Ionizing radiation damages DNA and other proteins directly, but does most of its dirty work through oxidative damage when a storm of free radicals are generated by the effect of radiation on water molecules inside the cells. That makes the best protection from ionizing radiation a comprehensive approach that optimizes intrinsic resources for ameliorating oxidative and mutagenic damage. Additionally, it is well known that iodine (potassium iodide) can help to protect the thyroid gland by displacing radioactive forms of the element, but should it be taken preventively? In fact, there is a substantial amount of scientific evidence that great care must be taken when recommending iodine for any health concern. Most clinicians that practice according the functional model are aware that the widespread surge in autoimmune disease presents a specific risk because iodine supplementation can trigger latent or aggravate pre-existing autoimmune thyroiditis (Hashimoto’s disease), as illustrated by a paper published recently in the journal Hormones. The authors state:

“Epidemiological studies have linked increased iodide intake from dietary or other sources to the development of hypothyroidism, and it appears that in several—though not all—cases, this phenomenon has an autoimmune basis.”

They further note:

“Within an immunological context, iodine may mediate thyroiditis induction via at least two mechanisms: a) by increased post-translational modification of thyroglobulin (Tg), an event which may enhance the immunopathogenicity of this molecule as detailed further in this review; and b) via apoptotic/necrotic effects of thyrocytes, a step that could initiate presentation of thyroid antigens at immunostimulatory levels.”

All clinicians who manage conditions for which supplemental iodine therapy is contemplated should bear in mind the authors’ conclusion:

“High dietary iodide intake may lead to the development of thyroid autoimmunity via at least two pathways. First, iodide may epigenetically modify the Tg molecule and create iodinated neoantigenic determinants to which immune tolerance has not been established or alter the processing of Tg to facilitate generation of pathogenic but cryptic Tg determinants that may not contain iodine. Second, iodine may precipitate apoptotic/necrotic effects on thyrocytes, thus releasing increased amounts of thyroid antigens that can activate autoreactive T cells in situ or in thyroid-draining lymph nodes. The genetic background of the host may be permissive to one or both of these pathways that may act in synergy or independently of each other.”

The authors of a study published in the Journal of Clinical Endocrinology & Metabolism also weigh in on the subject of hypothyroid due to thyroiditis from high iodine intake:

“Twenty-two patients with spontaneously occurring primary hypothyroidism were studied to evaluate the spontaneous reversibility of the hypothyroid state. Twelve (54.5%) became euthyroid [normal thyroid] after restriction of iodine intake for 3 weeks (reversible type).”

Of particular interest is the finding that:

“Seven patients with the reversible type were given 25 mg iodine daily for 2–4 weeks; all became hypothyroid again...The patients with reversible hypothyroidism had focal lymphocytic thyroiditis changes in the thyroid biopsy specimen, whereas those with irreversible hypothyroidism had more severe destruction of the thyroid gland.”

Their conclusion is consonant with those of the previously mentioned study, and implies that milder forms of thyroiditis may recover if iodine is discontinued:

“These results indicate the existence of a reversible type of hypothyroidism sensitive to iodine restriction and characterized by relatively minor changes in lymphocytic thyroiditis histologically. Attention should be directed to this type of hypothyroidism, because thyroid function may revert to normal with iodine restriction alone.”

Another study published in the journal Biological Trace Element Research finds more evidence for the role of iodine in promoting hypothyroidism. The authors first state:

“Excessive iodine intake is known to induce hypothyroidism in people who have underlying thyroid disorders. However, few studies have been performed on subjects with normal thyroid function without a history of autoimmune thyroid disease. We hypothesized that high iodine intake may cause a subtle change in thyroid function even in subjects with normal thyroid function.“

They examined 337 subjects with normal levels of thyroid antibodies for urinary iodine excretion, free T4 (FT4), and thyroid-stimulating hormone (TSH).

“The results showed urinary iodine excretion had negative correlation with FT4 and showed a positive trend with TSH. We found that 61.7% of subjects had circulating TPO-Ab within normal reference range. In all subjects, TPO-Ab levels were negatively correlated with FT4 and positively with TSH.”

