ENDOMETRIOSIS — GENETIC RISK

Endometriosis Genetic Risk — affecting 1 in 10 women of reproductive age with approximately 50% heritability and an average diagnostic delay of 7-10 years, where genetic risk awareness can accelerate the path to diagnosis and treatment.

Whole genome sequencing evaluates all identified endometriosis risk variants — WNT4, GREB1, CDKN2B-AS1, ESR1, and 40+ GWAS loci — providing a genetic risk profile that supports clinical suspicion in the setting of chronic pelvic pain and infertility.

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About this condition

Endometriosis — Genetic Risk

Endometriosis is a chronic inflammatory condition in which endometrial-like tissue grows outside the uterus — on the peritoneum, ovaries, bowel, bladder, and occasionally at distant sites. It affects approximately 190 million women worldwide (~10% of reproductive-age women), causing chronic pelvic pain, dysmenorrhea, dyspareunia, and infertility. Despite its prevalence, endometriosis has an average diagnostic delay of 7-10 years from symptom onset — one of the longest diagnostic delays of any common condition — because symptoms overlap with many other conditions and definitive diagnosis historically required laparoscopic surgery.

Endometriosis has strong genetic underpinnings — approximately 50% heritability based on twin studies, with first-degree relatives of affected women having 7-10x increased risk. Genome-wide association studies have identified >40 risk loci, including WNT4 (a key regulator of female reproductive tract development), GREB1 (a growth regulator involved in estrogen signaling), CDKN2B-AS1 (cell cycle regulation, also associated with endometrial cancer risk), ESR1/ESR2 (estrogen receptors), VEZT (cell adhesion), and FN1 (fibronectin — extracellular matrix remodeling). Polygenic risk scores combining these variants can identify women at 2-4x elevated relative risk.

While endometriosis is polygenic (no single gene is causative), genetic risk profiling has important clinical utility. In a woman presenting with chronic pelvic pain and infertility, elevated genetic risk for endometriosis can support clinical suspicion and accelerate referral for specialist evaluation — potentially reducing the devastating 7-10 year diagnostic delay. Additionally, emerging evidence suggests that genetic subtypes of endometriosis may respond differently to hormonal therapies (GnRH agonists, aromatase inhibitors, progestins) and surgical approaches — early steps toward genetically informed endometriosis treatment.

First-degree relatives of women with endometriosis have 7-10x increased risk. If you have a mother or sister with endometriosis and experience chronic pelvic pain, genetic and clinical evaluation should not wait for the typical 7-10 year diagnostic delay.

Gene locus
WNT4 (1p36.12), GREB1 (2p25.1), CDKN2B-AS1 (9p21.3), ESR1 (6q25.1-q25.2), VEZT (12q22), FN1 (2q35)

Endometriosis takes 7-10 years to diagnose on average. Genetic risk profiling can support earlier clinical suspicion in women with symptoms — cutting through the diagnostic delay that causes years of unnecessary suffering.

Genetic risk profiling accelerates the diagnostic pathway — reducing the 7-10 year delay that characterizes endometriosis diagnosis

Women with symptoms suggestive of endometriosis (chronic pelvic pain, painful periods, painful intercourse, infertility) often see multiple physicians over many years before the diagnosis is made. An elevated polygenic risk score for endometriosis — particularly in combination with family history — provides objective genetic evidence supporting clinical suspicion and specialist referral. This genetic information shifts the clinical calculation from 'watch and wait' toward 'investigate and treat' — potentially eliminating years of diagnostic limbo.

Emerging evidence links endometriosis genetic subtypes to differential treatment response — the foundation for precision endometriosis medicine

Preliminary research suggests that endometriosis associated with specific genetic risk variants may respond differently to hormonal therapies. WNT4 pathway-associated endometriosis may have different biology than GREB1/estrogen-signaling-associated endometriosis — with potential implications for choice between progestins, GnRH agonists, and aromatase inhibitors. While this pharmacogenomic endometriosis research is still emerging, establishing a patient's complete genetic profile through WGS creates a permanent resource for ongoing clinical reanalysis as precision endometriosis medicine matures.

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