Low Androgens in Females: Symptoms, Causes, and Treatments

Women produce androgens every day of their lives, and when those levels fall too low, the effects can ripple across sexual health, mood, energy, and bone strength. Testosterone is the androgen that gets the most attention, but it is only one member of a family that includes DHEA, DHEA-S, and androstenedione, all of which serve distinct roles in the female body. Despite growing research, there is still no universally agreed-upon clinical diagnosis of “female androgen deficiency,” which makes the topic both practically important and medically contentious.

Where Female Androgens Come From

The two main factories for androgen production in women are the adrenal glands and the ovaries. The adrenals sit on top of the kidneys and churn out DHEA-S, DHEA, androstenedione, and a small amount of testosterone. The ovaries produce DHEA, androstenedione, and testosterone under the influence of luteinizing hormone, with output shifting somewhat across the menstrual cycle.¹ DHEA also acts as a raw material that gets converted into more potent androgens in tissues throughout the body, so the picture is not as simple as two organs pumping out a single hormone.²

Because androgens depend on two separate organ systems, anything that disrupts either one can lower overall levels. This dual-source design also means that losing one source, say the ovaries to surgery, does not zero out androgen production entirely. The adrenals keep contributing. But the loss is still significant, and the body does not fully compensate.

Symptoms Linked to Low Androgens

The symptom that has received the most research attention is reduced sexual desire, clinically called hypoactive sexual desire disorder (HSDD). Multiple trials have demonstrated that low androgen states in postmenopausal women correlate with diminished desire, and that restoring testosterone can produce a modest but meaningful improvement.³ In the largest of these trials, women receiving a testosterone patch reported roughly two more satisfying sexual episodes per month compared to those on placebo, along with improvements in desire and reductions in personal distress about their sex lives.

Beyond libido, many clinicians and patients report that low androgens contribute to persistent fatigue, low motivation, and a general sense of reduced vitality. These are harder to study because they overlap with so many other conditions, from thyroid disorders to depression. A pilot study of transdermal testosterone in peri- and postmenopausal women found that roughly half reported mood improvements and about 40 percent noticed cognitive gains after treatment, though the study was small and uncontrolled enough that it serves more as a signal than proof.⁴

The cognitive angle is particularly murky. A systematic review of observational studies looking at testosterone and cognitive performance in postmenopausal women found the results inconsistent and inconclusive, with the majority of studies reporting no clear association.⁵ That does not mean testosterone plays no role in brain function, but it does mean we cannot confidently tell someone that raising their testosterone will sharpen their thinking.

Bone health is another area where androgens appear to matter. Multiple studies using U.S. national health data and other large cohorts have found that higher testosterone levels are positively associated with bone mineral density at the spine and hip in women aged 40 and older.⁶ In older women specifically, higher free testosterone has been linked not only to denser bones but also to greater lean body mass and total fat mass, with differences of more than 10 percent between those at the highest and lowest ends of the free testosterone range.⁷ The relationship between testosterone and lumbar spine density appears to be nonlinear, with the strongest benefit seen below roughly 30 ng/dL.⁸

What Causes Androgens to Drop

The most universal cause is simply aging. Androgen precursors decline steadily starting in the late reproductive years. A cross-sectional study of women at midlife found that median testosterone dropped from about 0.56 nmol/L in the early 40s to about 0.42 nmol/L by the late 50s. Androstenedione and DHEA fell even more steeply, declining by roughly half and a third, respectively, between the early 40s and late 60s.⁹ Interestingly, testosterone itself showed a modest rebound after its nadir around age 58–59, while the precursor hormones continued their downward slide. This suggests the ovary may not completely stop making testosterone even after menopause.

Surgical removal of both ovaries (bilateral oophorectomy) causes a sharper, more abrupt drop. One study found testosterone levels were about 25 percent lower in women who had undergone bilateral oophorectomy compared to women with natural menopause.¹⁰ Another found reductions of more than 40 percent in both total and bioavailable testosterone in women who had undergone hysterectomy with bilateral oophorectomy compared to women with intact ovaries.¹¹ Hysterectomy alone, even with ovarian conservation, was associated with intermediate testosterone levels, possibly because the surgery disrupts blood flow to the ovaries.

