Testosterone Levels (Women) and Your Genetics

Written by Scott Peeples, BS Biomedical Sciences · ExomeDNA Founder Reviewed by ExomeDNA Editorial Process Last reviewed: May 26, 2026

Postmenopausal testosterone is shaped by a different set of biological processes than testosterone in younger women — primarily by peripheral conversion of adrenal androgens rather than direct ovarian synthesis. Genetic variants influencing the enzymes that govern this conversion, including those near AKR1C3 and AKR1D1, are among the heritable signals for testosterone concentrations in postmenopausal women identified through cross-ancestry genome-wide research in approximately 230,000 women from the UK Biobank.^[1] These enzyme variants help explain why testosterone levels in postmenopausal women vary substantially between individuals with otherwise similar health backgrounds. Below: how inherited enzyme variation shapes postmenopausal androgen biology, what population research shows, and what the evidence suggests about hormonal health after menopause.

What is postmenopausal testosterone?

Testosterone is a key androgen in women's physiology throughout life — not just before menopause. Before menopause, the ovaries contribute substantially to testosterone production alongside the adrenal glands. After menopause, ovarian hormone production declines dramatically, and testosterone levels shift to depend primarily on adrenal androgen production — particularly androstenedione — and its peripheral conversion to testosterone in non-gonadal tissues including adipose, liver, and muscle.

This peripheral conversion is carried out primarily by aldo-keto reductase enzymes, with AKR1C3 playing a central role: it catalyzes the conversion of androstenedione and other adrenal androgens into active testosterone in peripheral tissues. AKR1D1 — a steroid 5-beta reductase — participates in the parallel inactivation pathway, converting steroids into less active forms and influencing how much active testosterone is available in different tissues.

In postmenopausal women, absolute testosterone concentrations are lower than in premenopausal women, but testosterone continues to influence bone density, muscle mass, libido, energy levels, and mood. Its decline after menopause is one factor contributing to the musculoskeletal and quality-of-life changes many women experience in later decades. Genetic variation in the enzymes that synthesize and break down testosterone directly shapes how much circulating testosterone a postmenopausal woman's body maintains.

The genetics of testosterone in postmenopausal women

The genetic architecture of postmenopausal testosterone reflects the peripheral biology of androgen production after ovarian function declines. Loci near AKR1C3, which encodes aldo-keto reductase family 1 member C3, appear among the heritable signals for postmenopausal testosterone concentrations.^[1] AKR1C3 is expressed in adipose tissue, liver, and other peripheral tissues — precisely the sites where adrenal androstenedione is converted to testosterone after menopause. Variants in this region that alter enzyme activity or expression directly affect the efficiency of this peripheral synthesis pathway, influencing how much testosterone is produced from adrenal precursors.

229,966 women from the UK Biobank were analyzed in a cross-ancestry genome-wide study of sex hormone concentrations in pre- and postmenopausal women, identifying genetic loci for testosterone and other sex hormones across European and African ancestry cohorts.^[1]

AKR1D1 — aldo-keto reductase family 1 member D1, also called steroid 5-beta reductase — encodes an enzyme involved in the 5-beta reduction and inactivation of steroid hormones. Variants near AKR1D1 in the postmenopausal testosterone genetic landscape reflect how the inactivation side of steroid hormone metabolism is just as heritable as the synthesis side. Higher-activity variants at this locus may shift the equilibrium toward more rapid inactivation of active androgens, influencing the net testosterone balance.

GWAS signals for testosterone concentrations in postmenopausal women show enrichment in genes expressed in adipose tissue — consistent with peripheral adipose conversion of adrenal androgens being the dominant source of testosterone after menopause, and reflecting how inherited variation in peripheral enzyme activity shapes androgen levels in this life stage.^[1]

AKR1C2, which encodes another aldo-keto reductase family member involved in inactivating potent androgens including dihydrotestosterone, also appears in this trait's genetic landscape. Together, the AKR1C cluster of genes — AKR1C2 and AKR1C3 at adjacent genomic positions on chromosome 10 — reflects how the balance between androgen synthesis and inactivation in peripheral tissues is heritable, and how variants in this cluster influence the net androgen environment in postmenopausal women.

