Raina Kranz, C.P.T., Contributor
Thyroid Nation
Raina discusses the effects of Iodine Deficiency on your body and your thyroid. 


Iodine is an element that is needed for the production of thyroid hormone. Our bodies do not make iodine, so it is an essential that we get in our diet. A wide variety of food we eat contains iodine and without enough iodine in your body, you cannot make enough thyroid hormone.  Iodine deficiency can lead to enlargement of the thyroid, also known as a Goiter and cause hypothyroidism. Expectant mothers that are deficient in iodine, can lead to mental retardation in infants and children.

Foods that contain Iodine:

  • Cheese
  • Cow’s milk
  • Eggs
  • Frozen yogurt
  • Ice cream
  • Iodine containing vitamins
  • Iodized salt
  • Salt water fish
  • Seaweed
  • Kelp
  • Dulce
  • Nori
  • Shellfish
  • Soy milk
  • Soy sauce
  • Yogurt

Iodine is present naturally in soil and seawater and the availability of iodine in foods differs in various regions of the world. Individuals in the United States can maintain adequate iodine in their diet by using iodized table salt (unless they have to restrict the amount of salt in their diet), by eating foods high in iodine, particularly dairy products, seafood, meat, some breads, and eggs, and by taking a multivitamin containing iodine . However, the amount of iodine in foods is not listed on food packaging in the U.S., and it can be difficult to identify sources of iodine in foods.

Before the 1920s, iodine deficiency was common in the Great Lakes, Appalachian, and Northwestern U.S. regions and in most of Canada. Treatment of iodine deficiency by the introduction of iodized salt has virtually eliminated the “goiter belt” in these areas. However, many other parts of the world do not have enough iodine available through their diet and iodine deficiency continues to be an important public health problem globally. Approximately 40% of the world’s population remains at risk for iodine deficiency. Iodine deficiency is diagnosed across populations and not specifically in individuals. Since iodine is released from the body through the urine, the best way to determine iodine deficiency across a large population is to measure the amounts of iodine in urine samples. Iodine deficiency is defined as a median urinary iodine concentration less than 50 μg/L in a population

Median Urinary Iodine Concentration (μg/L)  /corresponding Iodine uptake (μg/day) /Iodine Nutrition
< 20                      < 30 Severe Deficiency
20-49                      30 -74 Moderate Deficiency
50-99                    75 – 149 Mild Deficiency
100- 199                    150- 299 Optimal Deficiency
200 – 299                    300-449 More Than Adequate
>299                      >449 Possible Excess


All of the symptoms of iodine deficiency are related to its effect on the thyroid gland and its function:

Goiter Without adequate iodine, the thyroid progressively enlarges (develops a goiter) as it tries to keep up with demand for thyroid hormone production. Worldwide, iodine deficiency is the most common cause of thyroid enlargement and goiter. Within a goiter, nodules can develop. Patients with a large goiter may experience symptoms of choking, especially when lying down, and difficulty swallowing and breathing.

Hypothyroidism As the body’s iodine levels fall, hypothyroidism may develop, since iodine is essential for making thyroid hormone. While this is uncommon in the United States, iodine deficiency is the most common cause of hypothyroidism worldwide.

Pregnancy-related problems Iodine deficiency is especially important in women who are pregnant or nursing their infants. Severe iodine deficiency in the mother has been associated with miscarriages, stillbirth, preterm delivery, and congenital abnormalities in their babies. Children of mothers with severe iodine deficiency during pregnancy can have mental retardation and problems with growth, hearing, and speech. In the most severe form, an underactive thyroid can result in cretinism (a syndrome characterized by permanent brain damage, mental retardation, deaf mutism, spasticity, and short stature), though this is not seen in the United States. Congenital hypothyroidism due to iodine deficiency is the most common preventable cause of mental retardation in the world. Even mild iodine deficiency during pregnancy, which may be present in some women in the United States, may be associated with low intelligence in children.

In traditional medicine, there are no tests to confirm if you have enough iodine in your body. When iodine deficiency is seen in an entire population, it is best managed by ensuring that common foods that people eat contain sufficient levels of iodine. Since even mild deficiency during pregnancy can have effects on delivery and the developing baby, all pregnant and breastfeeding women should take a multivitamin containing at least 150 μg iodine per day.


As with many diseases, it is better to prevent the problem rather than have to treat it. Over the last 80 years, world-wide efforts have been made to eliminate iodine deficiency. Indeed, elimination of iodine deficiency has been a major goal of the World Health Organization. Iodized salt has been the mainstay of treatment for iodine deficiency worldwide, including in the United States. Injections of iodized oil are occasionally used in regions of the world where widespread iodized salt use is not possible. Iodination of water supplies also has been effective in some places.

