Reverse T3’s role in the body

Normal, healthy people produce reverse T3, it is not poison, and it is a normal pathway for the breakdown of T4.  It is actually abnormal to have no reverse T3! [7]

One purpose of reverse T3 is to reduce metabolism, to prevent starvation in cases of famine.  Anyone on a severe caloric restriction diet will reach a weight plateau at some point because reverse T3 naturally rises in this condition. [8]

Marathon athletes can also have high reverse T3 levels for the same reason—the body is trying to conserve energy to prevent starvation.  People on strict diets who overexercise should expect higher reverse T3 levels. [9]

Studies show that there are many other causes of high reverse T3 levels:

  • aging
  • burns/thermal injury
  • chemical exposure
  • cold exposure
  • chronic alcohol intake
  • free radical load
  • hemorrhagic shock (often from severe blood loss)
  • insulin-dependent diabetes mellitus
  • liver disease
  • kidney disease
  • severe or systemic illness
  • severe injury
  • stress
  • surgery
  • toxic metal exposure
  • certain drugs like amiodarone and beta blockers
  • and high cortisol. [10,11,12,13]

It’s much healthier to address and correct the conditions just listed, than to take T3 only.  Diabetics typically have high reverse T3 levels that drop once their glucose is controlled. [14]

Reverse T3 levels can appear high in someone whose liver is not healthy, because reverse T3 is processed and eliminated in the liver. [4,5]  There are anecdotal accounts from people who have a suboptimal reverse T3 ratio, with both FT3 and reverse T3 over mid-range, but who feel fine. As long as the FT3 was optimal for them, it didn’t matter what the reverse T3 level was.


4. Visser TJ. Role of sulfation in thyroid hormone metabolism.  Chem Biol Interact. 1994, Jun;92(1-3):293-303.

5. The relationship between the thyroid gland and the liver. QJM: An International Journal of Medicine, 2002, Volume 95, Issue 9, Pp. 559-569.

7. L. Gavin, J. Castle, F. Mcmahon, P. Martin, M. Hammond and R. R. Cavalieri. Extrathyroidal Conversion of Thyroxine to 3,3′,5′-Triiodothyronine (Reverse-T3) and to 3,5,3 ‘-Triiodothyronine. J Clin Endocrinol Metab, 1977, Vol. 44 (4): 733-742.

8. Douyon L, Schteingart DE. Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion.  Endocrinol Metab Clin North Am. 2002 Mar;31(1):173-89.

9. Sander M, Röcker L. Influence of marathon running on thyroid hormones.  Int J Sports Med. 1988 Apr;9(2):123-6.

10. Greg Kelly. Peripheral Metabolism of Thyroid Hormones: A Review. Alternative Medicine Review, August, 2000.

11. Jayne A. Franklyn, J. R. Davis, M. D. Gammage, W. A. Littler, D. B. Ramsden, M. C. Sheppard.  Amiodarone And Thyroid Hormone Action.  Clinical Endocrinology.  Volume 22, Issue 3, pages 257–264, March 1985.

12. Perrild, J. Mølholm Hansen, L. Skovsted, L. Korsgaard Christensen. Different Effects Of Propranolol, Alprenolol, Sotalol, Atenolol And Metoprolol On Serum T3 And Serum Rt3 In Hyperthyroidism. Clinical Endocrinology.  Volume 18, Issue 2, pages 139–142, February 1983.

13. Westgren, U., Ahrén, B., Burger, A., Ingemansson, S. and Melander, A. Effects of Dexamethasone, Desoxycorticosterone, and ACTH on Serum Concentrations of Thyroxine, 3, 5, 3′-Triiodothyronine and 3, 3‘, 5’-Triiodothyronine. Acta Medica Scandinavica, 202: 89–92. 1977.

14. Kabadi UM, Premachandra BN, Maayan M. Low serum 3, 5, 3′-triiodothyronine (T3) and raised 3, 3′, 5′-triidothyronine (reverse T3 or RT3) in diabetes mellitus: normalization on improvement in hyperglycemia.  Acta Diabetol Lat. 1982 Jul-Sep;19(3):233-42.