The genes governing how your body produces and converts sex hormones determine your baseline hormonal environment.
Aromatase activity, DHT conversion rate, steroid biosynthesis capacity, and vitamin D receptor efficiency. Four variants with direct implications for hormone optimization.
The Biology
Sex hormones are not produced at fixed rates. Their synthesis and interconversion is regulated by enzymatic pathways encoded by genes that vary between individuals. The same testosterone molecule will be converted to estradiol at different rates in two people with different CYP19A1 aromatase activity. The same testosterone will be converted to DHT at different rates depending on SRD5A2 5-alpha reductase activity. These differences have implications for hormone optimization, fertility, hormone-sensitive conditions, and pharmacological interventions.
What Varia Analyzes
Four variants governing the primary sex hormone synthesis and conversion enzymes. CYP19A1/aromatase (rs4646), which controls the rate of testosterone-to-estrogen conversion; SRD5A2 (rs523349), which governs DHT production from testosterone via 5-alpha reductase type 2 and mirrors the pharmacological mechanism of finasteride; CYP17A1 (rs743572), which regulates a rate-limiting step in both androgen and estrogen biosynthesis; and VDR Fok1 (rs2228570), which determines vitamin D receptor transcriptional efficiency. Vitamin D functions as a steroid hormone with direct effects on sex hormone production, calcium metabolism, and immune modulation.
Why It Matters
For individuals pursuing testosterone optimization or managing estrogen levels, the CYP19A1 and SRD5A2 findings directly inform the expected degree of aromatization and DHT conversion at a given testosterone level. The VDR Fok1 finding provides context for how efficiently your receptor responds to a given 25(OH)D level. Relevant for anyone supplementing vitamin D, which encompasses most of the population in northern latitudes.
Key sources
- Haiman CA, et al. Genetic variation at the CYP19A1 locus predicts circulating estrogen levels. Cancer Res. 2007.
- Makridakis NM, et al. Association of mis-sense substitution in SRD5A2 gene with prostate cancer. Lancet. 1999.
- Arai H, et al. A vitamin D receptor gene polymorphism in the translation initiation codon: effect on protein activity. J Bone Miner Res. 1997.