doctor check a woman for hyperthyroidism



Last Section Update: 01/2020

Contributor(s): Maureen Williams, ND; Colleen Mazin, MS/MPH; Shayna Sandhaus, PhD

1 Overview

Summary and Quick Facts for Hyperthyroidism

  • Up to 1% of the global population has hyperthyroidism, or overactive thyroid, which can contribute to troublesome symptoms like unintentional weight loss, nervousness, and sleep disturbances. An enlarged thyroid, known a a goiter, may also occur in some people.
  • This protocol reviews thyroid function and what happens when there is too much thyroid hormone activity in your body. You will learn about causes of hyperthyroidism, including Graves' disease, and strategies for treating the underlying cause of hyperthyroidism.
  • Selenium plays a key role in protecting the thyroid gland, and supplementation can help ensure the thyroid has access to adequate levels of this nutrient.

What Does the Thyroid Do?

The thyroid is an organ in the neck responsible for regulating metabolism by controlling the rate of oxygen and calorie conversion to energy. The metabolic rate of every cell in the body is controlled by thyroid hormones, particularly T3. The thyroid produces the hormones T3 and T4 in response to stimulation by thyroid stimulating hormone (TSH), which is produced in the pituitary gland. The thyroid requires iodine and L-tyrosine to synthesize T3 and T4.

Hyperthyroidism is a condition where the thyroid produces too much thyroid hormone, significantly accelerating metabolism. Hyperthyroidism has detrimental effects on the body. Fortunately, thyroid function tests (e.g. TSH, T3, and T4) can help identify an underlying thyroid condition as well as help direct proper treatment to improve symptoms.

Nutrients such as selenium and coenzyme Q10 may help support healthy thyroid function.

What are Signs and Symptoms of Hyperthyroidism?

  • Sudden weight loss
  • Rapid heartbeat
  • Thinning hair and nails
  • Frequent urination
  • Shortness of breath
  • Sweating
  • Nervousness or irritability
  • If left untreated, hyperthyroidism can lead to a goiter. Extreme hyperthyroidism can cause elevated heart rate and blood pressure, extreme exhaustion, and high fever. This condition sharply increases the risk of stroke and heart attack, and it can be fatal in up to half of all cases.

What are Conventional Medical Treatments for Hyperthyroidism?

  • Anti-thyroid drugs, such as methimazole or propylthiouracil, to inhibit the production of T3
  • Radioactive iodine to destroy the overactive thyroid gland
  • Surgical removal of the thyroid
  • Βeta-blockers to control high blood pressure and increased heart rate

Which Nutrients Support Thyroid Health?

Note: Certain supplements, including iodine and biotin, should be used with caution by those with hyperthyroidism. On the other hand, there’s evidence suggesting the following supplements may be helpful in cases of hyperthyroidism.

  • Selenium. This micronutrient is an essential component for converting T4 into T3 and for overall thyroid health. A literature review found that supplementing with selenium improved antibody levels and quality of life in patients with autoimmune thyroiditis.
  • Vitamin D. Vitamin D deficiency is associated with the autoimmune thyroid disease called Graves’ disease. Some research indicates supplementation might be beneficial for those with hyperthyroidism, including a study that showed better vitamin D status was associated with a lower relapse rate for those being treated for Graves’ disease.
  • Coenzyme Q10 (CoQ10). CoQ10 deficiency has been suggested as a factor in complications of hyperthyroidism, including heart failure. Preclinical research and a small clinical study indicate CoQ10 supplementation may help improve cardiac performance in those with hyperthyroidism.
  • Magnesium. Magnesium levels are decreased in patients with hyperthyroidism and may lead to an increased risk of complications following thyroid surgery.
  • Vitamin E. Many of the damaging effects of hyperthyroidism are related to oxidative stress, so supplementing with antioxidants is an area of research. In a preclinical study, vitamin E and curcumin improved antioxidant gene expression in animals with hyperthyroidism.
  • Bugleweed. Lycopus europaeus, or bugleweed, has been used traditionally to relieve symptoms of hyperthyroidism. It may work by inhibiting antibodies associated with Graves’ disease. Preliminary clinical studies indicate it may help normalize thyroid lab values in patients with mild hyperthyroidism.
  • Lemon Balm. Some laboratory research suggests lemon balm may prevent antibodies associated with Graves’ disease from stimulating the thyroid.

2 Introduction

The thyroid is a small gland located at the base of the neck that produces thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3). Thyroid hormones exert considerable influence over most aspects of human physiology.1,2 Hyperthyroidism, or overactive thyroid, is a condition in which the thyroid gland produces too much of these hormones. Because thyroid hormones affect so many parts of the body, hyperthyroidism can have serious consequences.

An estimated 20 million Americans have some form of thyroid disease. Globally, up to 1% of the population has hyperthyroidism.3,4 While people of all races and ages can develop thyroid issues, women are more likely than men to have thyroid problems: one in eight women will develop a thyroid problem during her lifetime.2 Stress, unhealthy diet, and even normal aging can compromise healthy thyroid function.

Because thyroid hormones have an up-regulating effect on metabolism, hyperthyroidism can lead to nervousness and irritability, weight loss, a racing heart, sleep disturbances, and vision issues among other concerns.5 Graves’ disease, the most common cause of hyperthyroidism, is an autoimmune disease that causes the immune system to make antibodies that trigger excessive thyroid hormone production.6 Graves’ disease and other types of hyperthyroidism are generally treated with anti-thyroid drug therapy or thyroid ablative (destructive) therapies, which include radioactive iodine and surgery.5,7,8

Hypothyroidism, or underactive thyroid, occurs when the thyroid does not produce enough thyroid hormone. Hypothyroidism can cause fatigue, depression, weight gain, cognitive deficits, and several other concerns.9 Many people who require treatment for hyperthyroidism will develop hypothyroidism as a result of that treatment and require thyroid hormone supplementation to maintain healthy thyroid hormone levels.10 Please refer to the Hypothyroidism protocol for more information about hypothyroidism.

In this protocol, you will learn how the thyroid gland works and what happens when there is too much thyroid hormone activity in your body. You will also learn how simple blood tests can assess thyroid function, and what treatments are available for hyperthyroidism. In addition, you will discover several integrative interventions and dietary and lifestyle changes that can support healthy thyroid function.

3 Background: Understanding the Thyroid

Thyroid hormone production is regulated by two specific brain regions: the hypothalamus and the pituitary gland. To ensure stable levels of thyroid hormones, the hypothalamus monitors circulating thyroid hormone levels and responds to low levels by releasing thyrotropin-releasing hormone (TRH). TRH stimulates the pituitary to release thyroid stimulating hormone (TSH), which in turn stimulates the thyroid gland to increase triiodothyronine (T3) and thyroxine (T4) secretion. When thyroid hormone levels increase, pituitary production of TSH decreases, which slows the release of hormones from the thyroid gland.11-13 This interconnected system is known as the hypothalamic-pituitary-thyroid (HPT) axis.