Combined oral contraceptives are another common and often underappreciated cause. The pill works in part by boosting a liver protein called sex hormone-binding globulin (SHBG), which binds to testosterone and makes it unavailable to tissues. A systematic review and meta-analysis found that free testosterone dropped by an average of about 61 percent during oral contraceptive use, regardless of which pill formulation was studied.¹² Different pill types raised SHBG by varying amounts, but the end result on free testosterone was remarkably similar across formulations.¹³ For many women this never becomes a problem, but for those already on the lower end of androgen production, oral contraceptives can push free testosterone to very low levels.

Less common but clinically important is hypopituitarism, where the pituitary gland fails to produce the hormones that signal the ovaries and adrenals to make androgens. Women with both gonadotropin deficiency and secondary adrenal insufficiency face the steepest androgen losses because both major sources are compromised simultaneously.¹⁴ Primary adrenal insufficiency (Addison’s disease) can produce a similar shortfall from the adrenal side alone.

Why Diagnosis Is So Difficult

One of the most frustrating aspects of low androgens in women is that there is no widely accepted blood-test cutoff that defines “too low.” A 2002 Princeton consensus statement tried to define female androgen insufficiency as a combination of clinical symptoms plus decreased bioavailable testosterone in a woman with normal estrogen levels, but acknowledged that available assays were not reliable enough at the low concentrations found in women.¹⁵ More than two decades later, the situation has improved technically but not clinically. Mass spectrometry methods can now accurately measure the very low testosterone concentrations found in healthy women.¹⁶ The problem is that most commercial labs still run standard immunoassays that were designed for male-range testosterone. When applied to female-range values, these assays show an average bias of more than 20 percent compared to the gold-standard mass spectrometry method.¹⁷

Adding to the confusion, testosterone levels in women fluctuate with time of day and season.¹⁸ A single blood draw can land on a peak or a trough and give a misleading snapshot. For all of these reasons, most expert guidelines say that clinicians should not diagnose androgen deficiency in women based on a lab number alone. The current approach leans heavily on symptoms, particularly distressing low sexual desire, and uses testosterone levels mainly to rule out other conditions or to ensure levels are not excessively high.

The Ongoing Controversy Over Whether “Female Androgen Deficiency” Exists

The entire concept has vocal skeptics in the endocrinology community. A prominent editorial in the Journal of Clinical Endocrinology & Metabolism called the female androgen deficiency syndrome “an unproven hypothesis,” pointing to the striking lack of consensus on how to define androgen deficiency quantitatively in women and noting that the FDA had declined to approve a female testosterone patch.¹⁹ Critics argue that because no threshold has been established, clinicians may be treating symptoms that are not actually driven by androgens, or that a diagnosis built on subjective complaints without a clear biochemical marker is too vague to be useful.

On the other side, proponents point out that the absence of a clean diagnostic cutoff does not mean the underlying biology is imaginary. Testosterone receptors exist throughout the female brain, bone, muscle, and genitalia. The therapeutic evidence for testosterone improving sexual desire in selected women is robust enough that several international professional societies now endorse its careful use for HSDD.²⁰ The honest picture is that the science of female androgens is about 40 years behind the science of female estrogens, and the gap is closing slowly.

Treatment Options

Transdermal testosterone, delivered through a cream, gel, or patch, is the most studied treatment for low androgen symptoms in women. A systematic review of randomized trials found that transdermal testosterone increased the frequency of satisfying sexual episodes, desire, and orgasms while reducing personal distress in both naturally and surgically menopausal women with HSDD.²¹ Transdermal delivery is preferred over oral pills because testosterone taken by mouth undergoes extensive liver processing that can shift lipid profiles unfavorably. The doses used in women are a fraction of what men receive, typically aiming to restore testosterone to a premenopausal physiological range rather than push it into male territory.

DHEA is the other therapeutic option, though it works by a different route. Because DHEA is a precursor hormone, supplementing it lets the body convert what it needs into testosterone and estradiol locally. A meta-analysis of randomized controlled trials found that DHEA supplementation raised testosterone by an average of about 24 ng/dL in postmenopausal women, with larger increases seen at doses of 50 mg per day or more.²² In women with hypopituitarism specifically, low-dose DHEA restored DHEA-S levels to normal age-related ranges and produced visible androgen effects on skin, hair, and behavior. Partners of the treated women reported improvements in alertness, stamina, and initiative compared to placebo.²³ Still, the overall evidence for DHEA is thinner than for testosterone. A review noted that DHEA trials in women with adrenal insufficiency have been limited by short durations and small sample sizes, and called for larger, better-designed studies.²⁴

Safety Considerations

The most common side effects of testosterone therapy at physiological doses in women are mild and cosmetic: a bit of extra facial hair growth and occasional acne. These rarely lead women to stop treatment. The more serious questions revolve around breast cancer and cardiovascular risk.

