Testosterone in Women: What It Does, When It's Low, and Whether It Matters for the Heart

Women produce testosterone throughout their lives, with ovarian production contributing approximately 50% of circulating levels. The Women’s Healthy Ageing Project (2022) followed community-dwelling women for 15 years and found those in the lowest testosterone tertile had 2-fold higher risk of acute cardiovascular events compared to women with higher levels. This association persisted after adjustment for estradiol and conventional risk factors. The 2019 Global Consensus Position Statement now recognizes testosterone deficiency in women as a clinical entity, though cardiovascular outcome trials remain absent.

She had never heard a doctor mention women and testosterone in the same sentence. Her cardiologist said: you have two sex hormones. We’ve only been talking about one of them.

She was 54. Fatigue that sleep could not fix. Muscle mass disappearing despite resistance training. Libido gone. Her cholesterol panel had shifted in ways her doctor called “typical for menopause.” Her total testosterone came back at 8 ng/dL. The lab flagged it as low. Her physician had no protocol for what to do next.

This is the blind spot. Women’s cardiovascular medicine has focused almost exclusively on estrogen. The conversation about hormone therapy centers on estrogen and progesterone. The research dollars follow. But women make testosterone. They make it every day of their lives. And when it disappears, something changes in the vessels, the muscles, and the metabolic machinery that protects the heart.

The Testosterone Women Were Never Told About

In premenopausal women, the ovaries produce approximately 50% of circulating testosterone. The adrenal glands contribute 25%. The remaining 25% comes from peripheral conversion of androstenedione in fat and muscle tissue Longcope 1986. The cells responsible are the theca interna cells surrounding each ovarian follicle.

The numbers matter. Normal total testosterone in reproductive-age women ranges from 15 to 70 ng/dL. In men, the range is 300 to 1,000 ng/dL Bhasin 2011. Women operate at roughly 5% of male testosterone levels. This small amount is not negligible. It is precisely calibrated.

Here is what most clinicians miss: testosterone decline in women begins decades before menopause. Total testosterone drops by approximately 50% between ages 20 and 40 Davison 2005. The steepest decline occurs in the third decade of life. By the time a woman reaches perimenopause, she has already lost half her testosterone. Menopause takes what remains.

Bilateral oophorectomy creates a different scenario entirely. Surgical removal of both ovaries causes immediate 50% reduction in circulating testosterone. The adrenal glands cannot compensate Laughlin 2000. A woman who undergoes oophorectomy at 40 experiences a hormonal amputation that natural menopause at 52 cannot replicate. The cardiovascular implications of this abrupt transition are covered in detail in surgical menopause cardiovascular crash.

The Cardiovascular Signal We Ignored

The Women’s Healthy Ageing Project (WHAP) is the study that changed the conversation. Researchers followed community-dwelling Australian women, mean age over 70, for approximately 15 years. They measured total testosterone at baseline and tracked cardiovascular events.

The finding: women in the lowest tertile of total testosterone had a 2-fold higher risk of acute cardiovascular events compared to women with higher testosterone levels (hazard ratio approximately 2.0, 95% CI 1.2 to 3.3) Bell 2022. This association held after adjustment for age, BMI, smoking, diabetes, hypertension, and estradiol levels.

The same study documented the metabolic profile accompanying low testosterone. Women in the lowest tertile had lower HDL cholesterol and higher triglycerides. These lipid changes occurred independent of estradiol status and traditional cardiovascular risk factors.

The Study of Women’s Health Across the Nation (SWAN) identified the metabolic mechanism. Women in the lowest quartile of free testosterone had 1.7-fold higher odds of developing metabolic syndrome (95% CI 1.2 to 2.4) compared to women in the highest quartile Janssen 2010. The primary driver was increased visceral adiposity. Low testosterone predicted fat accumulation in the abdomen, around the organs, where metabolic damage accelerates.

