Iodine Deficiency is an extremely common problem and the effects can be hidden. Iodine is an essential for life and is important for the synthesis of thyroid hormones. Deficiency can lead to hypothyroidism, goiters, and some lesser known problems. Some food sources can inhibit iodine absorption and are termed “goitrogenic”. 

Iodine is found in the upper crust of the earth as a trace element. Because of glaciation and flooding during the Ice Age, it was distributed mostly in the soil and waters of coastal areas (Leung et al., 2012). Food sources that are high in iodine include seafood such as oysters, shrimp, fish, and seaweed. It is also found in livestock in coastal regions depending on the soil, but because of intensive cropping and the use of alkaline fertilizers, iodine levels have been depleted (Kapil, 2007).

The role of iodine in production of thyroid hormones is well established, and deficiency can cause decreased production of T3 and T4. T3 is an important hormone that affects many tissues of the body and regulates body temperature, heart rate, metabolism, and development of fetuses and children. T3 increases the basal metabolic rate, so when it is low from an iodine deficient state, it can slow metabolism. The pituitary gland detects that T3 is low and in response, secretes TSH (thyroid stimulating hormone) in an attempt to reestablish balance. This can lead to hypertrophy of the thyroid and endemic goiter. 

Prior to the 1920s, iodine deficiency had become prevalent in the Great Lakes, Appalachians, and Northwest regions of the U.S. This area became known as the “goiter belt” and between 26-70% of the children had a visible goiter. For decades, most table salts have been sprayed with iodine to counteract iodine deficiency. In May of 1924, iodized salt first became available, however in 1926 there were reports of thyrotoxicosis (Leung et al., 2012). Perhaps the pendulum swung too far in the opposite direction. As usual, there is probably too much of a good thing and there is such a thing as iodine toxicity. Some salts such as Redmond, contain naturally occurring iodine (as it is mined from underground) and may be a good alternative to table salt.

That being said, iodine deficiency and hypothyroidism are much more common. There is another variable to this equation and it comes from sources that compete with iodine. There is a class of foods that are “goitrogenic”. Glucosinolates are a compound that are found in the plant order Brassicales. This is a natural plant defense and when the plant is chewed or cut, the glucosinolate is converted to isothiocyanate which can inhibit iodine uptake (Felker et al., 2016). Brassicales include foods such as the cruciferous vegetable; broccoli, kale, bok choy, brussel sprouts, and cauliflower. Fully cooking these vegetables significantly reduces these defense chemicals, but it unfortunately also reduces the beneficial nutrients. 

Another potential problem is fluoride. Both iodine and fluoride are halogens and compete with each other in the body. Unless you are living on a property with a well, water is fortified with fluoride, and it is in most toothpastes. Fluoride toxicity has been linked to thyroid disease (Singh et al. 2014). 

References: 

Felker P, Bunch R, Leung AM. Concentrations of thiocyanate and goitrin in human plasma, their precursor concentrations in brassica vegetables, and associated potential risk for hypothyroidism. Nutr Rev. 2016;74(4):248-258. doi:10.1093/nutrit/nuv110

Kapil U. Health consequences of iodine deficiency. Sultan Qaboos Univ Med J. 2007;7(3):267-272.

Leung AM, Braverman LE, Pearce EN. History of U.S. iodine fortification and supplementation [published correction appears in Nutrients. 2017 Sep 05;9(9):]. Nutrients. 2012;4(11):1740-1746. Published 2012 Nov 13. doi:10.3390/nu4111740

Singh N, Verma KG, Verma P, Sidhu GK, Sachdeva S. A comparative study of fluoride ingestion levels, serum thyroid hormone & TSH level derangements, dental fluorosis status among school children from endemic and non-endemic fluorosis areas. Springerplus. 2014;3:7. Published 2014 Jan 3. doi:10.1186/2193-1801-3-7