In other words, as iodine went up the thyroid hormone free T4 went down and TSH (thyroid stimulating hormone)—bother markers for hypothyroid disease. Additionally, while 38.3% had high levels of thyroid peroxidase antibody (proof of autoimmune thyroiditis), for everyone higher levels of TPO-Ab correlated with lower free T4 and higher TSH. (Personally, I have observed that the standard reference ranges for thyroid antibodies are too ‘generous’.) They authors summarize the implications of their data:

“In conclusion, high iodine intake can negatively affect thyroid hormone levels in subjects with normal thyroid function.”

I have heard the Japanese consumption of seaweed cited as evidence for allowing higher levels of iodine intake, but a study published in the Endocrine Journal (of the Japanese Endocrine Society) contradicts this assumption.

“The effect of ingesting seaweed “Kombu” (Laminaria japonica) on thyroid function was studied in normal Japanese adults. Ingesting 15 and 30 g of Kombu (iodine contents: 35 and 70 mg) daily for a short term (7-10 days) significantly increased serum thyrotropin (TSH) concentrations, exceeding the normal limits in some subjects…During long term daily ingestion of 15 g of Kombu (55-87 days), the TSH levels were elevated and sustained while the FT4 and FT3 levels were almost unchanged. Urinary excretion of iodine significantly increased during ingestion of Kombu. These abnormal values returned to the initial levels 7 to 40 days after discontinuing the ingestion of Kombu.”

In other words, a diet  heavy on the seaweed Kombu can introduce enough iodine to suppress thyroid function. The authors conclude by recommending:

“Based on these findings that thyroid function was suppressed during ingestion of Kombu, though the effect was reversible, we recommend Japanese people avoid ingesting excessive amounts of seaweed.”

Their findings are echoed in a paper published recently in The Medical Journal of Australia which reports…

“…a series of cases of thyroid dysfunction in adults associated with ingestion of a brand of soy milk manufactured with kombu (seaweed), and a case of hypothyroidism in a neonate whose mother had been drinking this milk. We also report two cases of neonatal hypothyroidism linked to maternal ingestion of seaweed made into soup. These products were found to contain high levels of iodine.”

Happily, in both cases the TSH returned and the patients recovered after discontinuing the seaweed enriched soy milk. The conclude with this alert:

“Despite increasing awareness of iodine deficiency, the potential for iodine toxicity, particularly from sources such as seaweed, is less well recognised.“

Another paper just published in the Journal of Paediatrics and Child Health reports a similar phenomenon and offers a balanced conclusion:

“Mild iodine deficiency is a recognised problem in Australia and New Zealand. However, iodine excess can cause hypothyroidism in some infants. We highlight two cases which illustrate the risks of excess dietary iodine intake during pregnancy and breastfeeding. They also describe a cultural practice of consuming seaweed soup to promote breast milk supply. Although most attention recently has been on the inadequacy of iodine in Australian diets, the reverse situation should not be overlooked. Neither feast nor famine is desirable.“

Caution should be used even when applying topical iodine as an antiseptic as reported in a paper published in the journal Anales española de pediatría. They note that iodine-containing antiseptics are still common in obstetrics and neonatology, and that…

“Topical iodine given both to the mother before delivery and to the neonate causes iodine overload. The absorption of maternal iodine through the skin is so fast that iodine in the blood of the umbilical cord increases by 50% a few minutes before delivery. Iodine overload also occurs in the mother. Urinary and breast-milk iodine are increased more than 10-fold in the days after delivery if providone-iodine is used in episiotomy. The overload in the neonate is even higher if breast-fed….this overload can produce thyroid blockade…”

The effects of thyroid blockade in the infant are potentially very serious, especially considering the importance of thyroid function for brain development. The authors conclude with a warning:

“Attention should be drawn to the undesirable effects of iodine antiseptics and their use in the perinatal period should be avoided.“

Of course there is a place for iodine supplementation in cases of deficiency conditions (which can manifest in a variety of ways) along with prophylaxis for disastrous exposure to ionizing radiation, but generally speaking, how much is enough? A very nice study on a chronically iodine-deficient population was recently published in the journal Endokrynologia Polska (Polish Journal of Endocrinology):

“Until 1997, Poland was one of the European countries suffering from mild/moderate iodine deficiency. In 1997, a national iodine prophylaxis programme was implemented based on mandatory iodisation of household salt with 30 ± 10 mg KI/kg salt, obligatory iodisation of neonatal formula with 10 μg KI/100 mL and voluntary supplementation of pregnant and breast-feeding women with additional 100-150 μg of iodine. Our aim in this study was to evaluate the iodine status of pregnant women ten years after iodine prophylaxis was introduced.“

They examined 100 healthy pregnant women between the fifth and the 38th week of pregnancy for serum TSH, fT(4), fT(3), thyroglobulin (TG), anti-peroxidase antibodies (TPO-Ab), anti-thyroglobulin antibodies (TGAb), urinary iodine concentration (UIC) and thyroid volume and structure by ultrasonography. This really was an iodine-deficient population—28% of the subjects had a goiter. What did their data show?

