Iodine

Iodine is a trace mineral that is necessary for various functions in the body. It is acquired from the diet, and intake is primarily from iodized table salt in the U.S. Yet, with the new heightened awareness about sodium restriction and the fact that iodine from iodized salt is not very bioavailable, deficiency of this crucial mineral is becoming a very real health concern. Iodine deficiency is implicated in numerous health problems including hypothyroidism, goiter (enlarged thyroid gland), cognitive disorders, neurological disorders, ADHD, breast and prostate diseases and stomach cancer. In addition, iodine deficiency during pregnancy can result in numerous complications as well as severe neurological defects and cretinism (severely stunted physical and mental growth). Iodine is found in each of the trillions of cells in the body. Without adequate iodine levels, life itself is not possible.

The statistics show that iodine deficiency is at an alarming level among the population. According to the National Health and Nutrition Examination Surveys (NHANES), from NHANES I (1971-1974) to NHANES III (1988-1994), the median urinary iodine concentration in the U.S. decreased by 50 percent. Furthermore, the number of individuals with unacceptable urinary iodine excretion levels below 5 mcg/dL increased by 4.5-fold. This included 6.7 percent of pregnant mothers and 14.9 percent of women of child-bearing age with urinary iodine excretion below 5 mcg/dL.¹ The most recent NHANES (2001-2006) indicated that iodine levels in pregnant women in the U.S. were only borderline sufficient.²

Despite the fact that many Americans consume large amounts of sodium, many of the processed foods high in sodium do not use salt in the iodized form. Iodine deficiency can be caused by a decrease in iodine intake or uptake by the intestines. Causes may include low iodine levels in the soil and water, salt-restricted diets or intake of large amounts of goitrogens—substances that cause goiter (enlarged thyroid)—such as cruciferous vegetables, cassava, millet and soy, which affect iodine uptake and utilization. Also, several elements found in the environment are similar to iodine in structure and compete for uptake from the intestines.

In this article, the first in a two-part series, I will discuss the negative effects of iodine deficiency on cognition and GI health as well as the reasons why iodine uptake can be blocked in the body. Next month, I will discuss the ways that iodine deficiency can destroy the health of the breast and prostate.

Thyroid and Cognition

The most notable physiological function of iodine is the incorporation into thyroid hormones. Iodine deficiency results in insufficient thyroid hormone synthesis and hypothyroidism, a problem widespread across the population. In pregnant women, maternal iodine deficiency and hypothyroidism is detrimental to the developing fetus, and can cause abnormal central nervous system development and maturation, with permanent mental retardation, neurologic defects and growth abnormalities known as cretinism. Even a mild iodine deficiency in the fetus can impair cognitive ability.²

In one study, researchers assessed iodine levels and IQ in schoolchildren. They showed that urinary iodine levels above 100 mcg/L was associated with significantly higher IQ, while children with urinary iodine levels less than 100 mcg/L had an increased risk of IQ below 70.³ A similar study found that children from severe iodine deficient areas had a loss in IQ scores of 12.45 points.⁴ Another interesting study compared the prevalence of ADHD in children in mildly and moderately iodine deficient areas. In the children from the moderately iodine deficient area, 68.7 percent were diagnosed with ADHD, compared to no children diagnosed from the mildly deficient area. Also important, this study showed that of the children diagnosed with ADHD, 63.6 percent were born to mothers who had become hypothyroid in early gestation.⁵ Research has also shown that children in a severely iodine deficient area had lower levels of the thyroid hormone thyroxine (T4) and higher thyroid stimulating hormone (TSH) levels and were slower learners with lower scores on achievement motivation tests compared to children in a mildly iodine deficient area.⁶

Iodine and Gastrointestinal Health

The cells that line the stomach and small intestines actively accumulate iodine. Some stomach conditions such as atrophic gastritis result in less uptake of iodine by the tissue, and are associated with iodine deficiency and goiter.⁷ Thus, gastrointestinal health is important for iodine sufficiency. In addition, research has shown that iodine uptake inhibitors such as nitrates, thiocyanate and salt increase the risk of gastric cancer.⁸ One study found that goiter was associated with double the risk of gastric non-cardia adenocarcinoma.⁹ Another study showed that as iodine intake increased, both the incidence of goiter and stomach cancer decreased.¹⁰ A third study demonstrated that severe iodine deficiency was present in 49 percent of individuals with stomach cancer compared to 19.1 percent in the control group.¹¹

Common Culprits Behind Deficiency

Iodine is an element in the halogen family, members of which also include fluorine, chlorine, bromine and astatine. These other halogens can compete with iodine for uptake from the intestines and can replace iodine in physiological reactions.

