Testosterone: Vital to female physiology

Abstract

The vital role of testosterone in normal female physiology and wellbeing is largely ignored by researchers and healthcare providers. The lack of recognition of the importance of testosterone in female health creates a health disparity. Androgens are the most abundant sex hormone in all humans, including females. However, the traditional view that testosterone is a male hormone and estrogen is a female hormone is not supported by scientific evidence. Emerging research shows that testosterone plays a crucial role in female reproduction, cardiovascular health, bone remodeling, muscle mass, and brain function. This article aims to review the literature on the physiological role of testosterone in females, the challenges in measuring testosterone levels, and the implications for female health. The authors conducted a review of the literature on testosterone in female physiology, including its biosynthesis, measurement, and effects on various bodily functions. There is a significant gap in research and understanding of the role of testosterone in female health. Barriers to recognizing the importance of testosterone include a male-centric medical system, the lack of standard reference ranges for testosterone during the menstrual cycle, and the general lack of understanding of endogenous testosterone in female endocrinology. There is a clear need for further research and clinical trials to address this health disparity.

Keywords

endogenous testosterone androgens female physiology women’s health

Introduction

The Sex and Gender Equity in Research (SAGER) and the National Institutes of Health’s (NIH) office of Research on Women’s Health (ORWH) define sex as a multidimensional grouping of biological attributes and emphasize the importance of function and reproductive/sexual anatomy.^1–3 For consistency with the SAGER and NIH guidelines, this article will use the terms male and female to refer to sex. Sex in this context is a biological variant and refers to reproductive organs, external genitalia, genotype of the 23rd chromosome, SRY gene presence or absence, endogenous hormone production by the gonads, and hormone exposure.^2–5 Gender is an important cultural and social variable in understanding health and has implications for identity, perception of self and others, distribution of resources, power, and roles that affect health outcomes.^1–4,6,7 Because this article is specifically focused on sex steroids and hormones, the authors will be discussing the variable of sex and not the variable of gender. When discussing ovaries and testes, we will use the gender-neutral term of gonad when the effect of testosterone is not sex specific. Therefore, instead of discussing the hypothalamic-pituitary-ovarian (HPO) axis, we will use the non-gendered description of the hypothalamic-pituitary-gonadal (HPG) axis.

The etymology of the word androgen is from Greek, meaning male produced or generated.⁸ However, there is no scientific basis for the traditional dichotomy holding that androgens are male and estrogens are female.⁹ In fact, all humans have the same sex hormones: androgens (including testosterone), estrogen, and progesterone.¹⁰ While it is common knowledge that testosterone is the dominant sex steroid in males, few know that testosterone levels far exceed levels of estradiol in females.^8,10–13 Endogenous testosterone is a vital hormone for total well-being in all humans, regardless of sex, and its role in human health goes well beyond sexual function and male physiology.^9,13,14 Testosterone is crucial for female reproduction, cardiovascular health, bone remodeling, muscle mass, and brain function.⁸

Review of the literature of endogenous testosterone in females

Due to the limited research on endogenous testosterone in females, the authors chose a perspective review in order to include studies that met the broad aims of the article. The perspective review format also allowed for a narrative summation and critique of the evidence. A preliminary search was undertaken in PubMed and then expanded to CINAHL and Web of Science. Various keywords were used including testosterone, female, benefits, physiology, and endogenous. The National Library of Medicine¹⁵ Medical Subject Heading (MeSH) description of testosterone is, “a potent androgenic steroid and major product secreted by the Leydig cells of the testis.” Other MeSH entry terms associated with testosterone are all male-related words and medications. Searches were limited to full text articles in English primarily from 2019–2025. Further searches were undertaken using references found in located articles. Studies were not restricted by research method. Approximately 3,000 articles resulted from these searches. Articles were eliminated that had a focus on the following: gender-affirming care (both for transgender women and transmasculine individuals); exogenous testosterone treatment; male contraception; animal research not in relation to humans; and male testosterone. Many remaining article topics focused on female hypoactive sexual disorder, sports and athletics, Polycystic Ovarian Syndrome (PCOS), and menopause.

