Vitamin D and Endometriosis
Endometriosis is a chronic oestrogen-dependent inflammatory disease affecting roughly 10% of women of reproductive age. Vitamin D receptors are expressed in endometrial tissue, and vitamin D modulates several pathways implicated in the disease — immune regulation, cell proliferation, angiogenesis, and prostaglandin synthesis.
Observational data
Cross-sectional studies find lower 25(OH)D in women with endometriosis than in matched controls, and lower levels correlate with disease stage (rASRM) and pain severity. A 2018 case-control study reported women in the highest 25(OH)D quartile had a 24% lower odds of endometriosis than the lowest quartile.
RCT evidence
- Almassinokiani 2016 — 45 women post-laparoscopy; 50,000 IU cholecalciferol every 2 weeks for 12 weeks did not reduce pelvic pain vs placebo. Small trial.
- Nodler 2020 — pilot RCT of adolescents with dysmenorrhoea including endometriosis; vitamin D 60,000 IU/week reduced pain scores.
- 2020 meta-analysis — significant reduction in dysmenorrhoea VAS scores overall; endometriosis-specific data more limited.
Practical dosing
- Test 25(OH)D — many endometriosis patients are deficient.
- Correct to at least 30 ng/mL with 2,000–4,000 IU/day for 8–12 weeks.
- Vitamin D is not a substitute for evidence-based endometriosis therapy — NSAIDs, combined hormonal contraceptives, progestin-only options, GnRH agonists/antagonists, and laparoscopic excision remain the core interventions.
- Consider in the fertility workup — see the women's page.
Mechanism
Vitamin D suppresses NF-κB signalling in endometrial stromal cells, reduces cyclooxygenase-2 expression (which drives menstrual pain via PGE2), and modulates NK-cell function that may affect ectopic implant survival. It also increases VDR expression in endometriotic tissue, offering a plausible route for locally antiproliferative effects.