• Weakness, sweating, weight loss, nervousness, loose stools, heat intolerance, irritability, fatigue
• Racing heartbeat; warm, thin, moist skin; stare; tremor
• Diffuse enlargement of the thyroid, nonpainful goiter
• Increased blood levels of thyroid hormones
Hyperthyroidism is a condition characterized by increased levels of thyroid hormones: thyroxine (T4) and triiodothyronine (T3). The autoimmune disorder Graves’ disease accounts for up to 85% of all cases of hyperthyroidism. Although no single immunological abnormality explains all of the clinical features of the disease, the common denominator is the presence of antibodies against receptors in the thyroid for thyroid-stimulating hormone (TSH). TSH receptor antibodies (TSH-R Ab) or thyroid-stimulating immunoglobulins (TSI) are present in 80% of cases of Graves’ disease. About 25 to 30% of people with Graves’ disease will also suffer from Graves’ ophthalmopathy (a protrusion of one or both eyes), in which the eye muscles become inflamed, attacking autoantibodies.
There are definite patterns of susceptibility for Graves’ disease. In particular, it is eight times more common in women than in men and typically begins between the ages of 20 and 40. The classic clinical presentation of Graves’ disease is a young adult female complaining of nervousness, irritability, sweating, palpitations, insomnia, tremor, frequent bowel movements, and unexplained weight loss.
Physical signs of hyperthyroidism include a smooth, diffuse, nontender goiter in the neck; a racing pulse, especially after exercise; loud heart sounds; and mild protrusion of the eyes with lid retraction. Other signs and symptoms include muscle weakness and fatigue, anxiety, heat intolerance, and fluid retention. The skin can also become moist, warm, and finely textured. Perspiration increases as a response to the increased body temperature. Pigment changes such as vitiligo (areas with loss of pigment) can be associated with Graves’ disease, as well as increased pigmentation of areas such as skin creases and the knuckles. Hair may thin or fall out in patches or all over the scalp. Nails may separate prematurely from the nail bed.
Causes
One of the key causes of hyperthyroidism and/or Graves’ disease is recent stress. This association has been recognized as a precipitating factor ever since Graves’ disease was first recognized. In fact, the most common precipitating event is an “actual or threatened separation from an individual upon whom the patient is emotionally dependent.”1 Studies now support the long-held observation that the onset of Graves’ disease often follows some kind of emotional shock, in particular some sort of loss, such as divorce, death, or difficult separations.2,3
The next most common cause of hyperthyroidism is a toxic nodular goiter. Other causes of hyperthyroidism include early Hashimoto’s thyroiditis (see the chapter “Hypothyroidism”).
People with certain types of genetic markers are statistically more prone to develop Graves’ disease, while people with other types of markers seem to be less frequently affected. In identical twins, if one twin is affected, the other has a 50% chance of manifesting the disease. In fraternal twins, if one twin is affected, the other has a 9% chance of having it as well.
Smoking is known to raise the risk and severity of Graves’ ophthalmopathy.4–6
Several studies have shown that dietary iodine supplementation, usually through consumption of iodized salt, in areas where there is already sufficient iodine in the food supply can increase the incidence of hyperthyroidism in susceptible individuals. In one study, the effects of consuming iodized salt were studied in 267,330 inhabitants of Galicia. The incidence of hyperthyroidism increased throughout the study period, with 4.89 new cases per 100,000 people, though the increase was due to larger numbers of both nodular and diffuse goiters rather than Graves’ disease. Also, iodine from other sources in doses above 600 mcg, such as potassium iodide, iodine supplements, medications such as amiodarone, and imaging contrast agents, can trigger Graves’ disease and toxic multinodular goiter.7
Therapeutic Considerations
Conventional treatment of hyperthyroidism in the United States focuses on destroying the thyroid gland with radioactive iodine (radioactive iodine ablation, RIA). Advantages include the high rate of response and the fact that there is no need for ongoing suppression. Disadvantages include progression to hypothyroidism, elevated risk of nonlocalized cancers, and risk for parathyroid disease. We do not recommend surgery to remove the thyroid unless there are significant extenuating circumstances. It carries with it too many risks compared with RIA.
We feel that prior to RIA a trial of antithyroid drugs should be attempted. This drugs work by entering the thyroid and blocking the formation of thyroid hormones; specifically, they inhibit binding of iodine to tyrosine. In many parts of the world, including Europe and Japan, antithyroid drugs are the first-line treatment for hyperthyroidism, as many cases of hyperthyroidism resolve spontaneously within 18 months. Some people develop hypothyroidism after treatment with antithyroid drugs, and some go on to require RIA.
The chief objective of the natural treatment of Graves’ disease and hyperthyroidism is to reduce symptoms while trying to reestablish normal thyroid status. We recommend use of antithyroid drugs to reduce the immediate severity of hyperthyroid symptoms. Recommended dietary and lifestyle measures may lower the required dose or duration of antithyroid drugs, or raise the likelihood of disease remission with conventional treatment.
Practical steps include reduction of risk factors (stress, smoking, excess iodine intake). Stress control is important in normalization of the thyroid, and counseling can prevent a return to stress-generating life strategies. Increase the amount of rest you get, including a nap after lunch and a full night’s sleep.