Bromine and chlorine are both widespread environmental contaminants. In addition to its use as a flame retardant, bromine has also replaced iodine as a dough softener in bread making. Animal models indicate that with increased intake, bromide replaces iodine in the thyroid.¹² Bromide treatment in iodine-deficient rats induces hypothyroid symptoms including decreased T4 and increased thyroid gland size. Similarly, animal models have shown that bromine can induce goiter, decrease iodine concentration in the thyroid¹³ and increase iodine excretion.¹² Also, research indicates that supplementation with iodine and selenium decreased the amount of bromine taken up by the thyroid gland by 50 percent compared to non-supplemented rats.¹⁴

Chlorine, particularly in the form perchlorate, is an environmental contaminant ingested through water, milk and produce. Perchlorate is a competitive inhibitor of the iodide/sodium symporter (NIS), which means it inhibits the uptake of iodide in the thyroid resulting in decreased thyroid function.¹⁵ The NIS has a 30-fold higher affinity for perchlorate than for iodide, thus if perchlorate is present, it is much more likely to be taken up into the thyroid gland than iodide.¹⁶

One study measured perchlorate levels in dairy milk and breast milk. They found that the majority of the dairy milk samples and all of the breast milk samples tested positive for perchlorate. More importantly, this study showed that due to the mean perchlorate level in breast milk and the recommended maximum daily “safe” intake levels of perchlorate established by the National Academy of Science, the average breast-fed infant consumes more than double the maximum daily safe intake.¹⁷

Some data suggests that perchlorate may affect thyroid function. One study demonstrated that newborns in an area with 100 percent contamination of the drinking water with perchlorate had elevated TSH levels compared to newborns in an area without contaminated drinking water.¹⁸ Another study found that in iodine-deficient women, higher levels of perchlorate in the urine was associated with increased TSH and decreased T4 levels.¹⁹

Fluorine is added to the majority of drinking water in the U.S. and is used in the prevention of dental disease, primarily in the form of fluoride. Research has shown that consumption of drinking water with raised fluorine content affects the pituitary-thyroid axis resulting in an increase in TSH and a reduction of the thyroid hormone triiodothyronine (T3), the strongest form of thyroid hormone that is 3 to 5 times stronger than T4. The researchers concluded that increased fluorine intake was a risk factor for acceleration of thyroid pathology.^20-21 Animal models support this finding, showing that increased fluoride intake in iodine-deficient mice results in increased levels of thyroid hormones.²²

Restoring Iodine Levels

In iodine-deficient individuals, iodine supplementation can re-establish optimal levels. Both clinical experience and research support the use of inorganic, non-radioactive iodine (Iodoral®).²³ Like the noted iodine researcher Guy Abraham, MD, I consider Iodoral to be a superior form of iodine supplementation. To prevent gastric irritation, the iodine/iodide preparation is absorbed into a colloidal silica excipient, and to eliminate the unpleasant taste of iodine, the tablets are coated with a thin film of pharmaceutical glaze. Prior to supplementation, one can identify iodine levels in the body via a 24-hour iodine sufficiency test.

It is important to note that the cofactors required for thyroid hormone synthesis, including riboflavin and niacin (as found in ATP Cofactors), should also be supplemented together with iodine. Selenium, when taken with iodine, can decrease the amount of bromine taken up by the thyroid gland and therefore should be added to this regimen.

Conclusion

Iodine deficiency is at epidemic proportions and iodine deficiency or sub-clinical deficiency is more common than previously believed. Due to the variety of health conditions associated with this deficiency, taking an iodine sufficiency test to determine iodine status and optimizing iodine levels with Iodoral, ATP Cofactors and selenium should be considered as part of any health maintenance plan.

References

1. Hollowell JG, Staehling NW, Hannon WH, et al. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994) J Clin Endocrinol Metab. 1998 Oct;83(10):3401-8.

