Graves’ disease is an autoimmune disease in which the body’s metabolism speeds up. It's possible that vitamin D deficiency may play a role in the development of Graves' disease — there is some evidence to suggest this, but it's not yet proven.
Graves’ disease is caused by an antibody that makes the thyroid gland produce too much thyroid hormone — the antibody activates the thyroid stimulating hormone (TSH) receptor. Graves’ disease is often accompanied by eye disease and skin disease.
Under normal circumstances, the pituitary gland in the brain makes TSH, which goes through the bloodstream to stimulate the thyroid gland (located in the neck) to make thyroid hormone. Thyroid hormone regulates metabolism in the body.
Normally, if the thyroid isn’t making enough hormone, the pituitary secretes more TSH. If the thyroid makes too much, TSH is suppressed. In Graves’ disease the antibody mimics the effect of too much TSH even though the real level of TSH is very low.
Signs and symptoms of Graves' disease
Graves’ disease is ten times more common in women than men. It usually begins between ages 30 and 60. It’s hereditary, passing from mother to daughter, but sometimes skips a generation. What is inherited is the tendency for autoimmune attack on the thyroid to occur, but a trigger to initiate the autoimmune attack is still needed.
Known triggers for Graves’ disease include stress, illness, pregnancy, and other factors. Oddly enough, the risk of hypothyroidism is also increased in the same families that are at high risk for Graves’ disease.
The signs and symptoms of Graves’ disease include the following:
Swollen knees with a waxy appearance
Bulging eyes with the whites showing above and below the pupil
Persistently high body temperature
Weight loss resulting from muscle loss
Moist, warm skin from increased sweating
Rapid pulse felt as palpitations of the heart
Fine tremor of the fingers
Weakness
Miscarriage of a pregnancy if uncontrolled
Increased bowel movements and sometimes diarrhea
Increased appetite, but weight loss because of the increased metabolism
Loss of bone from increased breakdown, with increased fracture rate
Increased urination and thirst
Increased reflexes
Changes in hair (thinner, falling out) and nails (breaking easily, separating from nail bed)
Doctors diagnose Graves’ disease by measuring the amount of free (active) thyroid hormone and the amount of TSH in the blood. In Graves’ disease, active thyroid hormone is elevated, TSH is suppressed, and a thyroid scan shows the gland to be enlarged.
Levels of antibodies against the TSH receptor can also be measured and will be elevated, but this test is usually done in exceptional circumstances such as pregnancy (because the antibody can cause Graves’ disease in the fetus).There are other causes of hyperthyroidism apart from Graves’ disease, including toxic nodules, multinodular goiters, and autoimmune thyroiditis.
Treating Graves’ disease
Doctors use three major forms of treatment for Graves’ disease:
Antithyroid pills, either methimazole or propylthiouracil: These drugs suppress the thyroid’s ability to make thyroid hormone and return the blood levels to normal. During the time that the thyroid is suppressed, in some patients the autoimmune attack lets up and the patient is effectively cured (it doesn’t seem to be a direct effect of the drug, though).
But in others the condition relapses weeks to years after the medication is stopped, and the patient needs to be retreated for a longer interval or indefinitely. This is the only treatment that can potentially cure the disease.
Radioactive iodine: Thyroid hormone is made out of iodine, and the thyroid avidly takes up most of the iodine in the diet. When a radioactive form of iodine goes into the thyroid, it kills thyroid cells and cures the overactive thyroid that way. Most patients end up with low thyroid function and have to take thyroid hormone in the form of a pill for life.
Surgical removal of the thyroid: This treatment usually results in low thyroid function because removing just enough thyroid to control Graves’ disease is difficult. It’s rarely done to treat Graves’ disease except in unusual circumstances, such as for a pregnant woman and those unable to tolerate the antithyroid medication (radioactive iodine cannot be safely used because it may destroy the fetal thyroid).
Vitamin D and Graves’ disease
There’s not a whole lot of evidence linking vitamin D to Graves’ disease; still, there’s enough that it’s worth considering. All of the following may link vitamin D and Graves’ disease:
Vitamin D deficiency has been seen among female Graves’ disease patients from Japan.
Variations in the genes responsible for calcitriol signaling or calcitriol action have been associated with a high incidence of Graves’ disease in some studies. This suggests that when calcitriol can’t work well in cells, a person might be more likely to get Graves’ disease. However, no one has tested to see if treating with vitamin D will prevent the onset of Graves’ disease or reduce its severity after it has occurred.