United States Recommendations – The Institute of Medicine has set the Recommended Dietary Allowance (RDA) for iodine in adult men and women at 150 μg per day. Individuals who add tablet salt to their food regularly should use iodized salt. One teaspoon of iodized salt contains approximately 400 μg iodine. Most iodine-containing multivitamins have at least 150 μg iodine, but only about half of the types of multivitamins in the U.S. contain iodine.

The RDA is 220 μg iodine per day for pregnant women and 290 μg iodine per day for breastfeeding women. Because the effects of iodine deficiency are most severe in pregnant women and their babies, the American Thyroid Association has recommended that all pregnant and breastfeeding women in the U.S. and Canada take a prenatal multivitamin containing 150 μg iodine per day.

Are there problems with taking in too much Iodine?

Taking too much iodine can also cause problems. This is especially true in individuals that already have thyroid problems, such as nodules, hyperthyroidism and autoimmune thyroid disease. Administration of large amounts of iodine through medications (ie Amiodarone), radiology procedures (iodinated intravenous dye) and dietary excess (Dulce, kelp) can cause or worsen hyperthyroidism and hypothyroidism.

In addition, individuals who move from an iodine-deficient region (for example, parts of Europe) to a region with adequate iodine intake (for example, the United States) may also develop thyroid problems since their thyroids have become very good at taking up and using small amounts of iodine. In particular, these patients may develop iodine-induced hyperthyroidism.

Iodine solutions such as saturated potassium iodide solutions (SSKI) or potassium iodide ( lugols’s solution)  replaced burnt sponge extracts in the 19th century as a treatment for endemic  goiter and sometimes used to treat Graves’ disease. By the end of the 19th century they were considered to be a dangerous form of treatment. Then in the 1920’s these treatments returned as a pre-operative and Today, Iodine solutions play a minor role in the treatment of hyperthyroidism.

Iodine and its Action on Thyroid

In hyperthyroid patients, Iodine acutely inhibits hormonal secretion within a few hours – 1-2 days of administration. How this actually happens is unknown.  This is an ACUTE effect of iodine on thyroid status.

A secondary effect of iodine therapy involves the inhibition of thyroid hormone synthesis. In normal subjects without thyroid disease, the administration of pharmacologic amounts of iodine leads to a temporary interruption organification in the thyroid gland.  Organification is a process in the thyroid gland where iodide is oxidized and incorporated into tyrosyl residues( tyrosine) of thyroglobulin . Organification is catalyzed by the enzyme thyroid peroxidase.  In turn it diminishes thyroid hormone biosynthesis ( a conversion of glycoprotein in the thyroid resulting in the formation of thyroglobulin)

This is called a Phenomenon called the Wolff- Chaikoff Effect, the decreased formation and release of thyroid hormone in the presence of an excess of iodine.

However, within 1-2 weeks of continual exposer to excess iodine, the organification process and the thyroid hormone biosynthesis resume back to normal.  This is called escape from Wolff – Chaikoff Effect.

This is why iodine is not used to treat hyperthyroid long term.

Graves’s patients/hyperthyroid patients are more sensitive to the pharmacological doses of iodine than normal healthy subjects, making iodine effective for some with this disease. In addition, pharmacological amounts of iodine may acutely improve hyperthyroidism by blocking hormone release.

Graves Disease and Iodine

The most extreme example of this is called Jod-Basedow Phenomenon, and it is caused by taking iodine. This occurs when people who are iodine-deficient also have high levels of thyroid antibodies. When they take this supplement, their immune system goes nuts. If you have Graves’ disease caused by autoimmune disease and you take iodine, you could be creating more harm than good.

The Jod-Basedow effect (also Jod-Basedow syndrome and Jod-Basedow phenomenon) is hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as contrast medium. This phenomenon is thus iodine-induced hyperthyroidism, typically presenting in a patient with endemic goiter (due to iodine deficiency), who relocate to an iodine-abundant geographical area. People who have Graves disease, toxic multinodular goiter, or various types of thyroid adenoma are also at risk of Jod-Basedow effect when they ingest extra iodine. The Jod-Basedow effect also been seen as a side effect of administration of the iodine-containing contrast agents, or amiodarone, an antiarrhythmic drug.The Jod-Basedow effect does not occur in persons with normal thyroid glands who ingest extra iodine in any form.

