organic and inorganic iodine. Kelp/seaweeds contains just organic iodine as well as many other rare essential trace minerals that your body also needs. I would be much harder, if not impossible, to overdose on iodine from kelp. I don’t think it’s necessary to take more than 1mg daily, unless you need to flush out other metals that’s interfering with your thyroid or when you want to lower excessive estrogen. Under those circumstance you could increase your dosage until you see the symptoms diminish and you have found your sweet spot.