A systematic review and meta-analysis by Panico et al. (2020) confirmed the pattern across multiple populations. Circulating androgens in women correlate inversely with metabolic syndrome components. Lower testosterone means higher fasting glucose, higher triglycerides, lower HDL, and larger waist circumference Panico 2020.

The data establish association, not causation. No randomized trial has tested whether restoring testosterone in women with low levels prevents cardiovascular events. This is the gap. We know low testosterone correlates with cardiac risk. We do not yet know if treating low testosterone reduces that risk.

What Low Testosterone Actually Does to a Woman’s Body

The clinical presentation of testosterone deficiency in women is non-specific but recognizable once you know the pattern. The 2019 Global Consensus Position Statement identified the core features: persistent fatigue unresponsive to rest, reduced motivation, depressed mood, and diminished sense of well-being Davis 2019. These symptoms overlap with perimenopause, depression, thyroid dysfunction, and chronic illness. Context matters.

The sexual domain is where the evidence is strongest. Hypoactive sexual desire disorder in postmenopausal women responds to testosterone therapy. A systematic review and meta-analysis of randomized controlled trials found testosterone increased satisfying sexual events by approximately 0.85 per month (95% CI 0.52 to 1.18) and improved desire and arousal scores Islam 2019. The effect size is modest but real.

Muscle is the overlooked casualty. Testosterone is anabolic. It builds and maintains skeletal muscle. Women lose approximately 3% to 8% of their muscle mass per decade after age 30. The decline accelerates after menopause. Low testosterone compounds this loss. Sarcopenia, the clinical term for pathologic muscle loss, predicts falls, fractures, disability, and death. It also predicts heart failure with preserved ejection fraction, the predominant heart failure phenotype in older women.

The connection between muscle, metabolism, and cardiovascular risk is direct. Skeletal muscle is the largest glucose disposal organ in the body. Less muscle means less capacity to clear glucose from the bloodstream. Less glucose clearance means higher insulin levels. Higher insulin levels drive fat storage, inflammation, and vascular dysfunction. This cascade links testosterone deficiency to the metabolic syndrome that precedes cardiovascular disease.

Women don’t die from what they have. Women die from what they hold.

The metabolic burden accumulates silently. Visceral fat secretes inflammatory cytokines. Insulin resistance stresses the endothelium. HDL drops. Triglycerides rise. The vascular system ages faster than the calendar suggests. By the time cardiovascular disease declares itself, the damage spans decades.

For strategies to preserve muscle mass during this transition, see creatine for women over 40. For a complete overview of the metabolic changes driving cardiovascular risk, see metabolic syndrome in women explained.

The Evidence for Testosterone Therapy in Women

The 2019 Global Consensus Position Statement represents the current scientific agreement. Testosterone therapy is indicated for postmenopausal women with hypoactive sexual desire disorder after other causes have been excluded Davis 2019. The recommended approach: transdermal testosterone at doses that maintain testosterone levels within the normal premenopausal range. No other indication has sufficient evidence.

The 2024 updated recommendations from the Endocrine Society and International Society for the Study of Women’s Sexual Health (ISSWSH) reinforce this position Wierman 2024. The expert panel acknowledges testosterone deficiency in women as a clinical entity. It recommends against testosterone therapy for non-sexual indications including fatigue, mood, cognition, and cardiovascular protection. The evidence is not there.

What the trials show: testosterone therapy in postmenopausal women at physiologic doses is well-tolerated. The Islam et al. meta-analysis (2019) found no significant increase in adverse events including acne, hair growth, voice changes, or cardiovascular events in trials lasting up to 24 months. Longer-term safety data do not exist.

The formulation matters. Transdermal testosterone, typically a cream or gel applied daily, allows dose titration and maintains stable blood levels. Oral testosterone undergoes first-pass hepatic metabolism and is not recommended. Injectable testosterone produces supraphysiologic peaks followed by troughs, creating an unstable hormonal environment.

Testosterone pellets deserve specific mention because they have become widely marketed. Pellets are compressed testosterone cylinders implanted subcutaneously. They deliver testosterone for 3 to 6 months. The problems: dosing is imprecise, levels cannot be adjusted once implanted, and pellets frequently produce supraphysiologic testosterone concentrations. The Global Consensus Statement specifically recommends against testosterone pellets in women.

