T3-only side effects

The problem with T3-only treatment is that one must usually take high doses of T3, which results in T3 levels above the reference range.  These high T3 levels compensate for the lack of T4 in the body.  People on thyroid internet forums that have been on T3-only protocols have reported the following side effects:

  • erythrocytosis (thick blood or high RBC, hematocrit, and hemoglobin) [34]
  • osteoporosis [35] – A study where subjects were given 50-75 μg of T3 showed increased bone resorption and fecal calcium loss.
  • muscle weakness [36,39] – (especially the thigh or upper arm muscles–difficult to climb stairs or rise from sitting; or to hold arms above head to wash hair)  A study found that doses of 60 μg/day or more of T3 enhanced muscle catabolism (breakdown) during fasting.  In other words, high T3 can cause muscle wasting.  The heart is a muscle and is not immune from this effect.
  • insulin resistance [37,38] – A study found that both plasma glucose and insulin increased after T3 ingestion, which is not a desirable effect. A correlation was found between higher Free T3 and Free T4 levels and insulin resistance in the early stages of Type 2 diabetes. [58]
  • fast heart rate or palpitations [39]
  • intolerance to exercise [39]
  • shortness-of-breath [39]
  • insomnia [39]
  • hair loss/thinning [39]
  • elevated liver enzymes (AST and/or ALT) [57]
  • brain fog or hyperthyroid dementia– can’t remember things that just happened, or trouble solving problems (math, scheduling. etc.) [40,41,59]

These are symptoms that anyone on T3-only therapy should be aware of, and are actually classic symptoms of hyperthyroidism.  Hypothyroidism presents with some of these same symptoms, so it can be difficult for patients to tell whether they are over or undermedicated.  Like hydrocortisone, there are side effects to this therapy that one should know about before undertaking this protocol.  Many have ended up feeling worse than before they started.  Because hydrocortisone helps one tolerate thyroid hormone, there is the potential problem of taking more and more hydrocortisone to tolerate more and more T3, ultimately resulting in a serious overdose of both hormones.  In fact, high T3 levels lowered cortisol levels to the point of adrenal insufficiency in hyperthyroid Graves’ patients.  Cortisol levels returned to normal when thyroid levels were brought back into the normal range with antithyroid medications. [61]

One of the dangers of T3-only therapy is the potential to “run out” of thyroid hormone in the event of an emergency.  The half-life of T3 is approximately one day, whereas the half-life of T4 is 5-7 days. [42]  Without any T4 reserves, constant T3 dosing is essential.  An incident where one was rendered unconscious or could not access their medication (natural disasters) would result in rapidly declining thyroid levels in the body after only 24 hours.  This severe hypothyroid state would hinder any recovery.

 

34. B. Brenner, J. Fandrey, W. Jelkmann. Serum immunoreactive erythropoietin in hyper- and hypothyroidism: Clinical observations related to cell culture studies. European Journal of Haematology.  Volume 53, Issue 1, pages 6–10, July 1994. http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0609.1994.tb00171.x/abstract

35. Steven R. Smith, Jennifer C. Lovejoy, George A. Bray, Jennifer Rood,Marlene M. Most, Donna H. Ryan. Triiodothyronine increases calcium loss in a bed rest antigravity model for space flight. Journal of Metabolism. Volume 57,Issue 12, Pages 1696-1703 (December 2008). http://www.metabolismjournal.com/article/S0026-0495%2808%2900283-7/abstract

36. Kenneth D. Burman, Leonard Wartofsky, Richard E. Dinterman, Phyllis Kesler and Robert W. Wannemacher Jr. The effect of T3 and reverse T3 administration on muscle protein catabolism during fasting as measured by 3-methylhistidine excretion.  Metabolism, Volume 28, Issue 8, August 1979, Pages 805-813.  http://www.ncbi.nlm.nih.gov/pubmed?term=454518

37. Gabriela Brenta. Diabetes and thyroid disorders.  British Journal of Diabetes & Vascular Disease 2010, 10: 172. http://dvd.sagepub.com/content/10/4/172.full.pdf

38. Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J. Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.  Am J Physiol. 1985 May;248(5 Pt 1):E593-601.  http://www.ncbi.nlm.nih.gov/pubmed/3887944?dopt=Abstract

39. Mihaela Simu, Elena Cecilia Rosca, Daniela Reisz. Thyroid Myopathy – A Case Study.  Timisoara Medical Journal.  Number 1-2 Year 2008. http://www.tmj.ro/article.php?art=3166304599124496#abstract

40. Toshiya Fukui, Yukihiro Hasegawa, Hiroki Takenaka. Hyperthyroid dementia: clinicoradiological findings and response to treatment.  Journal of the Neurological Sciences – 15 February 2001 (Vol. 184, Issue 1, Pages 81-88).  http://www.jns-journal.com/article/S0022-510X%2800%2900487-1/abstract

41. Karolina Jabłkowska, Małgorzata Karbownik-Lewińska, Katarzyna Nowakowska, Roman Junik, Andrzej Lewiński, Alina Borkowska. Working memory and executive functions in hyperthyroid patients with Graves’ disease. Archives of Psychiatry and Psychotherapy, 2009; 1 : 69–75.  http://www.archivespp.pl/uploads/images/2009_11_1/69_p_Archives_1_09.pdf

42. Lisandro Irizarry, Nadine A Youssef, Anton A Wray. Toxicity, Thyroid Hormone.  Emedicine.  Updated: Apr 23, 2010.  http://emedicine.medscape.com/article/819692-overview

43. Chopra IJ, Chopra U, Smith SR, Reza M, Solomon DH. Reciprocal changes in serum concentrations of 3,3′,5-triiodothyronine (T3) in systemic illnesses.  J Clin Endocrinol Metab. 1975 Dec;41(06):1043-9. http://www.ncbi.nlm.nih.gov/pubmed/812882

44. LoPresti JS, Gray D, Nicoloff JT. Influence of fasting and refeeding on 3,3′,5′-triiodothyronine metabolism in man.  J Clin Endocrinol Metab. 1991 Jan;72(1):130-6.  http://www.ncbi.nlm.nih.gov/pubmed/1986011

57. Kubota S, Amino N, Matsumoto Y, Ikeda N, Morita S, Kudo T, Ohye H, Nishihara E, Ito M, Fukata S, Miyauchi A. Serial changes in liver function tests in patients with thyrotoxicosis induced by Graves’ disease and painless thyroiditis. Thyroid. 2008 Mar;18(3):283-7.  http://www.ncbi.nlm.nih.gov/pubmed/18001177

58. Lambadiari V, Mitrou P, Maratou E, Raptis AE, Tountas N, Raptis SA, Dimitriadis G. Thyroid hormones are positively associated with insulin resistance early in the development of type 2 diabetes.  Endocrine. 2011 Feb;39(1):28-32. http://www.ncbi.nlm.nih.gov/pubmed/21072691

59. Ii Y, Ohira T, Narita Y, Kuzuhara S. [Transient dementia during hyperthyroidism of painless thyroiditis. A case report]. [Article in Japanese]  Rinsho Shinkeigaku. 2003 Jun;43(6):341-4.  http://www.ncbi.nlm.nih.gov/pubmed/14503353

61. Karl M, Onumah BM, Cole J, Golding J, Burman KD, Wartofsky L. Hypocortisolemia in Graves hyperthyroidism. Endocr Pract. 2009 Apr;15(3):220-4.  http://www.ncbi.nlm.nih.gov/pubmed/19364689