What the research says

Research base: Moderate. Cross-ancestry genome-wide analysis of postmenopausal testosterone provides an important evidence base — particularly for understanding sex hormone genetics in women outside European-ancestry populations, where earlier research was concentrated.^[1] The 229,966-participant UK Biobank study adds both scale and cross-ancestry breadth to the testosterone genetics literature for women. Moderate confidence reflects the current evidence resting primarily on a single large study for this specific postmenopausal phenotype, with further replication ongoing in the field. See our methodology page for how we evaluate and apply genetic evidence in your ExomeDNA profile.

An important note on interpretation: postmenopausal testosterone genetics specifically captures inherited factors influencing androgen levels in the post-ovarian context. These genetic signals are most applicable to the menopausal and postmenopausal transition — where the biology differs substantially from that governing testosterone in premenopausal women or in men.

How testosterone levels affect health after menopause

Testosterone remains a physiologically significant hormone in women after menopause, contributing to bone mineral density, lean muscle mass, sexual function, and mood. Its decline after menopause — both from lower gonadal production and from age-related changes in adrenal androgen output — is associated with changes in these domains over time.

Bone density is one of the clearest relationships: testosterone supports cortical bone formation, and lower androgen levels contribute to the accelerated bone loss that begins around menopause. Postmenopausal women with lower testosterone concentrations show more rapid bone density decline in some population studies, independent of estrogen levels.

Muscle mass maintenance is also relevant: testosterone is an anabolic hormone influencing protein synthesis and muscle fiber composition in both sexes, and its age-related decline contributes to the progressive muscle loss (sarcopenia) that accelerates after menopause.

Sexual function and libido are sensitive to androgen levels in women. The postmenopausal reduction in testosterone — partly genetic in its extent, as this trait captures — is one of the biological contributors to changes in libido and sexual responsiveness reported by many women in this life stage.

Because higher_is context-dependent for this trait, neither higher nor lower testosterone tendency carries a simple health interpretation. The effects of postmenopausal testosterone variation on specific health outcomes depend on the individual's broader hormonal, metabolic, and health context.

Working with your postmenopausal testosterone result

What research suggests about testosterone-supporting lifestyle factors in postmenopausal women

• Resistance training is the most evidence-backed modifiable factor for maintaining testosterone-driven anabolic signaling in postmenopausal women — strength exercise helps preserve muscle mass and bone density through pathways that partially overlap with androgen signaling.^[1]
• Dietary protein adequacy supports muscle protein synthesis; post-menopausal muscle preservation requires sufficient protein intake alongside exercise to compensate for lower anabolic hormone signaling.
• Body composition management: adipose tissue is the primary site of peripheral testosterone synthesis in postmenopausal women — the AKR1C3 pathway operates in adipose tissue. Healthy adipose tissue levels support peripheral androgen conversion, while excess adiposity can skew the hormonal environment toward estrogen through aromatase activity.
• Sleep quality matters for adrenal cortisol and DHEA rhythms that feed into the androgen precursor pool; disrupted sleep alters adrenal hormone output and may indirectly affect testosterone precursor availability.
• Nutritional support for adrenal health: zinc, magnesium, and healthy dietary fat provide substrates and cofactors for steroid hormone synthesis; deficiencies in these nutrients can limit adrenal androgen production.
• Hormone assessment with a clinician is the appropriate route for evaluating current testosterone status — serum total testosterone and SHBG measurement in a postmenopausal context provides the clinical picture that genetic estimates alone cannot supply.

Related traits and genes

Postmenopausal testosterone connects to several related traits in your ExomeDNA hormonal and bone health profile. Estrogen Metabolism shares the same steroid synthesis pathway — AKR1C enzymes participate in both estrogen and androgen interconversion, and the genetic architecture of postmenopausal estrogen and testosterone is partly overlapping. Bioavailable Testosterone covers the active fraction of testosterone relevant at any age, with AKR1C3 appearing across both traits. SHBG Levels directly modulates how much of whatever testosterone is produced remains bioavailable — SHBG tends to increase with age, reducing the active fraction even when total testosterone is maintained.