The Jod-Basedow effect typically occurs with comparatively small increases in iodine intake, in people who have thryoid abnormalities that cause the gland to function without the control of the pituitary (i.e., a thyroid gland that is not normally suppressed by thyroid hormone driven loss of TSH secretion from the pituitary). In some ways the Jod-Basedow phenomenon is the opposite of the Wolff-Chaikoff effect, which refers to the short period of thyroid-hormone suppression which happens in normal persons and in persons with thyroid disease, when comparatively large quantities of iodine or iodide are ingested. However, (unlike the Wolff-Chaikoff effect), the Jod-Basedow effect does not occur in persons with normal thyroid glands, as thyroid hormone synthesis and release in normal persons is controlled by pituitary TSH secretion, (which does not allow hyperthyroidism when extra iodine is ingested).The Jod-Basedow phenomenon is differentiated from Basedow’s disease, which is occasionally used as a synonym for Graves disease.

Thyroid Storm

There are really not many emergencies that we need to worry about regarding the thyroid gland – but thyroid storm is one of the rare exceptions. Thyroid storm is a medical emergency condition and needs to be treated immediately; even before all confirmatory diagnostic tests are performed.

Thyroid storm is a crisis or life-threatening condition characterized by an exaggeration of the usual physiologic response seen in hyperthyroidism. Whereas hyperthyroidism can cause symptoms such as sweating, feeling hot, palpitations and weight loss – symptoms of thyroid storm are more severe, resulting in complications such as:  fever, dehydration,  rapid heart rate, nausea/vomiting,  diarrhea,   irregular heartbeat, weakness, heart failure, confusion/disorientation, death.

Patients with thyroid storm should be treated in an ICU setting for close monitoring of vital signs and for access to invasive monitoring and inotropic support, if necessary. Initial stabilization and management of systemic decompensation is as follows:

If needed, immediately provide supplemental oxygen, ventilatory support, and intravenous fluids. Dextrose solutions are the preferred intravenous fluids to cope with continuously high metabolic demand. Correct electrolyte abnormalities and treat cardiac arrhythmia

If necessary, aggressively control hyperthermia by applying ice packs and cooling blankets and by administering acetaminophen (15 mg/kg orally or rectally every 4 h). Promptly administer antiadrenergic drugs (eg, propranolol) to minimize sympathomimetic symptoms.  Correct the hyperthyroid state. Administer antithyroid medications to block further synthesis of thyroid hormones (THs).

High-dose propylthiouracil (PTU) is preferred because of its early onset of action and capacity to inhibit peripheral conversion of T4 to T3. The US Food and Drug Administration (FDA) had added a boxed warning, the strongest warning issued by the FDA, to the prescribing information for PTU.

The boxed warning emphasizes the risk for severe liver injury and acute liver failure, some of which have been fatal. The boxed warning also states that PTU should be reserved for use in those who cannot tolerate other treatments such as methimazole, radioactive iodine, or surgery.

The decision to include a boxed warning was based on the FDA’s review of postmarketing safety reports and meetings held with the American Thyroid Association, the National Institute of Child Health and Human Development, and the pediatric endocrine clinical community.

The FDA has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with PTU. Among adults, 12 deaths and 5 liver transplants occurred; among the pediatric patients, 1 death and 6 liver transplants occurred. PTU is indicated for hyperthyroidism due to Graves disease. These reports suggest an increased risk for liver toxicity with PTU compared with methimazole. Serious liver injury has been identified with methimazole in 5 cases (3 resulting in death).

PTU is considered as a second-line drug therapy, except in patients who are allergic or intolerant to methimazole, or for women who are in the first trimester of pregnancy. Rare cases of embryopathy, including aplasia cutis, have been reported with methimazole during pregnancy. For more information, see the FDA Safety Alert.[10] The FDA recommends the following criteria be considered for prescribing

PTU: Reserve PTU use during first trimester of pregnancy, or in patients who are allergic to or intolerant of methimazole. Closely monitor PTU therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy. For suspected liver injury, promptly discontinue PTU therapy and evaluate for evidence of liver injury and provide supportive care. PTU should not be used in pediatric patients unless the patient is allergic to or intolerant of methimazole, and no other treatment options are available. Counsel patients to promptly contact their health care provider for the following signs or symptoms: fatigue, weakness, vague abdominal pain, loss of appetite, itching, easy bruising, or yellowing of the eyes or skin. Administer iodine compounds (Lugol iodine or potassium iodide) orally via nasogastric tube to block the release of THs (at least 1 h after starting antithyroid drug therapy). If available, intravenous radiocontrast dyes such as ipodate and iopanoate can be effective in this regard. These agents are particularly effective at preventing peripheral conversion of T4 to T3.

Administer glucocorticoids to decrease peripheral conversion of T4 to T3. This may also be useful in preventing relative adrenal insufficiency due to hyperthyroidism.