(Evidence: 3/Early for cardiovascular outcomes; 5/Solid for sexual function)

The gap between what we know and what we need to know is substantial. We have strong observational data linking low testosterone to cardiovascular risk. We have randomized trial data showing testosterone improves sexual function. We have no randomized trial data showing testosterone prevents heart attacks or strokes. Until that trial exists, testosterone therapy for cardiovascular protection remains speculative.

For a comparison of different hormone therapy formulations and their cardiovascular implications, see MHT types comparison.

The Clinical Framework: Testosterone as a Metabolic Marker

I use what I call the Androgen-Metabolic Axis assessment in my practice. The framework recognizes testosterone not primarily as a treatment target but as a metabolic signal.

Low testosterone in a woman tells me something about her metabolic health. It correlates with visceral adiposity, insulin resistance, and inflammatory burden. The question is not simply “is testosterone low?” but “what metabolic dysfunction accompanies this low level?”

The practical application: when I measure testosterone in a postmenopausal woman or a woman after oophorectomy, I also measure fasting insulin, fasting glucose, hemoglobin A1c, triglycerides, HDL, and high-sensitivity C-reactive protein. I want the metabolic context.

If testosterone is low and metabolic markers are abnormal, the path forward involves metabolic intervention first. Dietary modification targeting insulin sensitivity. Resistance training to build muscle mass. Sleep optimization to restore hormonal rhythms. Weight management to reduce visceral fat. These interventions can improve testosterone levels independent of exogenous hormone therapy.

If testosterone is low, metabolic markers are abnormal, and the woman has hypoactive sexual desire disorder affecting quality of life, testosterone therapy enters the conversation. The discussion includes: physiologic dosing, transdermal formulation, regular monitoring of testosterone levels to ensure they remain in the normal female range, and reassessment of benefits and risks at 6-month intervals.

If testosterone is low but metabolic markers are normal and sexual function is preserved, I monitor. Low testosterone in this context is a marker to track, not a problem requiring immediate treatment.

The cardiovascular calculation: treating the metabolic dysfunction almost certainly reduces cardiovascular risk. Treating low testosterone might reduce cardiovascular risk. We should prioritize interventions with proven benefit while remaining open to interventions with promising but unproven benefit.

What Happens at Menopause and After

The menopausal transition involves estrogen decline. This is the familiar story. But testosterone also changes, and the pattern differs.

Testosterone does not fall abruptly at menopause the way estrogen does. The ovaries continue producing some testosterone even after they stop producing estrogen. The dramatic testosterone decline occurred earlier, in the thirties. What menopause adds is the loss of estrogen’s moderating influence on testosterone action.

The practical result: some women experience relative androgen excess after menopause. Their testosterone levels are low by absolute standards but high relative to their estrogen levels. This imbalance can manifest as facial hair growth, acne, and scalp hair thinning. It does not mean testosterone is too high. It means the estrogen-testosterone ratio has shifted.

Surgical menopause creates a different picture entirely. Oophorectomy removes the primary testosterone production site. The adrenal contribution continues, but it cannot compensate for the ovarian loss. Women who undergo bilateral oophorectomy before natural menopause experience the most profound testosterone deficit.

The perimenopause window deserves particular attention. Women in perimenopause have irregular estrogen fluctuations overlaid on already-low testosterone. The metabolic consequences compound. Insulin resistance accelerates. Visceral fat accumulates. The cardiovascular risk trajectory steepens. For a detailed analysis of this transition, see perimenopause cardiovascular risk.

The Questions You Should Ask

At your next appointment, request a complete hormone panel if you are perimenopausal, postmenopausal, or have had your ovaries removed. The panel should include: total testosterone, free testosterone (calculated or measured by equilibrium dialysis), SHBG (sex hormone binding globulin), estradiol, FSH, and LH.