On a blood test, low TSH levels almost always indicate hyperthyroidism, or an overactive thyroid. This occurs when the thyroid is making too much T3 and T4, which suppresses the release of TSH by the pituitary gland. On the other hand, high TSH levels generally indicatehypothyroidism, or an underactive thyroid gland. In this condition, the pituitary keeps releasing TSH into the bloodstream in order to stimulate T3 and T4 production. In rare cases, abnormal TSH levels are a reflection of problems with the pituitary gland rather than the thyroid.1,14

The Primary Thyroid Hormones: T4 and T3

Thyroxine, or T4, produced solely by the thyroid gland, is the more common thyroid hormone in the blood. However, triiodothyronine, or T3, is the more biologically active thyroid hormone. T3 is formed by the removal of one of T4’s four iodine atoms. This process is mediated by selenium-dependent enzymes.15

T4 is found in the body in two forms: bound and free. Free T4 is not bound to any proteins and is able to enter into body tissues. Bound T4 is attached to proteins that render it biologically inactive. More than 99% of T4 in the body is in the bound, inactive form.16

High blood levels of T4 typically indicate hyperthyroidism and low levels are associated with hypothyroidism. However, pregnancy and oral contraceptive use can elevate thyroid hormone levels, while severe illness and certain medications can lower T4 levels.11,12 Elevated levels of cortisol, as seen during times of stress and in conditions such as Cushing’s syndrome, lower TRH, TSH, and thyroid hormone levels.17,18 Cold temperatures increase TRH levels, which is thought to be an intrinsic mechanism that helps keep people warm in cold weather.19


Hyperthyroidism affects about 1.3% of the U.S. population (0.5% clinical and 0.7% subclinical).19 In most people with hyperthyroidism, the thyroid gland produces too much thyroid hormone, which can significantly accelerate the body's metabolism. Typical symptoms of hyperthyroidism include sudden weight loss, a rapid heartbeat, thinning hair and nails, frequent urination, shortness of breath, sweating, nervousness or anxiety, and irritability. An enlarged thyroid gland, known as a goiter, may occur in some people. Goiters are characterized by neck swelling and discomfort and a sore throat, and severe cases may result in problems swallowing and breathing.21

Subclinical Hyperthyroidism

Subclinical hyperthyroidism is a condition marked by low TSH levels but normal circulating levels of thyroid hormones. This means the overactive thyroid is not producing excessive amounts of thyroid hormones as long as stimulation via TSH is abnormally low. People with subclinical hyperthyroidism may have no symptoms or very mild symptoms compared with those seen in overt hyperthyroidism. Subclinical hyperthyroidism also increases the risk of atrial fibrillation, heart failure, bone loss and osteoporotic fractures in older adults when TSH levels are very low or undetectable.22,23 Since treatment of subclinical hyperthyroidism does not appear to be universally beneficial, recommendations for treatment are limited to those with the lowest TSH levels. For those with moderately low TSH levels, the decision to treat is based on individual and clinical factors. For example, there is evidence to suggest some individuals over age 65 with subclinical hyperthyroidism may benefit from treatment, even if they are not symptomatic.22

4 Causes and Risk Factors

In most cases of hyperthyroidism, the thyroid gland is overactive even though it is not being stimulated by TSH. This is known as primary hyperthyroidism. Secondary hyperthyroidism is a less common condition caused by abnormally high levels of TSH, such as due to a TSH-producing pituitary tumor, which overstimulates the thyroid gland.24 The focus of this protocol is primary hyperthyroidism.

Risk factors for hyperthyroidism include family history, female gender, and having certain medical conditions such as type 1 diabetes and adrenal insufficiency. In addition, emotional or physical stress, pregnancy, smoking, and being under 40 increase the risk of Graves’ disease, the number one cause of hyperthyroidism.25-28

Graves’ disease is an autoimmune disorder that involves production of thyrotropin (TSH) receptor antibodies (TRAb) and, more specifically, thyroid stimulating immunoglobulins (TSI). These antibodies bind to and activate TSH receptors, disrupting normal regulation of thyroid function. Thyroid activity is then accelerated, increasing circulating levels of thyroid hormones in the blood.29 This condition is characterized by rapid heartbeat, sweating, nervousness, tremors, muscle weakness, sleep difficulties, increased appetite, and sudden weight loss.30 One telltale sign is Graves’ ophthalmopathy (also called orbitopathy), in which antibodies damage TSH receptors in the eye sockets and surrounding muscles, resulting in discomfort, visual problems, an inability to move the eyes, and bulging eye balls.31

Less commonly, hyperthyroidism is caused by conditions other than Graves’ disease, including toxic multinodular goiter, in which non-cancerous growths in the thyroid cause the gland to swell and make too much T4. This occurs more frequently in iodine-deficient regions. Thyroiditis (inflammation of the thyroid), which may occur in pregnancy or in the context of some autoimmune conditions, is another uncommon cause of hyperthyroidism.3,23

5 Complications and Associated Conditions

An overactive thyroid can cause anxiety, nervousness, restlessness, and irritability. Goiter, or thyroid enlargement, is common in people with Graves’ disease and can occur with other causes of hyperthyroidism as well.5,26-28,32,33 Research suggests diagnosed but untreated hyperthyroidism is associated with depression and anxiety.26,27,34

Complications of hyperthyroidism include heart problems, such as a rapid heartbeat, atrial fibrillation, and congestive heart failure; weak bones; skin changes; vision problems (including double vision) in those with Graves’ ophthalmopathy; and pregnancy complications, including preterm birth, stillbirth, congenital malformations, and pre-eclampsia.7,30 Infants of mothers with Graves’ disease have a risk of being born with hyperthyroidism, a condition known as neonatal hyperthyroidism.7

Extreme hyperthyroidism, or thyrotoxicosis, can progress to a life-threatening condition called thyroid storm. In this medical emergency, often brought on by stress, pregnancy, or thyroid trauma, patients suffer from an elevated heart rate and blood pressure, extreme exhaustion, and high fever. Thyroid storm sharply increases a patient’s risk for stroke and heart attack, and is fatal in up to 25% of cases, even with the best medical care.33

6 Testing Thyroid Function

Several tests are available to assess different aspects of thyroid health35:

  • Thyroid stimulating hormone (TSH) to evaluate overall thyroid function;
  • Total thyroxine (T4) to measure the total amount of T4 being produced by the thyroid;
  • Free thyroxine (T4) , a measure of the amount of available T4 not bound by transport proteins;
  • Free triiodothyronine (T3) to measure the amount of unbound T3 available;
  • Antibody tests to identify underlying autoimmune causes of thyroid dysfunction

Thyroid Stimulating Hormone (TSH)

Measuring TSH levels in the blood is the most common test of thyroid function. The normal range for TSH in healthy individuals is 0.45–4.5 µIU/mL.36 TSH levels below the normal range generally represent hyperthyroidism. Most cases of overt hyperthyroidism are marked by undetectable TSH levels (<0.1 μIU/L), but levels of 0.1–0.45 μIU/L may indicate subclinical hyperthyroidism. Undetectable levels in patients with subclinical hyperthyroidism are associated with a greater risk of progression to overt hyperthyroidism.22,23

TSH production can also fluctuate with time of day, infection, and various other factors. In a survey of nearly 350,000 people published in the Archives of Internal Medicine, abnormal TSH levels spontaneously returned to normal in more than 50% of subjects when the test was repeated at a later date.37 No single measurement of TSH should be considered diagnostic, and repeated testing may be necessary for optimal treatment.

