What is Graves’ Disease?
Graves’ disease, also called autoimmune hyperthyroidism, is an autoimmune disease that affects the thyroid gland by causing it to produce excessive levels of hormones. It is the most common cause of hyperthyroidism in Western countries, responsible for 4 out of every 5 cases.[1] Graves’ disease affects 1 in 200 people and occurs with 5–10 times higher frequency in women compared to men.[2] People with Graves’ disease are also at increased risk for developing other autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and type 1 diabetes.[3]
What are the main signs and symptoms of Graves’ disease?
Because thyroid hormones help to regulate multiple body systems, Graves’ disease causes a range of symptoms throughout the body.
The following symptoms are common in people with Graves’ disease:[4]
- Nervousness
- Moodiness or irritability
- Anxiety
- Rapid heartbeat
- Tremors
- Increased bowel movement frequency
- Intolerance for hot conditions and increased sweating
- Sleep difficulties
- Weight loss in spite of increased appetite
- Enlargement of the thyroid (goiter), which may interfere with breathing or swallowing
Up to half of people with Graves’ disease may have eye symptoms such as redness, dryness, irritation, and swelling. Women with Graves’ disease may also experience irregularities with their menstrual cycles.
A small number of people with Graves’ disease may develop a skin disorder called Graves’ dermopathy,[5] which causes localized thickening of the skin, typically in the legs and feet.[6]
How is Graves’ disease diagnosed?
When Graves’ disease is suspected based on a person’s symptoms (particularly skin and eye symptoms and an enlarged thyroid gland), a doctor will order testing to evaluate thyroid gland function. Blood tests will be performed to analyze levels of thyroid hormones and check for the presence of particular autoantibodies. Diagnosis can be confirmed through radioactive iodine uptake testing. The thyroid gland absorbs iodine to make thyroid hormones, and in people with Graves’ disease, overproduction of thyroid hormones increases iodine uptake by the thyroid gland, which can be measured with a thyroid scan. Doctors will also use the thyroid scan to analyze the pattern of iodine uptake, which can help to distinguish Graves’ disease from other thyroid disorders.[7]
What are some of the main medical treatments for Graves’ disease?
There are currently no cures for the chronic autoimmune process that causes Graves’ disease. However, there are treatment options for hyperthyroidism, including surgery, medications, and radioiodine therapy. Radioiodine therapy involves ingestion of a radioactive form of iodine, which destroys the cells in the thyroid gland that produce thyroid hormones. Medications such as beta blockers can reduce some of the symptoms of Graves’ disease, such as rapid heartbeat, tremors, and nervousness. Antithyroid medications that work by reducing the production of thyroid hormones are also commonly prescribed. Surgery is another common treatment for hyperthyroidism and involves removing part or most of the thyroid gland. [7]
Have any supplements been studied for Graves’ disease?
Selenium is a cofactor for enzymes in the body that function to neutralize reactive oxygen species,[8] and low vitamin D levels are associated with increased inflammation.[9] Because observational studies have noted low selenium and vitamin D levels in people with a new diagnosis of Graves’ disease,[10] one randomized controlled trial tested the effects of selenium and vitamin D supplementation in participants with Graves’ disease who had low levels of these nutrients. The trial found that selenium and vitamin D supplementation in combination with standard drug therapy was better than the drug therapy alone for treating hyperthyroid symptoms in participants.[11]
Additional supplements that have been studied for use in Graves’ disease include antioxidants,[12] omega-3 fatty acids,[13] and probiotics.[14]
How could diet affect Graves’ disease?
Because the thyroid gland uses iodine to synthesize thyroid hormones, people with Graves’ disease may be sensitive to foods or supplements that contain high amounts of iodine. Foods or supplements that are high in iodine, such as kelp or multivitamins, could potentially make hyperthyroidism worse.[15] The autoimmune protocol diet has shown positive effects on inflammation and disease symptoms in people with Hashimoto’s thyroiditis (a similar type of autoimmune thyroid disease) when used alongside a broader lifestyle intervention.[16] Treatment for hyperthyroidism is intended to ideally restore levels of thyroid hormones to normal ranges. However, therapy often results in hypothyroidism (an underactive thyroid gland),[7] which could potentially require dietary changes to mitigate weight gain in certain individuals. Hyperthyroidism can also potentially mask a predisposition for weight gain or obesity, which may require diet changes to avoid excessive weight after the hyperthyroidism is treated.[17]
Are there any other treatments for Graves’ disease?
