Grave’s Disease

February 2, 2017

Grave’s Disease also known as ‘Diffuse toxic goitre’ is characterized by hyperthyroidism and diffuse goiter. Graves’ disease is an autoimmune disorder where misplaced attacks from the immune system cause the thyroid gland to become overactive. It is caused by a generalized overactivity of the entire thyroid gland (hyperthyroidism). It is named for Robert Graves, an Irish physician, who described this form of hyperthyroidism about 150 years ago.

Graves’ disease is very common and affects about 1 in 200 people and is the most common cause of hyperthyroidism in the United States. Graves’ disease it is most often seen in women ages 20 to 40.

The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. The thyroid’s job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormone helps the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should.

With Graves’ disease, the immune system makes antibodies that act like thyroid stimulating hormone (TSH), causing the thyroid to make more thyroid hormone than your body needs. This is called an overactive thyroid or hyperthyroidism. An overactive thyroid causes every function of the body to speed up, such as heart rate and the rate your body turns food into energy. Graves’ disease is one cause of overactive thyroid. It is closely related to Hashimoto’s disease, another autoimmune disease affecting the thyroid.

Who gets Grave’s Disease?

Both men and women can get Graves’ disease. But it affects women 10 times more often than men. Graves’ disease occurs in people of all ages, but most often starts in the 20s and 30s. People who get Graves’ disease often have family members who have thyroid or other autoimmune diseases. People who get Graves’ disease sometimes have other autoimmune diseases, such as:

  • Vitiligo — A disease that destroys the cells that give the skin its color
  • Rheumatoid arthritis — A disease that affects the lining of the joints throughout the body
  • Addison’s disease — A disease that affects the adrenal glands, which make hormones that help the body respond to stress and regulate the blood pressure and water and salt balance
  • Type 1 diabetes — A disease that causes blood sugar levels to be too high
  • Pernicious anemia — A disease that keeps the body from absorbing vitamin B12 and making enough healthy red blood cells
  • Lupus — A disease that can damage many parts of the body, such as the joints, skin, blood vessels, and other organs




Genetic factors – High prevalence of Graves’ disease in family members and relatives of Graves’ disease and Hashimoto’s thyroiditis support that genetic factors are involved in causation of Graves’ disease. There is also evidence that occurrence rate of Graves’ disease is higher in monozygotic twins than dizygotic twins. The concordance rate in monozygotic twins is only 17-35% which indicate low penentrance of genes.

Environmental Factors – From very early it has been suggested that Graves’ disease is associated with infectious agents, but this hypothesis has not been confirmed. Incidence of viral infections is high in patients with Graves’ disease. The association of Graves’ disease with infectious agents can be explained by molecular mimicry. Infection might play a role in the onset of Graves’ disease, but no studies have shown infection to directly cause Graves’ disease.

Stress – Severe emotional and physical stress, like separation from the loved one or following road traffic accident, cause release of cortisol ad corticotrophin releasing hormone. So, stress is a relatively immune suppression state. Immune system overcompensates once stress is over which can precipitate disease similar to postpartum period. In conclusion there is limited but significant evidence that stressful life events can precipitate the onset of Graves’ disease in genetically susceptible individuals.

Gender – Typically Graves’ disease is more prevalent in females than males. It is about 5-10 times more common in females at any age. But Graves’ disease also occurs in men and postmenopausal women. These observations have suggested that it is the X-chromosome, not the sex steroids, which is responsible. But most of the x-linked disorders are only present in man, it has been thought that a gene with dose dependent effect on X-chromosome is responsible.

Pregnancy – Postpartum period is an important risk factor for both the onset and relapse of Graves’ disease. Postpartum period is associated with a fourfold to eightfold increased risk for the onset of Graves’ disease. However in women with Graves’ disease who became pregnant, successful pregnancy outcome is low because Graves’ disease causes increased pregnancy loss and its complications.

Smoking – Smoking is a minor risk factor for Graves’ disease; however it is a major risk factor for Graves’ ophthalmopathy. There are number of studies showing relationship between Graves’ disease, Graves’ ophthalmopathy and smoking.

Other Factors – Direct trauma to the thyroid gland, ethanol injection for the treatment of autonomously functioning thyroid nodules, or thyroid injury following radio-iodine treatment for toxic adenoma or toxic multinodular goiter are associated with an increased risk of Graves’ disease. Radio-iodine treatment may also cause onset or worsening of ophthalmopathy. Possible explanation is that thyroid injury by any means cause massive release of thyroid antigens, which in turn stimulate an autoimmune reaction to TSHR in susceptible individuals.