Tests for T4 and T3

Thyroid hormones can be tested in both their free and protein-bound forms. Tests for the protein-bound forms of T4 and T3 are generally referred to as total T4 and total T3, respectively; unbound forms are called free T4 and free T3. Each of these tests provides information about how the body is making, activating, and responding to thyroid hormone. The normal range for free T4 is 0.82–1.77 ng/dL, and the range for total T4 is 4.5–12.0 µg/dL.38-41

The feedback mechanisms by which the body regulates thyroid hormone levels are very sensitive, such that small changes in T4 levels lead to relatively large changes in TSH. Therefore, TSH is generally considered an excellent indicator of thyroid health in most people whose hypothalamus and pituitary gland are functioning normally.

Because T4 is converted to T3, and changes in levels of binding proteins do not affect free T4 levels, free T4 is typically the hormone measured in a clinical setting.13 The reason changes in binding protein levels typically do not affect free T4 levels is that the feedback mechanisms governing thyroid hormone levels either increase or decrease thyroid hormone release in response to fluctuations in free thyroid hormone levels.16 However, in some cases of hyperthyroidism, T4 levels are normal and T3 levels are high, so measuring both T3 and T4 may be useful in diagnosing or determining the severity of hyperthyroidism. The reference ranges are 2.0–4.4 pg/mL for free T3 and 71–180 ng/dL for total T3.40,41

Autoimmune Antibodies

Normally, the body’s immune system uses antibodies to attack foreign particles, such as bacteria and viruses, but in autoimmune disorders, dysfunctional antibodies are produced that attack healthy tissues, cells, or biomolecules. In people with autoimmune thyroid conditions, antibodies interfere with normal thyroid cell function, resulting in either stimulation or suppression of thyroid activity. In a hyperthyroid patient, testing for the presence of thyrotropin receptor antibody (TRAb) and thyroid-stimulating immunoglobulin (TSI, a type of TRAb) can help secure a diagnosis of Graves’ disease.29 Some people with celiac disease or gluten sensitivity are at increased risk for developing autoimmune thyroid disease.43

Elevated thyroid antibodies are often associated with chronic urticaria, or hives. Studies report that roughly 30–57% of patients with chronic urticaria also have anti-thyroid antibodies.44 Some of these patients manifest Graves’ hyperthyroidism, but more of them have autoimmune hypothyroidism.44,45

Basal Body Temperature

Measuring basal body temperature can sometimes provide some insight into thyroid function, although it should be used in conjunction with standard thyroid blood testing. Body temperature testing in the context of suspected thyroid issues was common before the development of accurate thyroid function blood tests.

Basal body temperature is measured when the body is at complete rest, immediately after waking, and before beginning any activity. Normal basal temperature is roughly 97.6–98.6º F. Some integrative practitioners suggest that basal body temperature readings below 97.6º F on five consecutive days may be a sign of hypothyroidism. Although it is less common for practitioners to recommend basal body temperature monitoring to identify hyperthyroid conditions, some suggest that a series of mildly elevated readings may be a sign of hyperthyroidism.

Additional Testing

Sometimes additional testing, such as biopsy or enzymatic studies, are required to establish a definite diagnosis of hyperthyroidism. Major abnormalities of the thyroid gland detected in a physical exam can be further assessed by other procedures, including ultrasound or scintigraphy.

Ultrasound may be used to more closely examine thyroid nodules (or lumps in the neck region) to determine if they are cancerous. Scintigraphy is a scan that can be used to look at the size and shape of the thyroid gland, as well as its position in the body. A small amount of radioactive iodine is used in this procedure to detect nodules and determine the cause of any thyroid issues.

The radioactive iodine uptake test may also be useful in diagnosing thyroid issues. As the thyroid takes up iodine from the bloodstream to produce T4, this action can be clinically measured by having a patient swallow a small amount of radioactive iodine. This allows the doctor to track where the iodine is going and measure thyroid function by determining how much radioactivity is taken up by the thyroid gland. The test is performed by taking a pill containing radioactive iodine. The thyroid is then scanned by a computer after several hours and usually again after a full day to assess the thyroid’s uptake of the radioactive iodine. A high level of radioactivity uptake is seen in those with hyperthyroidism, and a low level is seen in those with hypothyroidism.3,29,35,47

7 Treatment of Hyperthyroidism

Initial treatment of hyperthyroidism focuses on controlling dangerous manifestations of excessive thyroid hormone activity that can cause immediate problems. Longer-term management aims to suppress excessive production of thyroid hormone and keep thyroid hormone activity in a healthy range. The overall strategy will depend on what caused hyperthyroidism in the first place, and to what extent, if any, excessive thyroid signaling has already caused damage. Other factors that will inform the treatment strategy include the affected person’s age, health history, and, for women, desire to become pregnant.

Acute Management: Beta Blockers

Because pronounced hyperthyroidism can rapidly cause serious health problems, the aim of initial treatment is to counter high-risk manifestations of hyperthyroidism, such as heart rhythm irregularities. Beta blockers are typically used in the initial treatment of symptoms caused by pronounced hyperthyroidism. These drugs are commonly used to treat high blood pressure levels, but are also effective in relieving symptoms associated with hyperthyroidism such as tremors, rapid heart rate, and heart palpitations.30,48-51 Beta blockers are recommended in most patients with severe symptoms of hyperthyroidism, especially the elderly. Calcium channel blockers may be an acceptable alternative for initial symptom control in people who cannot tolerate beta blockers.7,52

Long-Term Management

Treatment options for reducing excess thyroid hormone levels include51:

  • anti-thyroid drugs, which prevent the thyroid from making hormones;
  • radioactive iodine, which destroys overactive thyroid cells, causing the thyroid to shrink and decreasing levels of thyroid hormone; and
  • surgery, in which the thyroid gland is removed.

The choice of treatment depends on the patient’s age and overall health, severity and cause of hyperthyroidism, and patient preference. Thyroid hormone replacement therapy to re-establish normal levels of T4, T3, and TSH may be needed following treatment in which thyroid tissue is destroyed or removed (thyroid ablation).5,26-28

In a long-term randomized trial, 179 people with Graves’ disease received treatment with either anti-thyroid medications, radioiodine, or surgery. An assessment 14‒21 years after treatment assignment determined that there were no significant differences in quality of life among the three treatment arms.53 In another trial, 131 people with Graves’ hyperthyroidism were randomized to receive medication, radioiodine treatment, or thyroid surgery, while all patients received levothyroxine (T4) as necessary. TSH antibodies were measured before treatment and for five years after therapy to determine TSH-receptor autoimmunity. Most people who took medication or had surgery experienced remission of TSH-receptor autoimmunity, while fewer people who had radioiodine therapy went into remission.54

Anti-thyroid drugs (thionamides). Anti-thyroid drugs (thionamides), such as methimazole (Tapazole) and propylthiouracil, prevent the thyroid gland from making too much T3 and T4. This allows symptoms of hyperthyroidism to improve within a few weeks to a few months, but treatment may need to be continued for up to a year or more. Some people may experience allergic reactions to these medications, and one possible side effect is liver damage.5,28 Agranulocytosis, a severe condition in which the number of white blood cells drops to a critical level, is a rare side effect of anti-thyroid drugs, especially when high doses are used.23 Thionamides and beta blockers are recommended for those with significant symptoms of hyperthyroidism and those at risk of complications (older individuals or people with cardiovascular disease). This may be followed by radioiodine or surgery.52,55

