Progestin vs. Progesterone

Progestin vs. Progesterone names the difference between two kinds of drugs used in reproductive care. Progesterone is the hormone that the body makes after ovulation. Progestins are synthetic drugs built to act like it on the lining of the uterus. They are the active ingredient in most suppressive medications and in many hormone treatments. Progestins are not built like progesterone. Many progestins also bind other hormone receptors, including the receptors for androgens, stress hormones, and salt balance.1 Action on those extra receptors may explain some of their side effects.1

Bioidentical (isomolecular) progesterone has the same structure as the progesterone that the body makes. Progesterone also acts on more than one receptor. It strongly blocks the salt-balance receptor (the mineralocorticoid receptor).2 Progesterone and the progestins differ in structure and in how tightly they bind each receptor. They also differ in their effects on the breast, bone, blood vessels, and nerves. They do not act as one class.3 One example is medroxyprogesterone acetate. In laboratory tests on immune cells, it acts on the stress-hormone receptor. It quiets inflammatory genes at levels found in women who use it. Progesterone does not.4 In Restorative Reproductive Medicine, clinicians generally favor the body's own progesterone when progesterone support is needed. The restorative principle is to work with the body's own chemistry rather than override it. Each compound carries its own safety record and its own effects. The two are not swappable.

Cited in this entry

  1. Africander D, Verhoog N, Hapgood JP. Molecular mechanisms of steroid receptor-mediated actions by synthetic progestins used in HRT and contraception. Steroids. 2011;76(7):636-52. Steroids. https://pubmed.ncbi.nlm.nih.gov/21414337/
  2. Quinkler M, Bumke-Vogt C, Meyer B, Bahr V, Oelkers W, Diederich S. The human kidney is a progesterone-metabolizing and androgen-producing organ. J Clin Endocrinol Metab. 2003;88(6):2803-9. The Journal of Clinical Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/12788891/
  3. Stanczyk FZ, Hapgood JP, Winer S, Mishell DR Jr. Progestogens used in postmenopausal hormone therapy: differences in their pharmacological properties, intracellular actions, and clinical effects. Endocr Rev. 2013;34(2):171-208. Endocrine Reviews. https://pubmed.ncbi.nlm.nih.gov/23238854/
  4. Hapgood JP, Ray RM, Govender Y, Avenant C, Tomasicchio M. Differential glucocorticoid receptor-mediated effects on immunomodulatory gene expression by progestin contraceptives: implications for HIV-1 pathogenesis. Am J Reprod Immunol. 2014;71(6):505-12. American Journal of Reproductive Immunology. https://pubmed.ncbi.nlm.nih.gov/24547700/

This content is for educational purposes only and does not constitute medical advice. Consult an RRM clinician or healthcare provider for guidance specific to your situation.