Current treatments for Graves’ disease all have drawbacks. Commonly used antithyroid therapies are associated with an increased risk that disease symptoms will return after treatment is stopped. The downside to ablative therapies such as radioiodine therapy or surgery is that many people will eventually develop hypothyroidism, which will require lifelong hormone therapy. Immunotherapies designed to treat the underlying autoimmune process that causes Graves’ disease are under development and are being designed with the goal of restoring immune tolerance to some of the self-proteins targeted by autoimmunity. If these immunotherapies are successful, stopping the underlying autoimmune process could potentially restore thyroid hormones back to normal, healthy levels without inducing hypothyroidism. Some of these therapies are being tested in early-phase clinical trials, with promising results.[18]
What causes Graves’ disease?
The thyroid is a gland in the lower neck that produces hormones that regulate many different body functions, including body temperature, body weight, and heart rate. In people with autoimmune hyperthyroid diseases such as Graves’, the immune system mistakenly generates an immune response against parts of the thyroid gland, resulting in the generation of autoantibodies. Some of the autoantibodies in people with Graves’ disease bind to and activate the thyroid gland, causing the overproduction of thyroid hormones. The symptoms of Graves’ disease are caused by both autoimmunity and hyperthyroidism.[7]
Examine Database: Graves’ Disease
Frequently asked questions
Graves’ disease, also called autoimmune hyperthyroidism, is an autoimmune disease that affects the thyroid gland by causing it to produce excessive levels of hormones. It is the most common cause of hyperthyroidism in Western countries, responsible for 4 out of every 5 cases.[1] Graves’ disease affects 1 in 200 people and occurs with 5–10 times higher frequency in women compared to men.[2] People with Graves’ disease are also at increased risk for developing other autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and type 1 diabetes.[3]
Because thyroid hormones help to regulate multiple body systems, Graves’ disease causes a range of symptoms throughout the body.
The following symptoms are common in people with Graves’ disease:[4]
- Nervousness
- Moodiness or irritability
- Anxiety
- Rapid heartbeat
- Tremors
- Increased bowel movement frequency
- Intolerance for hot conditions and increased sweating
- Sleep difficulties
- Weight loss in spite of increased appetite
- Enlargement of the thyroid (goiter), which may interfere with breathing or swallowing
Up to half of people with Graves’ disease may have eye symptoms such as redness, dryness, irritation, and swelling. Women with Graves’ disease may also experience irregularities with their menstrual cycles.
A small number of people with Graves’ disease may develop a skin disorder called Graves’ dermopathy,[5] which causes localized thickening of the skin, typically in the legs and feet.[6]
When Graves’ disease is suspected based on a person’s symptoms (particularly skin and eye symptoms and an enlarged thyroid gland), a doctor will order testing to evaluate thyroid gland function. Blood tests will be performed to analyze levels of thyroid hormones and check for the presence of particular autoantibodies. Diagnosis can be confirmed through radioactive iodine uptake testing. The thyroid gland absorbs iodine to make thyroid hormones, and in people with Graves’ disease, overproduction of thyroid hormones increases iodine uptake by the thyroid gland, which can be measured with a thyroid scan. Doctors will also use the thyroid scan to analyze the pattern of iodine uptake, which can help to distinguish Graves’ disease from other thyroid disorders.[7]
There are currently no cures for the chronic autoimmune process that causes Graves’ disease. However, there are treatment options for hyperthyroidism, including surgery, medications, and radioiodine therapy. Radioiodine therapy involves ingestion of a radioactive form of iodine, which destroys the cells in the thyroid gland that produce thyroid hormones. Medications such as beta blockers can reduce some of the symptoms of Graves’ disease, such as rapid heartbeat, tremors, and nervousness. Antithyroid medications that work by reducing the production of thyroid hormones are also commonly prescribed. Surgery is another common treatment for hyperthyroidism and involves removing part or most of the thyroid gland. [7]
Treatment is more complex for people with Graves’ disease who are pregnant because considerations need to be made for the thyroid function of both the mother and fetus. Antithyroid medications are the first line of treatment, and dosages are carefully adjusted to bring the mother’s thyroid hormone levels down to the upper limits of normal range (or slightly higher), without causing hypothyroidism in the developing fetus.[23] Radioactive iodine therapy is contraindicated during pregnancy because it can cause hypothyroidism in the fetus. Surgery may be considered if it is necessary for the mother’s health, but is not the first line of therapy. In cases in which surgery is warranted, it is generally delayed until the second trimester, when it poses less risk to the pregnancy.[24][25][23]