About 52% of hyperthyroidism patients treated with anti-thyroid drugs relapse. For these individuals, thyroid-ablative treatment with radioactive iodine or surgery may be needed.56 A study that followed 1,186 Graves’ disease patients for 6–10 years found more than half of those initially treated with anti-thyroid drugs later required thyroid-ablative treatment, and only 40% achieved normal thyroid hormone levels without thyroid hormone replacement therapy by the end of the study.57

Long-term low-dose treatment with anti-thyroid medication may be an alternative to thyroid-ablative treatments in patients whose hyperthyroidism returns after initial treatment. In a non-randomized retrospective study, 238 patients with Graves’ disease who experienced a relapse after anti-thyroid medication therapy either received radioiodine therapy followed by levothyroxine (T4) replacement (114 people) or low-dose methimazole (2.5‒7 mg/day) (124 people). The low-dose methimazole treatment was safe and effective, and was associated with less thyroid dysfunction than radioactive iodine treatment.58

Radioactive iodine. Radioactive iodine therapy involves orally consuming sodium iodide (I-131). I-131 is absorbed into the thyroid gland where it emits local radiation and damages thyroid cells over a period of 12 to 18 weeks. The damaged cells shrink, which decreases levels of thyroid hormones. Residual iodine is generally eliminated from the body within a period of weeks to months. Radioactive iodine treatment carries a small risk of thyroid storm due to radiation-induced thyroiditis. In addition, a small percentage of people treated with radioactive iodine experience thyroid swelling and sore throat.23,56

Radioactive iodine therapy is unsuccessful in about 8% of cases, as the remaining functional thyroid tissue sometimes overproduces thyroid hormones after treatment.23,56 In such cases, the treatment can be repeated or surgery may be performed. More often, radioactive iodine therapy induces a hypothyroid state, and many people who utilize this treatment require lifelong thyroid hormone replacement therapy to maintain healthy thyroid hormone levels.5,28,32,59 Radioiodine is the most common treatment for hyperthyroidism in the United States, and research has supported its use for over 70 years.60,61

Importantly, those who undergo radioiodine treatment should reduce exposure to other people for a period after taking the radioiodine, especially pregnant women. This helps reduce others’ exposure to radiation. The dose of radioiodine a patient receives informs how long he or she should limit contact with others. Consult your physician for more information.

Surgery (thyroidectomy). A thyroidectomy involves the removal of the thyroid gland. This is typically performed in people who cannot tolerate anti-thyroid medications, have large goiters, or are not candidates for radioactive iodine therapy. Potential risks of this surgery include damage to the vocal cords or parathyroid gland. Those who undergo this surgery require lifelong thyroid hormone replacement therapy to support normal levels of thyroid hormone.5,28,32 A meta-analysis of 35 studies involving over 7,200 subjects concluded that thyroidectomy is highly successful in treating hyperthyroidism in people with Graves’ disease.62 Research involving 99 people with Graves’ disease suggests thyroidectomy early in the course of treatment is not associated with complications, but rather improved biochemical recovery, as compared with delayed surgery.63

Treatment-Induced Hypothyroidism

Patients who undergo thyroid-ablative treatment like radioactive iodine or surgery typically experience overt or subclinical hypothyroidism after treatment. In most cases, treatment-induced hypothyroidism is permanent, but in some cases, thyroid function fluctuates over time.10 Thyroid hormone replacement therapy is used to manage treatment-induced hypothyroidism.3,9,64 This approach aims to replicate normal thyroid activity, prevent symptoms, and maintain normal TSH levels.65

Please refer to the Hypothyroidism protocol for more information about thyroid hormone replacement therapy.

8 Dietary and Lifestyle Changes

Dietary Considerations

In a large study that surveyed over 65,000 Seventh Day Adventists in the United States and Canada, eating a vegetarian diet was correlated with a lower risk of hyperthyroidism: those who excluded all animal products (vegans) were least likely to report having hyperthyroidism, and had 52% fewer hyperthyroidism cases than among omnivores. Vegetarians whose diets included fish (pesco-vegetarians) and whose diets included eggs and dairy products (lacto-ovo-vegetarians) also had less hyperthyroidism compared with omnivores, but these differences were smaller than for vegans.66 The possible association between vegetarian diet and lower risk of hyperthyroidism may be due to the high amounts of compounds such as antioxidants, phytochemicals, and prebiotic fibers present in plant foods. These types of compounds appear to protect against autoimmune diseases, including Graves’ disease—the most common cause of hyperthyroidism.67

Adequate iodine intake via foods such as iodized salt, seaweed, seafood, dairy products, eggs, blackstrap molasses, and some bread and grain products is necessary for healthy thyroid function. Although iodine deficiency is better known as a cause of hypothyroidism, mild hyperthyroidism is reported to be more common in iodine-deficient regions, suggesting low iodine intake may trigger excessive thyroid activity in some people.33 Eating excessive amounts of iodine-rich foods can also trigger increased thyroid hormone production in susceptible individuals. Cases have been reported in which daily intake of seaweed, particularly kelp, has resulted in iodine and thyroid hormone excess, but cases of iodine overdose from supplements are more common.68 Hyperthyroidism patients preparing to undergo radioactive iodine treatment may be instructed to eat a low-iodine diet.69,70 On the other hand, adequate iodine intake during treatment with anti-thyroid drugs was found in one study to help prevent relapse.71

Vegetables in the Brassica family, such as broccoli, cabbage, and Brussels sprouts, are well known to contain compounds called goitrogens that can interfere with the thyroid’s ability to absorb iodine. Goitrogens are less active after cooking, but eating large amounts of raw Brassicas may reduce production of thyroid hormones.72 While people with hypothyroidism are often encouraged to limit intake of raw Brassica vegetables, those with hyperthyroidism are sometimes told to increase raw Brassica consumption. In order to achieve large quantities of goitrogens, some individuals with hyperthyroidism consume fresh raw Brassica vegetable juices, such as cabbage juice; however, there is no evidence at this time that high intake of raw Brassica vegetables can effectively treat hyperthyroidism.


Thyroid hormones have a profound effect on cardiovascular function and performance. Chronic hyperthyroidism is associated with heart rhythm disturbances such as atrial fibrillation, changes to the heart muscle, and heart failure. In patients with hyperthyroidism, the heart’s ability to respond to increasing oxygen demands is diminished, resulting in reduced exercise capacity.72,73 Even those with subclinical hyperthyroidism have been found to have decreased cardiac capacity for physical activity, but cardiac capacity can improve after treatment.73,74 Because of the importance of physical activity on all parameters of health, hyperthyroidism patients should work with their health care provider to implement a regular exercise program that supports healthy cardiac function after appropriate therapy for their thyroid condition.

Stress Management

Stress may exacerbate thyroid dysfunction, and relaxation techniques may be a useful means of helping control symptoms of mild thyroid conditions. Stress appears to alter the regulation of the hypothalamic-pituitary-thyroid axis.75 Stress can be a trigger for the onset and exacerbation of Graves’ disease and may worsen the response to treatment.76 In one study, chronic social stress was associated with lower chance of recovery after one year of anti-thyroid drug therapy for a new diagnosis of Graves’ disease in women, but not men. In fact, women with the highest “daily hassles” scores were almost four times more likely to still have hyperthyroidism after a year of treatment than women with the lowest scores.77

Please refer to Life Extension’s Stress Management protocol for more information.

