Top 22 Reasons Not to Have RAI (Radio Active Iodine)
with permission from Jody
1. It’s permanent; once you swallow this there is no changing your mind and starting over.
2. Since the science is inexact and dosage a guess at best, it may take years to be fully effective, or it may have to be repeated (1)
3. Can bring on (induce or cause) thyroid storm as the dying gland “dumps” (releases) excess thyroid hormone and thyroid antibodies into the body; RAI also stimulates immune cells within the thyroid gland to produce more thyroid antibodies. (2)
4. Graves disease is an auto-immune disease, not a disease of the thyroid, so killing the thyroid doesn’t stop the disease process; without adequate thyroid tissue, the antibodies that cause hyperthyroidism may go on to affect orbital or dermal tissue, causing Graves’ ophthalmopathy and pretibial myxedema.
5. Results in hypothyroidism. Whoever said hypothyroidism is easy to treat, was mistaken. Because of the effects of thyroid antibodies, radiation-induced hypothyroidism is more difficult to treat than naturally occurring hypothyroidism. Hypothyroidism caused by treatment for hyperthyroidism is known to cause depression and anxiety. In one large Dutch study, “over one third of patients with a full-time job were unable to resume the same work after treatment. It appears that many of these patients are in need of psychological support. (3)
6. Being hypothyroid is neither less debilitating nor less dangerous than hyperthyroid. With hypothyroidism one is at risk of myxedema coma which can be more deadly than thyroid storm. This results from improper monitoring and labs tests, keeping us in a hypO state. After radiation-induced hypothyroidism develops, it takes only 6 weeks without thyroid replacement hormone for patients to fall into myxedema coma.
7. Increased antibody titers after RAI skew lab test results, adding to treatment difficulties. In particular, the widely-used TSH test is influenced by TSH receptor antibodies, causing falsely decreased levels.
8. RAI, aka spent nuclear fuel (“nuclear waste”, in other words) is absorbed by other organs and can cause cell death or DNA mutations. RAI is absorbed, in smaller amounts, by other organs besides the thyroid, including breast tissue, the genitals, pancreas, and the gastric mucosa.
9. For up to 4-8 weeks after dosage, we’re exposing those around us to radioiodine. This is demonstrated by patients registering measurable radioidine in airport and other screening devices.
10. Studies show an increase in cancers, especially of the thyroid gland and small bowel, after RAI. (4)
11. Possibility of damaging the parathyroid, causing hypoparathyroidism. (5)
12. RAI can cause difficulty with future attempts to become pregnant and carry pregnancies to term. RAI is known to affect the ovaries, which is why patients are recommended to avoid becoming pregnany for at least 6 months after RAI. The 6 months recommendation was increased to at least one year in early 2002
13. Chance of thyroid eye disease developing increases dramatically, as RAI doesn’t stop antibody production (6)
14. Chance of significant, unhealthy weight gain is increased Studies show that weight gain is inevitable after radioiodine-induced hypothyroidism (7)
15. Replacement hormone products currently on the market, both synthetic and glandular, are not comparable to our own hormone, and in some people, never feel “right”.
16. Ongoing problems as the gland gradually dies, necessitating close medical surveillance and replacement hormone dosage adjustments which usually does not happen unless a patient is educated and proactive in their disease and treatment. Within one year after RAI, most patients are on a dose of replacement hormone equivalent to 0.1mg levothyroxine; 5-6 years post RAI, most patients are on 0.175 mg levothyroxine because of the progression to autoimmune thyroid failure.
17. Increased risk of developing fibromyalgia like symptoms
18. For most GD patients, medication with ATD’s creates a euthyroid state similar to “normal life”, and can lead to long-term remission as well. (8)
19. As modern science explores the human genome, a cure for GD could be found, but after RAI kills the thyroid, it wouldn’t work. Current research is directed at modulating the cytokines, immune system chemicals released during the immune response and necessary for autoantibody production. Treatments of this nature are already being used successfully in Crohn’s disease.
20. I131 is so dangerous it’s transported in a lead container and kept at the hospital only for the briefest time before being dispensed by a doctor shielded in lead from head to toe.
21. When cats are given I-131, they must be kept in a contained facility for up to 6 weeks until they no longer set off warnings on a geiger counter, yet people, especially in the U.S.A. are released with in minutes of treatment on an unsuspecting population. Germany keeps I-131 patients for several days in a contained radiation facility until their radioactive numbers are in a *safe* level.