Across categories, Bone Density is a priority downstream trait — testosterone's direct anabolic effect on cortical bone makes genetic variation in postmenopausal testosterone directly relevant to bone health risk. Lean Muscle Mass is similarly downstream: the anabolic signaling that testosterone supports is a key determinant of muscle preservation in postmenopausal women. Vitamin D Metabolism interacts with the hormonal environment for bone protection, making these two traits important together for postmenopausal musculoskeletal health.

Frequently asked questions

How does testosterone change after menopause?

After menopause, ovarian hormone production declines substantially, and testosterone levels shift to depend primarily on adrenal gland androgen output — particularly androstenedione — and its peripheral conversion to testosterone by enzymes like AKR1C3 in adipose and other tissues. Total testosterone concentrations in postmenopausal women are lower than in premenopausal women on average, but the rate of decline and the level maintained vary substantially between individuals — and a meaningful portion of that variation is inherited, as this trait captures.

What role do AKR1C3 and AKR1D1 play in postmenopausal testosterone?

AKR1C3 is a peripheral testosterone synthesis enzyme: it converts adrenal-derived androstenedione and DHEA into active testosterone in adipose, liver, and muscle tissue. AKR1D1 (steroid 5-beta reductase) participates in the inactivation of steroid hormones, converting active steroids into reduced, less potent forms. Variants near both genes influence how efficiently this peripheral production-inactivation balance operates, directly shaping how much active testosterone is maintained in postmenopausal tissue environments.

Is testosterone important for women's health after menopause?

Yes. Testosterone continues to support bone mineral density, muscle mass, sexual function, and mood in women after menopause, even at lower absolute concentrations than in men. Population studies consistently link lower postmenopausal testosterone to faster bone density decline and muscle loss. It is one of several hormones — alongside estrogen and progesterone — that influence the trajectory of postmenopausal health, and its genetic architecture is a meaningful part of the broader postmenopausal hormonal picture.

Does genetic testosterone tendency in postmenopausal women affect health outcomes?

Genetic variants influencing postmenopausal testosterone levels are associated, at the population level, with differences in bone density, muscle mass, and other androgen-sensitive tissues. However, these are probabilistic population-level relationships — individual outcomes depend on the full hormonal, metabolic, and lifestyle context. Genetic susceptibility reflects a statistical tendency, not a fixed trajectory; lifestyle factors influencing adrenal health, exercise, nutrition, and body composition all modify how the inherited tendency translates into actual hormone levels.

Can lifestyle influence postmenopausal testosterone levels?

Yes, through several pathways. Resistance training supports anabolic signaling pathways that overlap with testosterone's effects. Body composition influences the peripheral AKR1C3 enzyme activity that synthesizes testosterone from adrenal precursors. Nutritional adequacy — particularly dietary fat, zinc, and protein — supports adrenal hormone precursor availability. Sleep and stress management affect adrenal cortisol and DHEA output, which feed the androgen precursor pool. Genetics shape the baseline tendency; lifestyle factors determine how that tendency expresses across years and decades.

References

1. Haas CB, et al. (2022). Cross-ancestry Genome-wide Association Studies of Sex Hormone Concentrations in Pre- and Postmenopausal Women. Endocrinology. PMID: 35192695. DOI: 10.1210/endocr/bqac034.

Data sources:

• GWAS Catalog (NHGRI-EBI, accessed 2026-05-26)
• Open Targets Platform (CC0 1.0, accessed 2026-05-26)
• ClinVar (NCBI, accessed 2026-05-26) — entries at ≥2-star review status
• ClinGen Gene-Disease Validity (CC0 1.0, accessed 2026-05-26)

This page is published by the ExomeDNA Research Team. Last reviewed: 2026-05-26.