Stop Smoking

Cigarette smoking is believed to impact thyroid function and may play a role in the development of autoimmune thyroid disease, particularly Graves’ disease. Smoking may induce changes in thyroid function tests, including a decrease in TSH levels and an increase in some thyroid hormone levels.78 One cohort study of over 4,000 participants in the sixth Korean National Health and Nutrition Examination Survey (2014‒2015) suggested a dose-related effect of smoking status (based on urinary cotinine levels) on thyroid function and autoimmunity. Urinary cotinine levels were positively associated with thyroid antibodies in male participants. The authors suggested smoking may influence many metabolic processes, including hormone synthesis, release, binding, transport, and storage.79

9 Nutrients

Certain supplements should be used with caution by those with hyperthyroidism. These include iodine and biotin. Excessive iodine intake can increase thyroid hormone production and trigger dangerous exacerbation of hyperthyroid symptoms.68 Taking large amounts of biotin can interfere with blood tests assessing thyroid function and may result in misdiagnosis and inappropriate treatment.80

On the other hand, a few nutritional and herbal supplements have scientific or historical evidence suggesting they may be helpful in cases of hyperthyroidism.


L-carnitine is an amino acid derivative that plays a critical role in mitochondrial energy metabolism. L-carnitine deficiencies have been linked with malfunction of several different organs, including the heart, liver, and thyroid.113 In thyroid-hormone-responsive cell lines, carnitine inhibited the nuclear uptake of thyroid hormones, which suggests that L-carnitine may limit tissue and organ susceptibility to excess thyroid hormone levels, potentially decreasing the signs and symptoms of hyperthyroidism.113,114

In clinical studies, L-carnitine has been shown to both reverse and prevent symptoms of hyperthyroidism.115,116 In a study of 50 women receiving TSH-suppressive L-T4 therapy, treatment with 2 or 4 g/day L-carnitine was shown to improve clinical and biochemical markers of hyperthyroidism relative to placebo.115 More recently, L-carnitine has been used in patients with Graves’-disease-related hyperthyroidism experiencing thyroid storms. Several case studies have reported the success of this approach, with L-carnitine both preventing progression and resolving symptoms in patients experiencing severe thyroid storms.117-119 L-carnitine may also be combined with other agents to address subclinical hyperthyroidism. After one month of treatment with L-carnitine and selenium, patients with subclinical hyperthyroidism had significant reductions in thyroid symptoms, which returned to baseline after treatment was discontinued.116


Selenium, an essential micronutrient found in Brazil nuts, cereals, mushrooms, and some fish (eg, tuna, halibut, and sardines), is a potent antioxidant that helps regulate thyroid hormone activation and deactivation, as well as immune function.81,82 The thyroid contains more selenium by weight than any other organ,83 and selenium is a necessary component of the enzymes that convert T4 into T3.84

Selenium also plays a role in protecting the thyroid gland from oxidative stress. The cells of the thyroid generate hydrogen peroxide during the process of making thyroid hormone, and selenium protects the thyroid gland from the oxidative damage caused by these reactions. Without adequate selenium, high iodine levels can destroy thyroid gland cells.85,86

A recent literature review regarding selenium’s role in promoting thyroid health found that selenium supplementation in those with autoimmune thyroiditis reduced antibody levels, improved presentation of the thyroid on ultrasound, and improved patient quality of life.83 In those with mild Graves’ ophthalmopathy, selenium supplementation may improve eye movement and delay disease progression.83,87

Vitamin D

Vitamin D is a fat-soluble vitamin that helps support bone growth and remodeling, enhance calcium absorption, promote immunity, and reduce inflammation. It is found in fatty fish and fish liver oil, and is produced naturally with exposure to sunlight.88 Vitamin D deficiency is associated with autoimmune thyroid disease, including Graves’ disease. In addition, impaired vitamin D signaling pathways have been indicated in thyroid cancer.89

Multiple studies have demonstrated a correlation between low vitamin D levels and risk of Graves’ disease and Graves’ ophthalmopathy.90-93 One study noted better vitamin D status was associated with lower risk of relapse in Graves’ disease patients treated with anti-thyroid drug therapy.94 In a randomized clinical trial, taking 2,800 IU (70 mcg) of vitamin D daily for nine months led to reduced arterial stiffness in Graves’ disease patients who were vitamin D insufficient at the beginning of the trial, but not those with sufficient vitamin D status. In addition, vitamin D lowered in-office blood pressures compared with placebo, but did not impact 24-hour blood pressures.95 A case report described a patient with Graves’ disease and vitamin D deficiency who was treated only with vitamin D supplementation. The patient was given 4,000 IU (100 mcg) vitamin D per day for six months, followed by 50,000 IU (3,750 mcg) per month for five months, after which 25-hydroxy vitamin D, TSH, free T4, and free T3 levels were all normal and thyroid antibodies were no longer detectable.96

Coenzyme Q10

Coenzyme Q10 (CoQ10) is needed for normal mitochondrial function in cells throughout the body and is especially concentrated in heart muscle cells. CoQ10 is depleted in conditions of high metabolic demand, including hyperthyroidism, and CoQ10 deficiency has been proposed as a contributing factor in complications of hyperthyroidism such as heart failure.97-99 Findings from animal research suggest CoQ10 supplementation can prevent the damaging effects of high thyroid hormone levels on heart muscle.100 In a preliminary clinical trial that included 12 women with untreated hyperthyroidism and related signs of heart failure, taking 120 mg CoQ10 daily for one week led to improvements in cardiac performance.101


Magnesium levels have been found to be decreased in patients with hyperthyroidism.102 In addition, surgical thyroid removal can further reduce magnesium levels, which may be linked to increased risk of long-term surgical complications.103 One report described cases in which supplementation with approximately 100 mg magnesium citrate and 200 mcg selenomethionine per day, along with stress reduction interventions, improved thyroid gland structure and reduced anti-thyroid antibody levels in women with Graves’ disease over a period of two to four years.104

Vitamin E

Vitamin E, a fat-soluble compound with natural antioxidant properties, plays a role in immune function, gene expression, and cellular metabolism.105 Many of the tissue effects and symptoms of hyperthyroidism are related to oxidative stress, and vitamin E may reduce cell and tissue injury by scavenging free radicals.106-108 In rats with experimental hyperthyroidism, supplementing with vitamin E plus curcumin (a carotenoid from turmeric) normalized expression of genes related to antioxidant enzyme production in liver cells.109 Whether or not vitamin E and other antioxidant supplements can have beneficial effects on the course of hyperthyroidism remains to be determined.


Bugleweed (Lycopus europaeus) is a European herb used historically to relieve symptoms of hyperthyroidism. Although the exact mechanisms behind its effects are not fully understood, bugleweed extract has been found to inhibit autoantibodies associated with Graves’ disease in the laboratory110 and increase urinary excretion of T4 in subjects with Graves’ disease.111 Findings from preliminary clinical trials suggest it may help reduce symptoms and normalize lab values in patients with mild hyperthyroidism.111,112

Lemon Balm

Lemon balm (Melissa officinalis) is a calming herb used traditionally to treat anxiety and insomnia. Laboratory research suggests lemon balm extract may prevent binding of Graves’ disease-associated antibodies, preventing them from stimulating the thyroid.110 Clinical research is needed to assess its potential benefit in the treatment of hyperthyroidism.