Add the metabolic markers: fasting insulin, fasting glucose, hemoglobin A1c, complete lipid panel including triglycerides and HDL, and high-sensitivity CRP.

If your testosterone is below 15 ng/dL and you have symptoms consistent with androgen deficiency, particularly if those symptoms include low libido, ask about the evidence for testosterone therapy. Understand that the indication with strongest evidence is hypoactive sexual desire disorder. Understand that cardiovascular benefit is biologically plausible but not proven in randomized trials.

If testosterone therapy is discussed, insist on transdermal formulation at physiologic doses. Testosterone levels should be monitored at 3 to 6 week intervals initially to ensure they remain in the normal female range (15 to 70 ng/dL). Decline pellet testosterone.

Document your baseline. Track your metabolic markers over time. The trajectory tells you more than any single measurement. Improving metabolic health improves cardiovascular outcomes regardless of testosterone status.

The conversation about testosterone in women is overdue. The evidence is incomplete. But the biology is clear: women make this hormone, they lose it as they age, and its absence correlates with metabolic and cardiovascular dysfunction. That correlation deserves clinical attention, not clinical silence.

Frequently Asked Questions

What is the normal testosterone level for women?

Normal total testosterone in reproductive-age women ranges from 15 to 70 ng/dL (0.5 to 2.4 nmol/L). This is approximately 5% of the male range of 300 to 1,000 ng/dL. The reference range varies slightly between laboratories based on the assay used. Free testosterone, the biologically active fraction, is typically 1% to 2% of total testosterone. Levels decline naturally with age, dropping approximately 50% between ages 20 and 40, with further reduction after menopause. Values below 15 ng/dL in a symptomatic woman warrant clinical attention and metabolic evaluation.

Does low testosterone increase heart disease risk in women?

Observational studies consistently link low testosterone to cardiovascular risk in women. The Women’s Healthy Ageing Project (2022) followed women for 15 years and found those in the lowest testosterone tertile had 2-fold higher risk of acute cardiovascular events. The SWAN study found low free testosterone associated with 1.7-fold higher odds of metabolic syndrome. The mechanism involves increased visceral fat, insulin resistance, lower HDL, and higher triglycerides. However, no randomized trial has tested whether testosterone replacement prevents cardiovascular events in women. The association is strong; causation remains unproven.

Should women take testosterone for heart health?

Current evidence does not support testosterone therapy specifically for cardiovascular protection in women. The 2019 Global Consensus Position Statement and 2024 Endocrine Society guidelines recommend testosterone only for hypoactive sexual desire disorder in postmenopausal women, using transdermal formulations at physiologic doses. While low testosterone correlates with cardiovascular risk, we lack randomized trial data showing treatment reduces that risk. Addressing the metabolic dysfunction accompanying low testosterone through diet, exercise, and weight management has proven cardiovascular benefit and should be prioritized.

What happens to testosterone after surgical menopause?

Bilateral oophorectomy causes immediate 50% reduction in circulating testosterone because the ovaries produce approximately half of a woman’s testosterone. The adrenal glands continue their contribution but cannot compensate for the ovarian loss. This abrupt decline differs from natural menopause, where testosterone falls more gradually and the ovaries continue producing small amounts even after estrogen production ceases. Women who undergo oophorectomy before natural menopause experience the most profound testosterone deficit, and this may accelerate metabolic dysfunction and cardiovascular risk.

Are testosterone pellets safe for women?

The 2019 Global Consensus Position Statement specifically recommends against testosterone pellets in women. Pellets deliver unpredictable doses that cannot be adjusted once implanted. Studies show pellets frequently produce supraphysiologic testosterone levels, sometimes exceeding the normal female range by 2 to 4 times. Elevated testosterone can cause irreversible side effects including voice deepening, clitoral enlargement, and male-pattern hair loss. Transdermal testosterone (cream or gel) allows precise dosing, easy adjustment, and stable blood levels within the physiologic female range. If testosterone therapy is indicated, transdermal formulation is the evidence-based choice.