Selenium is a cofactor for enzymes in the body that function to neutralize reactive oxygen species,[8] and low vitamin D levels are associated with increased inflammation.[9] Because observational studies have noted low selenium and vitamin D levels in people with a new diagnosis of Graves’ disease,[10] one randomized controlled trial tested the effects of selenium and vitamin D supplementation in participants with Graves’ disease who had low levels of these nutrients. The trial found that selenium and vitamin D supplementation in combination with standard drug therapy was better than the drug therapy alone for treating hyperthyroid symptoms in participants.[11]
Additional supplements that have been studied for use in Graves’ disease include antioxidants,[12] omega-3 fatty acids,[13] and probiotics.[14]
Because the thyroid gland uses iodine to synthesize thyroid hormones, people with Graves’ disease may be sensitive to foods or supplements that contain high amounts of iodine. Foods or supplements that are high in iodine, such as kelp or multivitamins, could potentially make hyperthyroidism worse.[15] The autoimmune protocol diet has shown positive effects on inflammation and disease symptoms in people with Hashimoto’s thyroiditis (a similar type of autoimmune thyroid disease) when used alongside a broader lifestyle intervention.[16] Treatment for hyperthyroidism is intended to ideally restore levels of thyroid hormones to normal ranges. However, therapy often results in hypothyroidism (an underactive thyroid gland),[7] which could potentially require dietary changes to mitigate weight gain in certain individuals. Hyperthyroidism can also potentially mask a predisposition for weight gain or obesity, which may require diet changes to avoid excessive weight after the hyperthyroidism is treated.[17]
Current treatments for Graves’ disease all have drawbacks. Commonly used antithyroid therapies are associated with an increased risk that disease symptoms will return after treatment is stopped. The downside to ablative therapies such as radioiodine therapy or surgery is that many people will eventually develop hypothyroidism, which will require lifelong hormone therapy. Immunotherapies designed to treat the underlying autoimmune process that causes Graves’ disease are under development and are being designed with the goal of restoring immune tolerance to some of the self-proteins targeted by autoimmunity. If these immunotherapies are successful, stopping the underlying autoimmune process could potentially restore thyroid hormones back to normal, healthy levels without inducing hypothyroidism. Some of these therapies are being tested in early-phase clinical trials, with promising results.[18]
The thyroid is a gland in the lower neck that produces hormones that regulate many different body functions, including body temperature, body weight, and heart rate. In people with autoimmune hyperthyroid diseases such as Graves’, the immune system mistakenly generates an immune response against parts of the thyroid gland, resulting in the generation of autoantibodies. Some of the autoantibodies in people with Graves’ disease bind to and activate the thyroid gland, causing the overproduction of thyroid hormones. The symptoms of Graves’ disease are caused by both autoimmunity and hyperthyroidism.[7]
Although the mechanism of hyperthyroidism in Graves’ disease is well understood, the autoimmune process that causes it is not. Autoimmunity occurs when the immune system loses tolerance to “self” molecules and instead interprets them as harmful invaders and targets the tissues where they’re present. The mechanisms that break self-tolerance in Graves’ disease are not clear. Similar to other autoimmune diseases, loss of tolerance to “self” is likely due to a combination of genetic and environmental factors. It has been proposed that the thyroid proteins targeted by the immune system in people with Graves’ disease may have properties that contribute to loss of immune tolerance.[19] However, direct evidence for this hypothesis is lacking. Although several animal models are known to develop autoimmunity against the thyroid gland,[20] they differ from Graves’ disease in that these models are associated with different antibodies and do not develop hyperthyroidism.[19]
Loss of self-tolerance may also occur via common mechanisms across different autoimmune diseases because up to 25% of people with one autoimmune disorder tend to develop additional ones.[21] This phenomenon has also been observed for Graves’ disease, in which 20% of patients also have at least one additional autoimmune disorder.[22]
References
Examine Database References
- Bone Mineral Density - Grove-Laugesen D, Ebbehoj E, Watt T, Hansen KW, Rejnmark LChanges in bone density and microarchitecture following treatment of Graves' disease and the effects of vitamin D supplementation. A randomized clinical trial.Osteoporos Int.(2024 Sep 12)