  • Jan: Comprehensive update & review

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.


  1. Shahid MA, Sharma S. Physiology, Thyroid Hormone. StatPearls Publishing. Published 2019. Updated March 23 2019. Accessed Aug. 27 2019.
  2. OWH. Office of Women's Health. Thyroid disease. Last updated 4/1/2019. Accessed 8/22/2019.  Accessed.
  3. American Thyroid Association (ATA). Hyperthyroidism (Overactive). Accessed 10/4/2019.
  4. Vadiveloo T, Donnan PT, Cochrane L, Leese GP. The Thyroid Epidemiology, Audit, and Research Study (TEARS): the natural history of endogenous subclinical hyperthyroidism. J Clin Endocrinol Metab. 2011;96(1):E1-8.
  5. Mayo Clinic. Hyperthyroidism. Published 2018. Accessed.
  6. Brent GA. Clinical practice. Graves' disease. The New England journal of medicine. 2008;358(24):2594-2605.
  7. Burch HB, Cooper DS. Management of Graves Disease: A Review. Jama. 2015;314(23):2544-2554.
  8. Mayo Clinic. Graves' Disease. Published 2018. Accessed.
  9. American Thyroid Association (ATA). Hypothyroidism (Underactive). Hypothyroidism FAQs. Copyright 2019. Accessed 9/10/2019.  Accessed.
  10. Sheehan MT, Doi SA. Transient Hypothyroidism after Radioiodine for Graves' Disease: Challenges in Interpreting Thyroid Function Tests. Clin Med Res. 2016;14(1):40-45.
  11. NIH. National Institute of Diabetes and Digestive Kidney Diseases. Hypothyroidism (Underactive Thyroid). 8/2016. Accessed 8/22/2019.  Accessed.
  12. NIH. National Institutes of Health. Iodine. Fact Sheet for Health Professionals. Updated 7/9/2019. Accessed 10/4/2019.
  13. NIH. National Institute of Diabetes and Digestive and Kidney Diseases. Thyroid Tests. 5/2017. Accessed 8/22/2019.  Accessed.
  14. Amlashi FG, Tritos NA. Thyrotropin-secreting pituitary adenomas: epidemiology, diagnosis, and management. Endocrine. 2016;52(3):427-440.
  15. Marsili A, Zavacki AM, Harney JW, Larsen PR. Physiological role and regulation of iodothyronine deiodinases: a 2011 update. Journal of endocrinological investigation. 2011;34(5):395-407.
  16. Refetoff S. Thyroid Hormone Serum Transport Proteins. South Dartmouth (MA):, Inc.; 2015.
  17. Tsigos C, Chrousos GP. Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. Journal of psychosomatic research. 2002;53(4):865-871.
  18. Roelfsema F, Pereira AM, Biermasz NR, et al. Diminished and irregular TSH secretion with delayed acrophase in patients with Cushing's syndrome. European journal of endocrinology / European Federation of Endocrine Societies. 2009;161(5):695-703.
  19. Arancibia S, Rage F, Astier H, Tapia-Arancibia L. Neuroendocrine and autonomous mechanisms underlying thermoregulation in cold environment. Neuroendocrinology. 1996;64(4):257-267.
  20. Hollowell JG, Staehling NW, Flanders WD, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). The Journal of clinical endocrinology and metabolism. 2002;87(2):489-499.
  21. American Thyroid Association (ATA). Clinical Thyroidology for Patients. Subclinical Thyroid Disease: Subclinical thyroid disease increases the incidence of heart failure in older persons. 3/2012. Accessed 8/22/2019.  Accessed.
  22. Donangelo I, Suh SY. Subclinical Hyperthyroidism: When to Consider Treatment. American family physician. 2017;95(11):710-716.
  23. Gilbert J. Thyrotoxicosis - investigation and management. Clinical medicine (London, England). 2017;17(3):274-277.
  24. Nygaard B. Hyperthyroidism (primary). BMJ Clin Evid. 2010;2010.
  25. Clinic M. Graves' Disease. 2018.
  26. Mayo Clinic. Hyperthyroidism (overactive thyroid). 11/3/2018. Accessed 8/21/2019.  Accessed.
  27. Mayo Clinic. Hyperthyroidism (overactive thyroid). Symptoms & causes. Updated 11/3/2018. Accessed 10/4/2019.
  28. Mayo Clinic. Hyperthyroidism (overactive thyroid): Diagnosis & treatment. Updated 11/3/2018. Accessed 10/4/2019.
  29. Soh SB, Aw TC. Laboratory Testing in Thyroid Conditions - Pitfalls and Clinical Utility. Ann Lab Med. 2019;39(1):3-14.
  30. Kravets I. Hyperthyroidism: Diagnosis and Treatment. American family physician. 2016;93(5):363-370.
  31. Turck N, Eperon S, De Los Angeles Gracia M, Obéric A, Hamédani M. Thyroid-Associated Orbitopathy and Biomarkers: Where We Are and What We Can Hope for the Future. Disease markers. 2018;2018:7010196.
  32. Clinic M. Hyperthyroidism. 2018.
  33. De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet. 2016;388(10047):906-918.
  34. Ittermann T, Volzke H, Baumeister SE, Appel K, Grabe HJ. Diagnosed thyroid disorders are associated with depression and anxiety. Soc Psychiatry Psychiatr Epidemiol. 2015;50(9):1417-1425.
  35. American Thyroid Association (ATA). Thyroid Function Tests. Copyright 2014. Accessed 8/22/2019.  Accessed.
  36. LabCorp. Thyroid-stimulating Hormone (TSH). Accessed 10/23/2019.
  37. Meyerovitch J, Rotman-Pikielny P, Sherf M, Battat E, Levy Y, Surks MI. Serum thyrotropin measurements in the community: five-year follow-up in a large network of primary care physicians. Arch Intern Med. 2007;167(14):1533-1538.
  38. LabCorp. Thyroxine (T4.). Copyright 2019.  Accessed.
  39. LabCorp. Thyroxine (T4), Free, Direct. Copyright 2019. Accessed 8/21/2019.  Accessed.
  40. LabCorp. Triiodothyronine (T3), Free. 2019.
  41. LabCorp. Triiodothyronine (T3). 2019.
  42. Kohrle J. The Colorful Diversity of Thyroid Hormone Metabolites. Eur Thyroid J. 2019;8(3):115-129.
  43. Meloni A, Mandas C, Jores RD, Congia M. Prevalence of autoimmune thyroiditis in children with celiac disease and effect of gluten withdrawal. J Pediatr. 2009;155(1):51-55, 55 e51.
  44. Najib U, Bajwa ZH, Ostro MG, Sheikh J. A retrospective review of clinical presentation, thyroid autoimmunity, laboratory characteristics, and therapies used in patients with chronic idiopathic urticaria. Ann Allergy Asthma Immunol. 2009;103(6):496-501.
  45. Aamir IS, Tauheed S, Majid F, Atif A. Frequency of autoimmune thyroid disease in chronic urticaria. Journal of the College of Physicians and Surgeons--Pakistan : JCPSP. 2010;20(3):158-161.
