Written by John – April 27, 1999
From here: Iodine
Selenium and iodine are two minerals which are critically important in the proper functioning of the thyroid. While the importance of iodine has been known a long time, the importance of selenium has only been discovered and explored since 1990. Much research is presently being conducted on the functions of these two minerals in thyroid function and it is becoming clear that there is an interaction between the two. Iodine has a seemingly simple role in the thyroid-it is incorporated into the thyroid hormone molecule.
A deficiency of iodine will cause hypothyroidism and if this is severe and occurs during pregnancy, the offspring will be mentally damaged and is called a cretin. Cretinism, or myxeodematous cretinism as it is sometimes called, is not only caused by an iodine deficiency, but is also influenced by a selenium deficiency. Iodine apparently has just one function in the body-in the thyroid.
Selenium, on the other hand, performs many functions. At the beginning of the 1990s it was discovered that the deiodinase enzymes which convert T4 (thyroxin, the thyroid prohormone) into T3 (triiodothyronine, the cellularly active hormone) and also convert T3 into T2, thereby degrading it, are selenium enzymes (formed with the amino acid cysteine). This discovery has led to a lot of research studies on the effects of selenium, iodine, and their interactions.
Selenium also performs other important roles in the body. The most important of these is probably as its role as the body’s best antioxidant (anti-peroxidant). It performs this role as part of glutathione peroxidase (GSHPx or GPX). As part of GPX, selenium prevents lipids and fats from being peroxidized (oxidized), which literally means that it prevents fats from going rancid (this can be seen on your skin as “age spots” or “liver spots” (autopsies show that skin “liver spots” are accompanied by similar spots of peroxidized fats in the liver.) Therefore selenium protects all of the cellular membranes, which are made up of fats, from peroxidation. Peroxidation of cellular membranes reduces the ability of the membrane to pass nutrients including minerals and vitamins, so selenium deficiency is the first step toward developing the many problems caused by nutrient deficiencies.
Joel Wallach considers a selenium deficiency combined with high intake of vegetable oils (salad dressings, margarine, cooking oils) as the “quickest route to a heart attack and cancer.” It seems that the body uses a lot of selenium to protect the fats from peroxidation. Polyunsaturated fats which are hydrogenated or heated become the same as rancid fats and large amounts of selenium are then needed to protect the body. Consumption of these dietary fats can thus lead to a selenium deficiency.
Selenium is also essential for the production of estrogen sulfotranserfase which is the enzyme which breaks down estrogen. A deficiency of selenium can thus lead to excessive amounts of estrogen, which may depress thyroid function, and also upset the progesterone-estrogen balance.
Wallach also lists other effects of selenium deficiency: anemia (red blood cell fragility), fatigue, muscular weakness, myalgia (muscle pain), muscular dystrophy (white muscle disease in animals), cardiomyopathy (sudden death in athletes), heart palpitations, irregular heartbeat, liver cirrhosis, pancreatitis, Lou Gehrig’s and Parkinson’s diseases (mercury toxicity), Alzheimer’s Disease (high intake of vegetable oil), sudden infant death syndrome (and possibly “breathlessness” in adults, jj), cancer, multiple sclerosis, and sickle cell anemia.
Selenium is essential for the production of testosterone. A deficiency seems to be involved in osteoarthritis. I’ve found studies linking selenium deficiency to alopecia (hair loss) and to degeneration of the knee joint (seen in Kashin-Beck disease). Since selenium is necessary to produce GPX which is a major detoxifier of man-made and environmental toxins, selenium deficiency can lead to chemical and drug sensitivities.
These are some of the non-thyroidal effects of selenium deficiency. The effects of selenium deficiency on thyroidal health is even more interesting. One study I read indicated that in experimental animals, selenium deficiency will increase T3 in the heart. This may be the reason that selenium deficiency causes heart palpitations and rapid heart beat, which is common in thyroid disease.
While we’ve seen that selenium deficiency will interfere with T4 to T3 conversion and lead to functional hypothyroidism (low T3 phenomenon), selenium plays another vital role in the thyroid as part of GPX. During the production of thyroid hormone, hydrogen peroxide (H2O2) is produced. H2O2 is important for the production of thyroid hormone, but excessive amounts lead to high production of thyroxin (T4) and also damage to the cells of the thyroid. GPX plays the extremely vital role of degrading H2O2 and thereby limiting hormone production and preventing damage to the thyroid cells. This seems to be the main way in which selenium protects the thyroid from sustaining damage which can lead ultimately to cancer.
Without selenium, the thyroid gland becomes damaged and it is through this mechanism that the main selenium and iodine interactions are found. An iodine deficiency will cause goiter, an enlargement of the thyroid gland produced by the body in an attempt to increase hormone production from limited amount of iodine. Selenium deficiency increases the weight of the thyroid in experimental animals, and a selenium deficiency combined with an iodine deficiency leads to a further increase in thyroidal weight (bigger goiter). In African countries like Zaire, there are areas where both iodine and selenium are very scarce in the soil (these deficiencies seem to run parallel in most areas). Consequently a high percentage of the people have goiters and hypothyroidism. An experimental attempt was made to correct the selenium deficiency and the result was that the hypothyroidism was made WORSE in the hypos and it produced hypothyroidism in some euthroid subjects. This was entirely unexpected and the experimenters issued a warning about supplementing with selenium (and not iodine) when both deficiencies exist concurrently.