The overproduction of thyroid hormones can have a variety of effects on the body due to the important role these hormones play to regulate a person’s metabolism.

The onset of Graves’ disease can have a number of effects on the body.

The influx of thyroid hormones can increase these processes, symptoms of this include –

  • Increased sweating
  • Weight loss
  • Nervousness
  • Hand tremors
  • Anxiety
  • An irregular or rapid heartbeat
  • Enlargement of the thyroid gland (goiter).

One distinct feature of Graves’ disease, compared with other causes of hyperthyroidism, is its effects on the eyes. Graves’ disease is the only type of hyperthyroidism that is associated with the swelling and inflammation of the eye tissue.

Graves’ eye disease is also known as ophthalmopathy (exophthalmos) and is a common symptom of patients with Graves’s disease with 30% of patients suffering from the condition. In this instance, the eyes become painful, red and watery. Patients may also experience extreme sensitivity to sunlight and blurred vision.



Conventional Treatment – People with Graves’ disease have three conventional treatment options – radioiodine therapy, medications, and thyroid surgery. Radioiodine therapy is the most common treatment for Graves’ disease in the United States. Graves’ disease is often diagnosed and treated by an endocrinologist—a doctor who specializes in the body’s hormone- secreting glands.

  • Radioactive iodine therapy – Radioactive iodine is taken orally and directly targets the thyroid gland. Iodine is required to produce the thyroid hormones. When medication is taken, the radioactive iodine soon accumulates in the thyroid gland and slowly destroys any overactive thyroid cells. This results in the reduction of the thyroid gland and fewer thyroid hormones being produced. Although there have been concerns regarding the relationship between head and neck irradiation and the increased risk of thyroid cancer, so far no study has revealed any relation.
  • Medications
    • Beta blockers.Health care providers may prescribe a medication called a beta blocker to reduce many of the symptoms of hyperthyroidism, such as tremors, rapid heartbeat, and nervousness. But beta blockers do not stop thyroid hormone production.
    • Anti-thyroid medications.Health care providers sometimes prescribe anti-thyroid medications as the only treatment for Graves’ disease.  Anti-thyroid medications interfere with thyroid hormone production but don’t usually have permanent results.  Use of these medications requires frequent monitoring by a health care provider.  More often, anti-thyroid medications are used to pretreat patients before surgery or radioiodine therapy, or they are used as supplemental treatment after radioiodine therapy
  • Thyroid Surgery – Surgery is the least-used option for treating Graves’ disease. Sometimes surgery may be used to treat
    • pregnant women who cannot tolerate anti-thyroid medications
    • people suspected of having thyroid cancer, though Graves’ disease does not cause cancer
    • people for whom other forms of treatment are not successful

Alternative Treatment


Lithium – Prescription lithium carbonate is well known to cause hypothyroidism. Small studies have shown that lithium carbonate is also effective at controlling symptoms of hyperthyroidism. There are also case reports where patients who were prescribed lithium for other reasons and went on to develop Graves’ disease remained asymptomatic while on lithium


Selenium – A dose of slenium may show effective in reducing symptoms of Graves’ disease, including ophthalmopathy.

Carnitine – L-carnitine helps to improve symptoms of hyperthyroidism.

Probiotics like acidophilus – These can help the immune system as well.

Omega-3 Fatty Acids – Omega-3s such as those that are found in fish oil decrease inflammation and improve immunity.

Iodine – Iodine is a vital nutrient in the body and essential to thyroid function; thyroid hormones are comprised of iodine. While autoimmune disease is the primary cause of thyroid dysfunction in the United States, iodine deficiency is the main cause worldwide.

Vitamin D – Hyperthyroidism, particularly Graves’ disease, is known to cause bone loss, which is compounded by the vitamin D deficiency commonly found in people with hyperthyroidism. This bone mass can be regained with treatment for hyperthyroidism, and experts suggest that adequate bone-building nutrients, such as vitamin D, are particularly important during and after treatment.

Goitrogens – Cruciferous vegetables such as broccoli, cauliflower, and cabbage naturally release a compound called goitrin when they’re hydrolyzed, or broken down. Goitrin can interfere with the synthesis of thyroid hormones. Soy is another potential goitrogen


Reference –

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