On breast cancer, the laboratory evidence is actually reassuring. Experimental studies show that androgens tend to inhibit breast cell proliferation and promote cell death through the androgen receptor, even though testosterone can theoretically be converted to estrogen.²⁵ A prospective 10-year cohort study of women treated with subcutaneous testosterone found the incidence of invasive breast cancer was significantly lower than the age-matched expected rate from national cancer data, at roughly 165 per 100,000 person-years compared to an expected 271 per 100,000.²⁶ A separate long-term study reached a similar conclusion, finding that testosterone pellet implants significantly reduced breast cancer incidence in both pre- and postmenopausal women.²⁷ These are observational findings, not randomized trials, so they cannot prove causation. But they push against the worry that testosterone therapy would fuel breast tumors.

Cardiovascular risk remains an open question. A review of subcutaneous testosterone implant therapy noted that long-term safety data on cardiovascular outcomes in women are still limited and the evidence is mixed.²⁸ No large randomized trial has been designed to answer the question definitively for women, which leaves clinicians and patients weighing theoretical concerns against the available safety signals, most of which have been neutral or mildly favorable over follow-up periods of several years.

The Regulatory Gap and Compounding

No testosterone product has been approved by the FDA specifically for women in the United States. More than 30 formulations are approved for men. This disparity means women who are prescribed testosterone typically receive either a male product at a fraction of the labeled dose or a custom-compounded formulation made by a specialty pharmacy.²⁹

Compounded hormones come with their own problems. An Endocrine Society scientific statement flagged the general lack of standardization and quality control in how custom-compounded bioidentical hormones are produced and administered, noting the possibility of overdosing, underdosing, or contamination.³⁰ When you get a testosterone cream from a compounding pharmacy, there is no guarantee that what is in the jar matches what is on the label to the same degree as an FDA-approved product. Some compounding pharmacies voluntarily pursue third-party testing, but it is not required. If you go this route, asking your prescriber about reputable compounders and checking for accreditation is worth the effort.

Oral Contraceptives and Androgens After Stopping

A question that comes up frequently in practice is whether androgen levels bounce back after discontinuing the pill. The mechanism is straightforward in theory: once the exogenous estrogen from the pill is gone, the liver should stop overproducing SHBG, and free testosterone should rise again. For most women this does happen within a few months. However, some researchers have noted that SHBG levels can remain elevated for a prolonged period after pill cessation, potentially keeping free testosterone suppressed longer than expected. The data on long-term post-pill androgen recovery are limited, and individual responses vary enough that no firm timeline can be quoted. If you stopped the pill and still feel low on energy or desire six months later, it is reasonable to have your hormone levels checked, ideally with a sensitive assay method.

Practical Steps If You Suspect Low Androgens

If you are experiencing a cluster of the symptoms discussed, particularly distressing low desire combined with fatigue and reduced sense of well-being, the first practical step is a conversation with a clinician who is familiar with female androgen physiology. Not all providers are, and the controversy around the diagnosis means some will dismiss the possibility outright. Asking for a referral to an endocrinologist or a menopause specialist can help.

When testosterone testing is ordered, request that it be done by a mass spectrometry method if your lab offers it, rather than a standard immunoassay. The difference in accuracy at female-range levels is substantial. Have blood drawn in the morning, when testosterone tends to be highest, and keep in mind that a single test is a snapshot. Other conditions that mimic low androgen symptoms should be ruled out: thyroid dysfunction, iron deficiency, depression, and sleep disorders can all produce overlapping complaints. Testosterone therapy, if pursued, should start at the lowest effective dose and be monitored with follow-up blood work to make sure levels stay within the physiological female range. Supraphysiological dosing carries risks of irreversible virilization, including voice deepening and clitoral enlargement, that low-dose therapy does not.