The body has a compensatory mechanism to maintain T3 levels when iodine is deficient–it increases the production of the deiodinase Type I enzyme (DI-I). This is not a small increase, but has been shown in cattle to be an increase of 10-12 times. This increase in ID-I increases the conversion of the existing T4 to T3 to maintain T3 levels, but also increases the conversion of T3 to T2 (the degraded by-product of T3). Because of the iodine deficiency, T4 is not replenished and T3 ultimately decreases from the lack of sufficient T4 leading to a worsening of the hypothyroidism.
This result is made worse by another phenomenon which hasn’t been thoroughly studied: a selenium deficiency causes an iodine deficiency to get worse. This may be a protective adaptation by the body to limit the damage caused to the thyroid when selenium is deficient and iodine is adequate. Let’s examine this part of the interaction.
We’ve all heard that many doctors tell hypo patients, especially those with Hashimoto’s thyroiditis, not to take iodine because it can aggravate their condition. The reason seems to be that selenium protects the thyroid gland from oxidative damage and this damage can increase significantly if iodine is supplemented. Taking iodine will increase thyroid hormone production and the production of H2O2 which damages the thyroidal cells. The lack of selenium prevents GPX from being able to protect the cells from this oxidative damage. While I doubt if most doctors realize why iodine should be restricted (it certainly seemed counter-intuitive to me at first), they have learned through experience that iodine can increase the thyroid damage in Hashimoto’s. The information that selenium should be supplemented along with iodine is so new that most of them are unaware of it.
Here’s what we have: Studies have shown that if iodine is low, selenium must also be kept low to prevent the hypothyroidism from becoming worse (from increased DI-I and T4 depletion, as explained above.) So if both minerals are low, then the person is hypo and gets a goiter, but the damage to the thyroid is kept to a minimum. More severe problems happen when either selenium or iodine is high and the other is low. If selenium is high and iodine low, then T4 to T3 to T2 conversion is accelerated without T4 being replenished, leading to a worsening of the hypoT. If iodine is high and selenium is low, then H2O2 is not degraded by GPX. Since H2O2 drives the thyroid hormone production, then the thyroid over-produces thyroid hormone (Grave’s hyperthyroidism), the thyroid is damaged from the oxidation by the H2O2, and the end result is that the damaged thyroid ultimately decreases activity and hypothyroidism results (Hashimoto’s thyroiditis). This could explain the observed progression of Grave’s to Hashimoto’s.
If a selenium deficiency causes an iodine deficiency, leaving you both selenium and iodine deficient, and supplementing with either selenium or iodine causes severe problems, then the only solution is to supplement both selenium and iodine simultaneously and gradually. Even then you could experience an immediate boost (from increased conversion of T4 to T3) with a subsequent letdown (lack of T4 production because of insufficient iodine or other necessary nutrient). You have to be prepared to ride out the tough times and continue increasing the selenium and iodine until those two deficiencies are corrected and the respective metabolic pathways are back working properly.
Everything that I’ve read about selenium indicates that it is absolutely essential for proper functioning of the thyroid. A deficiency of selenium may lead to either hyperthyroidism or hypothyroidism. I’ve always wondered if high intake of selenium can lead to hyperthyroidism and finally found someone who did the experiment. They found that a high intake of selenium will not increase T4 production and lead to hyperthyroidism.
If a person has hyperT, then it looks like taking selenium without iodine will result in a decrease in production of T4 (although there may be an initial transient increase in T4 to T3 conversion and hence higher T3). I would suggest to start with a small amount of selenium methionine (about 50 mcg) and gradually increase it. I cannot see any way that thyroid function can be normalized without selenium.
For hypos the important message is that a selenium deficiency may cause an iodine deficiency, so that even though you are taking iodine you may not be assimilating it unless selenium is also being taken. This would explain how people can have iodine deficiencies even though salt and many foods have iodine added. Supplement with both iodine and selenium. I would recommend starting with 100 mcg of selenium and one kelp tablet and gradually work up to 400-600 mcg of selenium and 2-4 tablets of kelp.
While I’ve found research on the interactions of iodine and selenium, there are two other minerals which need to be studied for their interactions with these two: zinc and copper. I found one study which examined the complex interactions of selenium, iodine, and zinc (there are interactions), but none which have looked at all four minerals in a 4 X 4 factorial design. Now that would be an interesting study! Hopefully someone will do that soon.
I think one lesson from studying the interactions of selenium and iodine is that the interrelationships between minerals are very complicated. Supplementing with one or two can cause further problems. You have to make sure that you correct every deficiency. Health is built from a chain of nutrients and, like a chain, health cannot be accomplished if one nutrient is missing. Sometimes it’s complicated putting the chain back together without running into problems (like supplementing with either selenium or iodine, but not both), but every deficiency has to be corrected.