  46. Kolkhir P, Metz M, Altrichter S, Maurer M. Comorbidity of chronic spontaneous urticaria and autoimmune thyroid diseases: A systematic review. Allergy. 2017;72(10):1440-1460.
  47. American Thyroid Association (ATA). Iodine Deficiency. Accessed 10/4/2019.
  48. Azim S, Nasr C. Subclinical hypothyroidism: When to treat. Cleveland Clinic journal of medicine. 2019;86(2):101-110.
  49. Cleveland Clinic. Thyroid Blood Tests. 2019.
  50. Cleveland Clinic. Thyroid Blood Tests. Copyright 2019. Accessed 8/22/2019.  Accessed.
  51. Cleveland Clinic. Hyperthyroidism: Management and Treatment. Published 2019. Accessed September 9, 2019.
  52. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343-1421.
  53. Abraham-Nordling M, Torring O, Hamberger B, et al. Graves' disease: a long-term quality-of-life follow up of patients randomized to treatment with antithyroid drugs, radioiodine, or surgery. Thyroid. 2005;15(11):1279-1286.
  54. Laurberg P, Wallin G, Tallstedt L, Abraham-Nordling M, Lundell G, Torring O. TSH-receptor autoimmunity in Graves' disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study. European journal of endocrinology / European Federation of Endocrine Societies. 2008;158(1):69-75.
  55. Abraham P, Acharya S. Current and emerging treatment options for Graves' hyperthyroidism. Therapeutics and clinical risk management. 2010;6:29-40.
  56. Smithson M, Asban A, Miller J, Chen H. Considerations for Thyroidectomy as Treatment for Graves Disease. Clin Med Insights Endocrinol Diabetes. 2019;12:1179551419844523.
  57. Sjolin G, Holmberg M, Torring O, et al. The long-term outcome of treatment for Graves' hyperthyroidism. Thyroid. 2019.
  58. Villagelin D, Romaldini JH, Santos RB, Milkos AB, Ward LS. Outcomes in Relapsed Graves' Disease Patients Following Radioiodine or Prolonged Low Dose of Methimazole Treatment. Thyroid. 2015;25(12):1282-1290.
  59. Bahn Chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. 2011;21(6):593-646.
  61. Brito JP, Schilz S, Singh Ospina N, et al. Antithyroid Drugs-The Most Common Treatment for Graves' Disease in the United States: A Nationwide Population-Based Study. Thyroid. 2016;26(8):1144-1145.
  62. Palit TK, Miller CC, Miltenburg DM. The Efficacy of Thyroidectomy for Graves' Disease: A Meta-analysis. Journal of Surgical Research. 2000;90(2):161-165.
  63. Vital D, Morand GB, Meerwein C, et al. Early Timing of Thyroidectomy for Hyperthyroidism in Graves’ Disease Improves Biochemical Recovery. World journal of surgery. 2017;41(10):2545-2550.
  64. American Thyroid Association (ATA). Thyroid Hormone Treatment. Accessed 10/4/2019.
  65. Clarke N, Kabadi UM. Optimizing treatment of hypothyroidism. Treat Endocrinol. 2004;3(4):217-221.
  66. Tonstad S, Nathan E, Oda K, Fraser GE. Prevalence of hyperthyroidism according to type of vegetarian diet. Public health nutrition. 2015;18(8):1482-1487.
  67. Alwarith J, Kahleova H, Rembert E, et al. Nutrition Interventions in Rheumatoid Arthritis: The Potential Use of Plant-Based Diets. A Review. Frontiers in nutrition. 2019;6:141.
  68. Leung AM, Braverman LE. Consequences of excess iodine. Nature reviews Endocrinology. 2014;10(3):136-142.
  69. American Thyroid Association (ATA). Iodine Deficiency. Copyright 2019. Accessed 8/22/2019.  Accessed.
  70. American Thyroid Association (ATA). Low Iodine Diet. Available at Accessed 10/15/2019.
  71. Huang H, Shi Y, Liang B, Cai H, Cai Q, Lin R. Optimal iodine supplementation during antithyroid drug therapy for Graves' disease is associated with lower recurrence rates than iodine restriction. Clin Endocrinol (Oxf). 2018;88(3):473-478.
  72. 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. Nutrition reviews. 2016;74(4):248-258.
  73. Osuna PM, Udovcic M, Sharma MD. Hyperthyroidism and the Heart. Methodist DeBakey cardiovascular journal. 2017;13(2):60-63.
  74. Kaminski G, Dziuk M, Szczepanek-Parulska E, Zybek-Kocik A, Ruchala M. Electrocardiographic and scintigraphic evaluation of patients with subclinical hyperthyroidism during workout. Endocrine. 2016;53(2):512-519.
  75. Sharif K, Watad A, Coplan L, et al. The role of stress in the mosaic of autoimmunity: An overlooked association. Autoimmun Rev. 2018;17(10):967-983.
  76. Vita R, Lapa D, Trimarchi F, Benvenga S. Stress triggers the onset and the recurrences of hyperthyroidism in patients with Graves' disease. Endocrine. 2015;48(1):254-263.
  77. Yoshiuchi K, Kumano H, Nomura S, et al. Psychosocial factors influencing the short-term outcome of antithyroid drug therapy in Graves' disease. Psychosomatic medicine. 1998;60(5):592-596.
  78. Sawicka-Gutaj N1 GP, Sowiński J, Wender-Ożegowska E, Czarnywojtek A, Brązert J, Ruchała M. Influence of cigarette smoking on thyroid gland--an update. Endokrynol Pol. 2014;65:54-62.
  79. Kim SJ, Kim MJ, Yoon SG, et al. Impact of smoking on thyroid gland: dose-related effect of urinary cotinine levels on thyroid function and thyroid autoimmunity. Sci Rep. 2019;9(1):4213.
  80. Barbesino G. Misdiagnosis of Graves' Disease with Apparent Severe Hyperthyroidism in a Patient Taking Biotin Megadoses. Thyroid. 2016;26(6):860-863.
  81. Mao J, Pop VJ, Bath SC, Vader HL, Redman CW, Rayman MP. Effect of low-dose selenium on thyroid autoimmunity and thyroid function in UK pregnant women with mild-to-moderate iodine deficiency. European journal of nutrition. 2016;55(1):55-61.
  82. Guastamacchia E, Giagulli VA, Licchelli B, Triggiani V. Selenium and Iodine in Autoimmune Thyroiditis. Endocr Metab Immune Disord Drug Targets. 2015;15(4):288-292.
  83. Ventura M, Melo M, Carrilho F. Selenium and Thyroid Disease: From Pathophysiology to Treatment. International journal of endocrinology. 2017;2017:1297658.
  84. Rayman MP. The importance of selenium to human health. Lancet. 2000;356(9225):233-241.
  85. Kohrle J. The trace element selenium and the thyroid gland. Biochimie. 1999;81(5):527-533.
  86. Zimmermann MB, Kohrle J. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid. 2002;12(10):867-878.
  87. Genere N, Stan MN. Current and Emerging Treatment Strategies for Graves' Orbitopathy. Drugs. 2019;79(2):109-124.