“Median UIC was significantly higher in the group receiving iodine supplements than in the group without iodine supplements…Serum TSH, fT(3) and fT(3)/fT(4) molar ratio increased significantly during pregnancy while fT(4) declined. Median serum TG was normal: 18.3 ng/mL (range 0.4-300.0 ng/mL) and did not differ between trimesters. Neonatal TSH performed on the third day of life as a neonatal screening test for hypothyroidism was normal.”

Thus the authors concluded:

“Iodine supplements with 150 μg of iodine should be prescribed for each healthy pregnant [Polish] woman according to the assumptions of Polish iodine prophylaxis programme to obtain adequate iodine supply.”

Here is a point worth noting for those who are aware of a recent trend for prescribing extremely high doses of supplemental iodine, as high as 50 mg per day and sometimes more: 50 mg = 50,000 μg (micrograms). That’s 333 times the amount recommended by the Polish study. This is not to say that there are never cases where megadoses of iodine may be indicated, but clinicians should maintain a biological perspective and exercise caution.

Regarding tools to support the practitioner’s thoughtful efforts to structure a careful approach to thyroid case management and iodine supplementation, can we rely on urinary iodine concentration (UIC) as a metric? A study published in Clinical Endocrinology suggests that we can’t. The authors set out to…

“…measure breast milk iodine (MI) and urinary iodine (UI) concentrations in healthy newborns and their nursing mothers from an iodine-sufficient region to determine adequacy and to relate these parameters to thyroid function tests in mothers and infants.”

Their study cohort included 48 healthy neonates of 37 to 42 weeks’ gestation and their mothers. Serum thyroid function tests and urinary iodine excretion were measured for infants and mothers, and maternal milk iodine concentration were measured. What did their data show?

“Neonatal and maternal UI did not correlate with serum thyroid function tests…Among euthyroid neonates, UI was adequate despite low median maternal UI and MI concentrations. There were no significant correlations between UI or MI and thyroid function tests in the mothers and infants.“

What about in cases where there is documented thyroid dysfunction? Is urinary iodine a correlative marker in this patient population. An interesting study published in the journal Endocrine implies that it is not. The authors state:

“The prevalence of thyroid dysfunction varies in different populations. The aim of this cross-sectional study was to analyze the prevalence of undiagnosed thyroid dysfunction and thyroid antibodies and their relationship with urine iodine excretion in a representative sample of 1,124 (55.5% women; mean age: 44.8 ± 15.2 years) non-hospitalized Mediterranean adults, in Catalonia (Spain).”

They measured free thyroxine (fT4), thyroid-stimulating hormone (TSH), thyroperoxidase and thyroglobulin antibodies, and urine iodine. Interestingly, they found thyroid dysfunction in 8.9% of their subjects with 5.3% previously undiagnosed (13.61% and 9.8% in those over age 60). Rough indicators of autoimmune thyroiditis were present: thyroperoxidase antibodies in 2.4% of men and 9.4% of women and thyroglobulin antibodies in 1.3% of men and 3.8% of women. What about the correlation with urine iodine?

“No differences were observed in urine iodine between groups with thyroid dysfunction and euthyroidism, or between subjects with positive or negative antibodies.“

In other words, urine iodine completely failed to discriminate between those with normal and abnormal thyroid function.

Here’s what the evidence boils down to: iodine supplementation has its place when used with sound clinical judgment and a biological perspective in the hands of a practitioner with the knowledge and experience to assess the need and tolerance of each individual patient with care. As for protection from harmful doses of ionizing radiation, clinicians who employ a functional medicine perspective are well equipped to evaluate your resources for ameliorating oxidative and mutagenic stresses.