FAI is a calculated snapshot of bioavailable testosterone
The Free Androgen Index (FAI) is a calculated number derived from a blood test; it is not a hormone itself. It uses two measured players: total testosterone, the main androgen made primarily by the testes or ovaries and also by the adrenal glands, and sex hormone–binding globulin (SHBG), a transport protein produced by the liver. By combining these two, FAI provides a shorthand view of how much testosterone is present relative to the body’s binding capacity (total testosterone and SHBG).
FAI matters because it estimates the share of testosterone that is readily available to tissues—the portion not tightly sequestered by SHBG and thus more able to enter cells and engage androgen receptors (free or bioactive testosterone). In simple terms, it reflects the balance between androgen supply and the proteins that carry and limit it, offering a practical snapshot of androgen bioavailability. This gives context to how strongly androgen signals may be felt across the body—affecting features like hair growth, skin oiliness, muscle and bone support, and aspects of libido and energy—without directly measuring the tiny unbound fraction.
Why the testosterone-to-SHBG balance carries clinical weight
The Free Androgen Index (FAI) estimates how much testosterone is available to act on tissues by relating total testosterone to sex hormone–binding globulin (SHBG). Because androgens shape muscle and bone, red blood cell production, skin and hair, mood, metabolism, and reproductive function, FAI gives a systems-level view of androgen signaling rather than just hormone supply.
Big picture: FAI integrates signals from the gonads, liver, thyroid, and metabolic state. It complements total testosterone to flag androgen excess or deficiency that influences fertility, bone and muscle health, and, especially in women, long-term metabolic and cardiovascular risk.
What low, mid-range, and high FAI usually point to
Reference intervals vary by lab, age, and sex: in adult women typical values are very low; in adult men they are several-fold higher. During pregnancy and with estrogen therapy, SHBG rises and FAI runs lower; in puberty it rises. For most people, results clustered near the middle of the sex- and age-specific range align most appropriate with balanced physiology.
When FAI is low, either testosterone is low or SHBG is high (as with estrogen exposure, hyperthyroidism, liver conditions, or undernutrition). Tissue-level androgen tone falls, and people may notice reduced strength, lower libido, low energy, and thinner bones over time. Men can have features of hypogonadism; women may experience low sexual desire and arousal; boys may show delayed pubertal progression.
When FAI is high, testosterone is elevated or SHBG is suppressed (commonly with insulin resistance, obesity, hypothyroidism, or androgen medications). Androgen-sensitive organs are overstimulated: women often develop acne, hirsutism, scalp hair thinning, and irregular or absent ovulation, as seen in polycystic ovary syndrome; men may show acne, oily skin, and hair loss.
Low values usually reflect either too little testosterone production or disproportionately high SHBG, which binds and reduces available hormone. In men this aligns with androgen deficiency physiology (lower libido and vigor, reduced muscle and hematocrit, lower bone turnover). In women it indicates low androgen availability (lower sexual desire, fatigue, reduced lean mass); during pregnancy FAI is typically low due to high SHBG.
Being in range suggests balanced androgen signaling relative to SHBG, supporting stable metabolic, musculoskeletal, cardiovascular, and reproductive function. In practice, values near the middle of the sex- and age-specific reference interval commonly align with eugonadal physiology when symptoms are absent.
High values usually reflect either excess testosterone or disproportionately low SHBG. In women this often signals androgen excess physiology (acne, hirsutism, ovulatory dysfunction) and can track with insulin resistance, commonly seen in polycystic ovary syndrome. In men it may reflect exogenous androgens or low SHBG states and can associate with increased erythropoiesis and oilier skin.
Where SHBG biology and assay choice complicate the number
FAI is a surrogate and depends heavily on SHBG; it is most useful in women. In men, calculated free testosterone or equilibrium dialysis is preferred when available. SHBG shifts with estrogen exposure, thyroid and liver status, insulin resistance/obesity, and pregnancy. Morning sampling and assay method affect interpretation.
Companion markers for a fuller androgen picture
FAI is best read with total testosterone, SHBG, and DHEAS, plus symptom context. Together these clarify whether a shift reflects gonadal output, adrenal androgens, or a binding-protein change, and help guide PCOS workup, fertility planning, or treatment tracking.
FAQs
FAI testing calculates a ratio from total testosterone and SHBG — FAI = (Total Testosterone ÷ SHBG) × 100 — to estimate how much androgen is available to tissues.
SHBG strongly influences how much testosterone is usable. FAI helps clarify symptoms related to androgen imbalance, supports PCOS assessment in females, flags low-androgen states in males, and tracks how medications or lifestyle changes affect SHBG and androgen exposure.
Establish a baseline, then recheck after meaningful changes (for example, 8–12 weeks after adjusting training, weight, or medications). For ongoing monitoring, many people retest every 3–6 months. Test in the early morning if male, and use consistent cycle timing if female.
FAI shifts with factors that alter SHBG or total testosterone, including thyroid status, liver function, insulin resistance, obesity, aging, oral estrogens (e.g., contraceptives), androgens, pregnancy, acute illness, and significant weight or training changes.
FAI itself does not require fasting. For appropriate consistency, males test in the morning; females should test at a consistent cycle phase (often early follicular) or maintain the same timing across tests.
Superpower currently offers at-home blood testing in the following states: Alabama, Arizona, California, Colorado, Connecticut, Delaware, District of Columbia, Florida, Georgia, Idaho, Illinois, Indiana, Kansas, Maine, Maryland, Massachusetts, Michigan, Minnesota, Missouri, Montana, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, South Carolina, Tennessee, Texas, Utah, Vermont, Virginia, Washington, West Virginia, and Wisconsin.
We’re actively expanding nationwide, with new states being added regularly. If your state isn’t listed yet, stay tuned.
References
- Rosner, W., Auchus, R. J., Azziz, R., Sluss, P. M., & Raff, H. (2007). Position statement: Utility, limitations, and pitfalls in measuring testosterone: An Endocrine Society position statement. The Journal of Clinical Endocrinology & Metabolism, 92(2), 405-413. https://doi.org/10.1210/jc.2006-1864
- Laurent, M. R., Hammond, G. L., Blokland, M., Jardí, F., Antonio, L., Dubois, V., Khalil, R., Sterk, S. S., Gielen, E., Decallonne, B., Carmeliet, G., Kaufman, J.-M., Fiers, T., Huhtaniemi, I. T., Vanderschueren, D., & Claessens, F. (2016). Sex hormone-binding globulin regulation of androgen bioactivity in vivo: Validation of the free hormone hypothesis. Scientific Reports, 6, 35539. https://doi.org/10.1038/srep35539
- Teede, H. J., Tay, C. T., Laven, J., Dokras, A., Moran, L. J., Piltonen, T. T., Costello, M. F., Boivin, J., Redman, L. M., Boyle, J. A., Norman, R. J., Mousa, A., & Joham, A. E. (2023). Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertility and Sterility, 120(4), 767-793. https://doi.org/10.1016/j.fertnstert.2023.07.025
- Hammond, G. L. (2016). Plasma steroid-binding proteins: Primary gatekeepers of steroid hormone action. The Journal of Endocrinology, 230(1), R13-R25. https://doi.org/10.1530/JOE-16-0070
- Marques, P., De Sousa Lages, A., Skorupskaite, K., Rozario, K. S., Anderson, R. A., & George, J. T. (2024). Physiology of GnRH and gonadotrophin secretion. In Endotext. MDText.com. https://www.ncbi.nlm.nih.gov/books/NBK279070/






































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