  88. NIH. US National Institutes of Health. Office of Dietary Supplements: Health Information: Vitamin D. Available at Last updated 11/10/2014. Accessed 06/01/2015. 2014.
  89. Kim D. The Role of Vitamin D in Thyroid Diseases. International journal of molecular sciences. 2017;18(9).
  90. Xu MY, Cao B, Yin J, Wang DF, Chen KL, Lu QB. Vitamin D and Graves' disease: a meta-analysis update. Nutrients. 2015;7(5):3813-3827.
  91. Planck T, Shahida B, Malm J, Manjer J. Vitamin D in Graves Disease: Levels, Correlation with Laboratory and Clinical Parameters, and Genetics. Eur Thyroid J. 2018;7(1):27-33.
  92. Mangaraj S, Choudhury AK, Swain BM, Sarangi PK, Mohanty BK, Baliarsinha AK. Evaluation of Vitamin D Status and its Impact on Thyroid Related Parameters in New Onset Graves' Disease- A Cross-sectional Observational Study. Indian J Endocrinol Metab. 2019;23(1):35-39.
  93. Heisel CJ, Riddering AL, Andrews CA, Kahana A. Serum Vitamin D Deficiency Is an Independent Risk Factor for Thyroid Eye Disease. Ophthalmic Plast Reconstr Surg. 2019.
  94. Ahn HY, Chung YJ, Cho BY. Serum 25-hydroxyvitamin D might be an independent prognostic factor for Graves disease recurrence. Medicine. 2017;96(31):e7700.
  95. Grove-Laugesen D, Malmstroem S, Ebbehoj E, et al. Effect of 9 months of vitamin D supplementation on arterial stiffness and blood pressure in Graves' disease: a randomized clinical trial. Endocrine. 2019.
  96. Alhuzaim ON, Aljohani N. Effect of vitamin d3 on untreated graves' disease with vitamin d deficiency. Clin Med Insights Case Rep. 2014;7:83-85.
  97. Menke T, Niklowitz P, Reinehr T, de Sousa GJ, Andler W. Plasma levels of coenzyme Q10 in children with hyperthyroidism. Hormone research. 2004;61(4):153-158.
  98. Pandolfi C, Ferrari D, Stanic I, Pellegrini L. [Circulating levels of CoQ10 in hypo- and hyperthyroidism]. Minerva endocrinologica. 1994;19(3):139-142.
  99. Littarru GP, Lippa S, Oradei A, Serino F. Coenzyme Q10: blood levels and metabolic demand. International journal of tissue reactions. 1990;12(3):145-148.
  100. Oztay F, Ergin B, Ustunova S, et al. Effects of coenzyme Q10 on the heart ultrastructure and nitric oxide synthase during hyperthyroidism. The Chinese journal of physiology. 2007;50(5):217-224.
  101. Suzuki H, Naitoh T, Kuniyoshi S, et al. Cardiac performance and coenzyme Q10 in thyroid disorders. Endocrinol Jpn. 1984;31(6):755-761.
  102. Abdel-Gayoum AA. Dyslipidemia and serum mineral profiles in patients with thyroid disorders. Saudi Med J. 2014;35(12):1469-1476.
  103. Hammerstad SS, Norheim I, Paulsen T, Amlie LM, Eriksen EF. Excessive decrease in serum magnesium after total thyroidectomy for Graves' disease is related to development of permanent hypocalcemia. World journal of surgery. 2013;37(2):369-375.
  104. Moncayo R, Moncayo H. Proof of concept of the WOMED model of benign thyroid disease: Restitution of thyroid morphology after correction of physical and psychological stressors and magnesium supplementation. BBA clinical. 2015;3:113-122.
  105. NIH. National Institutes of Health. Vitamin E. Fact Sheet for Consumers. Last updated 7/10/2019. Accessed 8/21/2019.  Accessed.
  106. Venditti P, Di Stefano L, Di Meo S. Vitamin E management of oxidative damage-linked dysfunctions of hyperthyroid tissues. Cellular and molecular life sciences : CMLS. 2013;70(17):3125-3144.
  107. Guerra LN, Rios de Molina Mdel C, Miler EA, Moiguer S, Karner M, Burdman JA. Antioxidants and methimazole in the treatment of Graves' disease: effect on urinary malondialdehyde levels. Clin Chim Acta. 2005;352(1-2):115-120.
  108. Bianchi G, Solaroli E, Zaccheroni V, et al. Oxidative stress and anti-oxidant metabolites in patients with hyperthyroidism: effect of treatment. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 1999;31(11):620-624.
  109. Subudhi U, Chainy GB. Expression of hepatic antioxidant genes in l-thyroxine-induced hyperthyroid rats: regulation by vitamin E and curcumin. Chem Biol Interact. 2010;183(2):304-316.
  110. Auf'mkolk M, Ingbar JC, Kubota K, Amir SM, Ingbar SH. Extracts and auto-oxidized constituents of certain plants inhibit the receptor-binding and the biological activity of Graves' immunoglobulins. Endocrinology. 1985;116(5):1687-1693.
  111. Beer AM, Wiebelitz KR, Schmidt-Gayk H. Lycopus europaeus (Gypsywort): effects on the thyroidal parameters and symptoms associated with thyroid function. Phytomedicine. 2008;15(1-2):16-22.
  112. Eiling R, Wieland V, Niestroj M. [Improvement of symptoms in mild hyperthyroidism with an extract of Lycopus europaeus (Thyreogutt(R) mono)]. Wien Med Wochenschr. 2013;163(3-4):95-101.
  113. Benvenga S, Feldt-Rasmussen U, Bonofiglio D, Asamoah E. Nutraceutical Supplements in the Thyroid Setting: Health Benefits beyond Basic Nutrition. Nutrients. 2019;11(9).
  114. Benvenga S, Lakshmanan M, Trimarchi F. Carnitine is a naturally occurring inhibitor of thyroid hormone nuclear uptake. Thyroid. 2000;10(12):1043-1050.
  115. Benvenga S, Ruggeri RM, Russo A, Lapa D, Campenni A, Trimarchi F. Usefulness of l-Carnitine, A Naturally Occurring Peripheral Antagonist of Thyroid Hormone Action, in Iatrogenic Hyperthyroidism: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial. J Clin Endocrinol Metab. 2001;86(8):3579-3594.
  116. Nordio M. A novel treatment for subclinical hyperthyroidism: a pilot study on the beneficial effects of l-carnitine and selenium. Eur Rev Med Pharmacol Sci. 2017;21(9):2268-2273.
  117. Kimmoun A, Munagamage G, Dessalles N, Gerard A, Feillet F, Levy B. Unexpected awakening from comatose thyroid storm after a single intravenous injection of L-carnitine. Intensive Care Med. 2011;37(10):1716-1717.
  118. Chee R, Agah R, Vita R, Benvenga S. L-carnitine treatment in a seriously ill cancer patient with severe hyperthyroidism. Hormones (Athens). 2014;13(3):407-412.
  119. Benvenga S, Lapa D, Cannavò S, Trimarchi F. Successive thyroid storms treated with L-carnitine and low doses of Methimazole. Am J Med. 2003;115(5):417-418.