Alternative Treatment for Graves Disease

Graves Disease is an autoimmune disorder that causes the immune system mistakenly attacked healthy tissue. Grave’s disease affects the thyroid gland which is located at the front of the neck. With Graves’s disease, the body overproduces the hormones thyroxine and triiodothyronine which control cell metabolism. This overproduction is known as hyperthyroidism.

Thyroid hormone affects metabolism, and its deficiency causes many of the body’s functions to slow down. An estimated twenty percent of the population suffers from thyroid conditions. It is more common among women than men.

Bari Shares Her Experience at Sunridge

Bari, Phoenix, Arizona The only option that Bari was given was to remove her diseased thyroid. This was not acceptable to her and she chose alternative treatments instead. Her autoimmune disease is now in remission and she still has her thyroid.

Symptoms of Graves Disease

Graves_Disease Treatment at sunridge medical The thyroid gland, which is located in the lower part of the neck, uses iodine (found in foods such as iodized salt, seafood and vegetables) to produce thyroid hormones. The two most important ones are thyroxine (T4) and triiodothyronine (T3). With Graves disease too much T4 is produced.
Several other hormones regulate the amount of thyroid hormone normally released into the bloodstream. Thyrotropin-releasing hormone (TRH), released by the hypothalamus, sends signals to the pituitary gland to release thyroid-stimulating hormone (TSH). TSH in turn “tells” the thyroid gland to release the thyroid hormones T3 and T4. Testing TSH levels is the standard blood work for detecting Graves disease.
Under normal conditions, TSH regulates the amount of thyroid hormone in the blood to allow for normal functioning. In a hypothyroid patient, on the other hand, TSH levels fall as the pituitary attempts to decrease thyroid hormone production. As a result, hypothyroid patients continuously have decreased blood levels of circulating thyroid hormone.
The onset of Grave’s disease can occur slowly or very suddenly. It is also frequently misdiagnosed. The cause of Grave’s disease is still not clear but it is believed that genes, gender and pregnancy may play vital roles. Also, there is a hereditary link present; when an identical twin comes down with Grave’s Disease, their twin has a 25-50% chance of developing the disease as well.

References

van Kinschot, C. M. J., Soekhai, V. R., de Bekker-Grob, E. W., Visser, W. E., Peeters, R. P., van Ginhoven, T. M., & van Noord, C. (2021). Preferences of patients and clinicians for treatment of Graves’ disease: a discrete choice experiment, European Journal of Endocrinology184(6), 803-812. Retrieved Mar 7, 2022, from https://eje.bioscientifica.com/view/journals/eje/184/6/EJE-20-1490.xml

Lee BC, Kang SI, Ahn YM, Doo HK, Ahn SY. An alternative therapy for graves’ disease: clinical effects and mechanisms of an herbal remedy. Biol Pharm Bull. 2008 Apr;31(4):583-7. Graves’ disease, the most common cause of hyperthyroidism, is an autoimmune disorder. Antithyroid drugs have been selected as the first-line treatment of Graves’ disease in Korea, Japan, and European countries. However, antithyroid drugs such as methimazole (MMI) and prophylthiouracil (PTU) have limitations in clinical applications because of their side effects. In this study, we performed a clinical trial and in vitro study to investigate the clinical effects and action mechanism of Ahnjeonbaekho-tang (AJBHT), an herbal remedy for Graves’ disease. In a clinical study of Graves’ disease patients who had side effects from antithyroid drugs, we found that treatment by AJBHT resulted in a reduction of serum triiodothyronine (T3) and free thyroxine (FT4) levels and an increase in thyroid stimulating hormone (TSH) levels (T3: p<0.0001, FT4: p=0.0012, TSH: p=0.0370, respectively). In vitro, AJBHT significantly inhibits FRTL-5 cell proliferation, DNA synthesis, cyclic AMP production, T4 synthesis, and the expression of thyroglobulin (Tg) mRNA in comparison with the control. These results suggest that AJBHT might suppress T(4) synthesis by modulating adenosine 3′,5′-cyclic monophosphate (cAMP) and Tg expression, and therefore, AJBHT could be an alternative therapy for Graves’ disease patients who have side effects from antithyroid drugs. doi: 10.1248/bpb.31.583. PMID: 18379045.  
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