2. Perrine CG, Herrick K, Serdula MK, et al. Some Subgroups of Reproductive Age Women in the United States May Be at Risk for Iodine Deficiency. J. Nutr. 2010 June 16. Published Online Ahead of Print.

3. Santiago-Fernandez P, Torres-Barahona R, Muela-Martinez JA, et al. Intelligence quotient and iodine intake: a cross-sectional study in children. J Clin Endocrinol Metab. 2004 Aug;89(8):3851-7.

4. Qian M, Wang D, Watkins WE, et al. The effects of iodine on intelligence in children: a meta-analysis of studies conducted in China. Asia Pac J Clin Nutr. 2005;14(1):32-42.

5. Vermiglio F, Lo Presti VP, Moleti M, et al. Attention deficit and hyperactivity disorders in the offspring of mothers exposed to mild-moderate iodine deficiency: a possible novel iodine deficiency disorder in developed countries. J Clin Endocrinol Metab. 2004 Dec;89(12):6054-60.

6. Tiwari BD, Godbole MM, Chattopadhyay N, et al. Learning disabilities and poor motivation to achieve due to prolonged iodine deficiency. Am J Clin Nutr. 1996 May;63(5):782-6.

7. Nicola JP, Basquin C, Portulano C, et al. The Na+/I- symporter mediates active iodide uptake in the intestine. Am J Physiol Cell Physiol. 2009 Apr;296(4):C654-62.

8. Venturi S, Venturi A, Cimini D, et al. A new hypothesis: iodine and gastric cancer. Eur J Cancer Prev. 1993 Jan;2(1):17-23.

9. Abnet CC, Fan JH, Kamangar F, et al. Self-reported goiter is associated with a significantly increased risk of gastric noncardia adenocarcinoma in a large population-based Chinese cohort. Int J Cancer. 2006 Sep 15;119(6):1508-10.

10. Gołkowski F, Szybinski Z, Rachtan J, et al. Iodine prophylaxis—the protective factor against stomach cancer in iodine deficient areas. Eur J Nutr. 2007 Aug;46(5):251-6.

11. Behrouzian R, Aghdami N. Urinary iodine/creatinine ratio in patients with stomach cancer in Urmia, Islamic Republic of Iran. East Mediterr Health J. 2004;10:921-924.

12. Pavelka S. Metabolism of bromide and its interference with the metabolism of iodine. Physiol Res. 2004;53(suppl1):S81-S90.

13. Kotyzova D, Eybl V, Mihaljevic M, et al. Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005 Dec;149(2):329-33.

14. Kotyzova D, Eybl V, Mihaljevic M, et al. Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005 Dec;149(2):329-33.

15. Crump C, Michaud P, Tellez R. Does perchlorate in drinking water affect thyroid function in newborns or school-age children? J Occup Environ Med. 2000;42:603-612.

16. Tran N, Valentín-Blasini L, Blount BC, et al. Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells. Am J Physiol Endocrinol Metab. 2008 Apr;294(4):E802-6.

17. Kirk AB, Martinelango PK, Tian K, et al. Perchlorate and iodide in dairy and breast milk. Environ Sci Technol. 2005 Apr 1;39(7):2011-7.

18. Brechner RJ, Parkhurst GD, Humble WO, et al. Ammonium perchlorate contamination of Colorado River drinking water is associated with abnormal thyroid function in newborns in Arizona. J Occup Environ Med. 2000 Aug;42(8):777-82.

19. Blount BC, Pirkle JL, Osterloh JD, et al. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Environ Health Perspect. 2006 Dec;114(12):1865-71.

20. Bachinskii PP, Gutsalenko OA, Naryzhniuk ND, et al. Action of the body fluorine of healthy persons and thyroidopathy patients on the function of hypophyseal-thyroid the system. Probl Endokrinol (Mosk). 1985 Nov-Dec;31(6):25-9.

21. Sidora VD, Shliakhta AI, Iugov VK, et al. Indices of the pituitary-thyroid system in residents of cities with various fluorine concentrations in drinking water. Probl Endokrinol (Mosk). 1983 Jul-Aug;29(4):32-5.

22. Zhao W, Zhu H, Yu Z, et al. Long-term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice. Endocr Regul. 1998;32:63-70.

23. Abraham GE. Facts about Iodine and Autoimmune Thyroiditis. The Original Internist. 2008 Jun;15(2):75-6.