22. Salivary and tear duct damage from I-131 (10)
(1) Radioiodine Therapy of Graves Disease; Milton D. Gross, John E. Freitas, James C. Sisson and B. Shapiro, Chapter 11, Page 160
“Despite a clinical experience now amounting to many hundreds of thousands of patients treated with 131 I for GD, there is still no unanimity as to the selection of the appropriate dose of 131 I.”
(2) Graves Disease, Pathogenesis and Treatment, edited by Basil Rappoport and Sandra M. McLachlan, published by Kluwer Academic Publishers. ISBN 0-7923-7790-7. Chapter 11, RAI Therapy of GD, Complications and Risks of RAI, pg. 162 (Acute radiation thyroiditis; Exacerbations of thyrotoxicosis (transient)); pg. 164 (thyroid storm)
(3) Werner and Ingbar’s The Thyroid A Fundamental and Clinical Text, Eighth Edition, page 703:
“Hypothyroidism may be considered an inevitable consequence of RAI therapy, rather than a side effect”
This section goes on to state that
“Hypothyroidism may develop in as many as 90% of patients within the first year after therapy” (Ref 243 Cunnien AJ, Hay ID, Gorman CA et al. Radioiodine induced hypothyroidism in Graves’ disease: factors associated with the increasing incidence. J Nucl Med 1982; 23:978), with a continuing rate of 2% to 3% per year thereafter.
Graves’ Disease, Pathogenesis and Treatment, edited by Basil Rappoport and Sandra M. McLachlan, published by Kluwer Academic Publishers. ISBN 0-7923-7790-7. Chapter 11, RAI Therapy of GD, Complications and Risks of RAI, pg. 164,
“Eventual hypothyroidism is an expected consequence of 131I treatment for many patients with Graves’ disease and can occur within a few weeks, months, or years after treatment. Since permenant hypothyroidism eventually occurrs in 5-20% of patients with ATDs, 131 I appears to exaggerate the natural history of GD”.
(REF Cooper DS. 1998 Antithyroid drugs for treatment of hyperthyroidism. Endocrinal Metab Clin North Amer. 27: 225-248).
(4) Werner and Ingbar’s The Thyroid A Fundamental and Clinical Text, Eighth Edition, page 703:
“One report from the Co-operative Thyrotoxicosis follow up study, with a mean length of 21 years, did find an excess risk of death from thyroid carcinoma in patients receiving RAI for hyperthyroidism due to toxic multinodular goiter.”
(262 Ron E, Doody MM, Becker DV, et al. Cancer mortality following treatment for adult hyperthyroidism. JAMA 1998: 280; 347)., Page 704, Exposure of the rest of the body to RAI 131-I:
“The whole body is exposed to radiation after RAI therapy with gonadal radiation of particular concern because of gamma irradiation from RAI in urinary bladder”
Women with Thyroid Cancer at Risk for Breast Carcinoma
(5) Am J Surg 1984 Oct;148(4):441-5 Related Articles, Links Induction of hyperparathyroidism by radioactive iodine. Rosen IB, Palmer JA, Rowen J, Luk SC. PMID: 6486309 [PubMed – indexed for MEDLINE]
(6) Werner and Ingbar¹s The Thyroid A Fundamental and Clinical Text, Eighth Edition. Page 704 -705. “Based on these results, patients with Graves’ thyrotoxicosis should be counseled that eye disease is more likely to occur after radioiodine therapy than antithyroid drug (or surgical) therapy. They should also be counseled about the risks and benefits of adjunctive glucocorticoid therapy.”
Therapy of Graves Ophthalmopathy By Leonard Wartofsky, Matthew D.Ringel, and Kenneth D. Burman, Chapter 19, page 272:
“Since our ability to predict which patient will get worsening ophthalmopathy is poor at best, we would urge clinicians to be sensitive to a possible worsening of ophthalmopathy after Radioiodine, and to counsel their patients on the risk and to document that counselling had been given. Based upon many reports of rising TSH receptor antibody titers after 131 I as important to underlying pathophysiology, and upon the weight of randomised prospective studies (Ref. 110, 120, 121) there exists some basis to believe that Graves’ Ophthalmopathy may be worsened by RAI until proven otherwise”
(7) Is excessive weight gain after ablative treatment of hyperthyroidism due to inadequate thyroid hormone therapy?
(8) According to P.Reed Larsen, writing in Williams’ Clinical Textbook of Endocrinology, most patients can achieve remission with anti-thyroid drugs. The drugs are used to both lower thyroid hormone levels and mildly suppress the immune system until remission is achieved. Most side effects of these drugs are related to inappropriately high doses.
(9) Radioiodine therapy of Graves’ disease–quality assurance and radiation protection.
(10) Salivary and lacrimal gland dysfunction (sicca syndrome) after radioiodine therapy.