Patients with autoimmune thyroid disease, either Graves’ disease or Hashimoto’s thyroiditis (the major cause of low thyroid function), are more likely than the general population to suffer from celiac disease and/or gluten sensitivity. Therefore, these conditions must be ruled out. See the chapter “Celiac Disease” for specific guidance. Also, identify food allergies and avoid problematic foods; see the chapter “Food Allergy.” Otherwise, the recommendations given in the chapter “A Health-Promoting Diet” are appropriate here. Keep in mind that the diet may need to be higher in calories to compensate for the increase in metabolism. We also recommend that you avoid caffeine and dietary sources of iodine (especially iodized salt, kelp and other seaweeds, seafood, and nutritional supplements that contain more than 300 mcg of iodine).
Dietary Goitrogens
Some foods contain goitrogens, substances that prevent the utilization of iodine. These compounds—primarily isothiocyanates, which are similar in action and structure to antithyroid drugs such as propylthiouracil—are found in such foods as turnips, cabbage, rutabagas, mustard greens, rapeseed, cassava root, soybeans, peanuts, pine nuts, and millet. However, these foods cannot reliably be used to treat hyperthyroidism for the following reasons:
• Their goitrogen content is quite low compared with the dosages of propylthiouracil required to treat hyperthyroidism.
• Cooking inactivates the goitrogens.
• No substantial documentation exists that these naturally occurring goitrogens interfere with thyroid function to any significant degree when dietary iodine levels are adequate.
Despite these shortcomings, some natural medicine practitioners may use naturally occurring goitrogens in mild cases instead of propylthiouracil and related drugs. Anecdotally, the typical recommendation is the equivalent of half a head of raw cabbage per day.
Carnitine
Carnitine is manufactured within the body, where it plays an important role in energy metabolism. Carnitine has been shown to be an antagonist of thyroid hormone in peripheral tissues, inhibiting the hormone’s entry into the cell nucleus. A six-month, randomized, double-blind, placebo-controlled study evaluated the use of carnitine in patients prescribed high doses of thyroid hormone.8 During this study, 50 women with benign nodular goiter who already had been prescribed a suppressive dose of thyroxine were randomly assigned to five groups of 10 subjects each. One group was given a placebo for six months. Two groups started with the placebo for two months, then were prescribed 2 or 4 g carnitine per day, then were returned to the placebo for the last two months. The last two groups were started with either 2 or 4 g carnitine per day for the first four months and then were given placebo for the last two months. Symptoms of hyperthyroidism, bone mineralization markers, and liver indicators were recorded.
In the second and third groups, the symptoms that had worsened while the subjects were on thyroxine plus the placebo returned to baseline once carnitine had replaced the placebo. In the fourth and fifth groups, symptoms remained stable or improved as long as carnitine was given with thyroxine, implying that the carnitine effect prevailed over the T4 effect. For those given supplemental carnitine, liver profiles improved, although cholesterol levels were virtually unaffected. Side effects were minor. Symptoms and biochemical variables only worsened in the placebo group.
Because carnitine has extremely low toxicity, the authors of this study recommend considering carnitine for Graves’ disease–induced thyrotoxicosis during pregnancy, during lactation, or in other conditions in which antithyroid drugs may be unwanted, such as liver disease and blood disorders.
There is a long list of plants used traditionally in the treatment of hyperthyroidism. Unfortunately, these plants have not been adequately evaluated in clinical studies. Rather than discuss these plants here, we would encourage anyone interested to consult a naturopathic physician to allow for proper monitoring.
QUICK REVIEW
• Hyperthyroidism is a condition characterized by increased levels of thyroid hormones.
• Graves’ disease accounts for up to 85% of all cases of hyperthyroidism.
• One of the key causes of hyperthyroidism and/or Graves’ disease is recent stress.
• Smoking is known to raise the risk and severity of Graves’ ophthalmopathy.
• Dietary iodine supplementation in iodine-sufficient areas can increase the incidence of hyperthyroidism in susceptible individuals.
• A trial of antithyroid drugs should be attempted before radioactive iodine ablation of the thyroid is considered.
• Stress control is important in the treatment of hyperthyroidism.
• Patients with autoimmune thyroid disease, either Graves’ disease or Hashimoto’s thyroiditis, are more likely than the general population to suffer from celiac disease and/or gluten sensitivity.
• Carnitine has been shown to counteract the effects of elevated thyroxine.
TREATMENT SUMMARY
Acute Graves’ disease is not easily treated by naturopathic methods. In severe cases, there is no guarantee that natural treatments will alleviate the symptoms adequately. In mild cases, natural therapeutics can manage symptoms well, but patients must be monitored carefully.
Rule out gluten sensitivity and then follow the guidelines in the chapter “A Health-Promoting Diet.” Higher calorie intake may be necessary to meet the hyperthyroid patient’s metabolic needs. In mild cases, consumption of large amounts of raw vegetables from the brassica (cabbage) family may be adequate to control symptoms when combined with restricted iodine consumption.
• Foundation supplement program as described in the chapter “Supplementary Measures”
• Carnitine: 2 to 4 g per day