Treat the underlying condition, if any, that precipitated thyroid storm and exclude comorbidities such as diabetic ketoacidosis and adrenal insufficiency. Infection should be treated with antibiotics.

Rarely, as a life-saving measure, plasmapheresis has been used to treat thyroid storm in adults.

Iodine preparations should be discontinued once the acute phase resolves and the patient becomes afebrile with normalization of cardiac and neurological status. Glucocorticoids should be weaned and stopped and the dose of thioamides adjusted to maintain thyroid function in the normal range. Beta-blockers may be discontinued once thyroid function normalizes.

If the patient is given PTU during treatment of thyroid storm, this should be switched to methimazole at the time of discharge unless methimazole is contraindicated. If there is a contraindication for the use of methimazole, alternative methods to treat hyperthyroidism should be considered after discharge, such as radioactive iodine or surgery.

In Patients with Autoimmune Disease,

There is an abnormal AUTO – Regulation of iodine economy. Iodine induced blockade of iodine organification persists and can result in or exacerbate hypothyroidism in patients with Hashimoto’s Thyroiditis.

Iodine Stimulates TPO (thyroid peroxidase) and Increases Immune Attack

In the body iodine is a major cofactor and stimulator for TPO. A cofactor is something (usually a vitamin, mineral, enzyme or nutrient) that is used to build something else inside the body. When you have Hashimoto’s, TPO is under attack by your immune system. Increased iodine, especially as a supplement, increases the immune attack on the thyroid.

Hashimoto’s and Iodine: No Intake of Iodine Can Actually Improve Symptoms

This also holds true for patients with Hashimoto’s. Reports have shown that too much iodine causes hypothyroidism in Hashimoto’s thyroiditis. A study from the Yonsei Medical Journal published in 2003 looked at how not taking this supplement affected patients with Hashimoto’s.

Here’s what they found: “….78.3% of patients with hypothyroidism due to Hashimoto’s thyroiditis regained a euthyroid state (meaning a normal thyroid state) with iodine restriction alone. Both a low initial serum TSH and a high initial urinary iodine concentration can be predictable factors for a recovery from hypothyroidism due to Hashimoto’s thyroiditis after restricting iodine intake.”

In other words, more than 3/4 of the patients returned to a normal thyroid state by just lowering the amount of iodine they took in.

Several Studies Worldwide Show Increased Iodine Equals Increased Autoimmune Thyroiditis

There are several studies with large numbers of people that have shown a direct link between increased iodine and autoimmune thyroid disease. Here are a few:

  • A study in China looked at 3,018 people and found that “…more than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.”
  • In Sri Lanka, researchers kept track of the effects of using iodine on thyroid function and they charted their findings for 3 years. This was the first study of its kind. It showed the changes in autoimmune markers as the study went on and showed the increases in autoimmune disease in these people.
  • In Turkey, a study looked at 1,733 adolescents and found that the elimination of iodine deficiency in the Eastern Black Sea region was also followed by an increase in autoimmune thyroiditis and thyroid dysfunction.

(Please consult your health care provider before supplementing with iodine.)

 About the Author

Adaptogenic-Herbs-And-Their-Interaction-With-MedicationsRaina Kranz, C.P.T. attended and is certified from the American College of Sports Medicine. She studied Kinesiology/Biomechanics. Living in Hollywood, Florida she is a full time personal trainer and coach. Find her at her website, Personal Fitness Training Florida. and wonderful online Facebook Group, Thyroid Discussion Group.

 Questions or anything to add about iodine deficiency? We want your thoughts in the comments section–Please! 

Help Thyroid Nation create awareness for thyroid disease and share the links below…

Surks M., Sievert R., Drugs and thyroid function, NEJM, 1995; 333(25):1688

Yoon SJ, Choit SR, Kim DM, et al. The effect of iodine restriction on thyroid functions in patients with hypothyroidism due to Hashimoto’s thyroiditis. Yonsei Med J. 2003 Apr 30;44(2):227-35.
Eur J Endocrinol. 2011 Jun;164(6):943-50. doi: 10.1530/EJE-10-1041. Epub 2011 Mar 28.
More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels.
Effect of iodine intake on thyroid disease diseases in China, NEJM, 2006, Jun 29;354(17);2783-93
Evolution of thyroid autoimmunity during iodine prophylaxis – the Sri Lankan experience. Eur J Endocrinology, 2003, Aug;149(2):103-10
High prevalence of thyroid dysfunction and autoimmune thyroiditis in adolescents after elimination of iodine deficiency in the Eastern Black Sea Region of Turkey. Thyroid, 2006 Dec;16(12):1265-71