The results of these searches demonstrate that research on testosterone is male-centric.¹⁵ An abundance of research shows that endogenous testosterone is vital for the general health and quality of life of males, yet comparatively little research investigates testosterone as a normal, physiologic, and necessary hormone in females.^9,10,13,14 No articles that resulted from these searches addressed testosterone in intersex individuals. Testosterone is common in the discussion of females when it relates to menopause or some form of pathophysiology -- specifically hyposexuality or polycystic ovarian syndrome (PCOS).^10,16 Emerging research on the significance of testosterone in female endocrinology debunks the myth of estrogen as the dominant female hormone.^9,16

One system-related issue inhibiting research is the lack of current agreed upon laboratory parameters for measuring testosterone in females.¹⁷ In fact, only four studies reported testosterone reference ranges according to menstrual phase using liquid chromatography-tandem mass spectrometry (LC-MS/MS).^17–21

Another systematic reason for the lack of research on the role of testosterone in female health is that until recently, the “vast majority of clinical research was conducted with exclusively or predominantly male participants.”¹⁵ Between 2016 and the 2025, countries such as the United States, United Kingdom, Germany, Canada, and Australia have adopted requirements that preclinical research include female animals and cell models.^3,6,22–25 Prior to the adoption of these guidelines in the last decade, findings from male animals, male cell models, and male participants were typically applied to females for conditions that affect all sexes.²⁶ This gap in clinical research has negative effects on the health of females, transgender individuals, and intersex populations.^3,25

Testosterone biosynthesis

The androgen group of hormones includes (in ascending order of potency): dehydroepiandrosterone sulphate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione (A), and the sex-steroids testosterone (T), and dihydrotestosterone (DHT).^11,27–29 In humans, the hypothalamus regulates gonadal secretion of testosterone through the secretion of gonadotropin-releasing hormone (GnRH).²⁶ This signals the anterior pituitary to release the gonadotropins: luteinizing hormone (LH) and follicle-stimulating hormone (FSH).^30–33 In males, this stimulates the testes to produce testosterone.⁹ LH and FSH stimulate the ovaries to produce estradiol, progesterone, and testosterone.¹⁰ HPG axis activity is regulated by positive and negative feedback loops with estradiol, progesterone, and testosterone.⁹ Adrenal androgen secretion is stimulated by adrenocorticotropic hormone (ACHT).⁸

In females, about half of testosterone is made in the reticular zone of the adrenals (25%) and the theca cells of ovarian follicle (25%).⁹ The other 50% of testosterone is produced by conversion of androgens in peripheral tissues.^{8,9,11,14,27,33} The physiological effects of testosterone are made directly by converting to DHT or androstenediol, or indirectly via aromatization to estradiol.^27,34 Aromatization is the process of potent androgens being converted into estrogens by the action of the enzyme aromatase, which is present in many tissues throughout the body.^8,29 The effects can be rapid, within minutes to seconds.¹³ Testosterone and DHT act directly on target cells via androgen receptors (AR) that are abundant in the human body.¹¹ The effect of the sex hormones on the tissue is dependent on many factors including bioavailability, androgen receptor expressivity, and aromatase activity.^8,26

Androgen biosynthesis in females has four known pathways: the classic pathway, the backdoor pathway, the c11-oxy and c11-oxy backdoor pathways.²⁸ Many different enzymes are needed to catalyze cholesterol and the individual androgens.^11,30,31 Androgen biosynthesis starts with cholesterol which synthesizes into pregnenolone, to 17 hydroxypregnenolone, and to DHEA, which synthesizes to DHEAS.^8,9,11,26,28 (see Figure 1). DHEAS is a precursor androgen, or a pro-androgen. Pro-androgens must be converted to testosterone or DHT via peripheral synthesis to express their effects.^10,11,29 It is produced primarily in the adrenal glands and is converted to DHEA, another pro-androgen.^10,12,30 DHEA is the most abundant adrenal androgen and is regulated by ACTH.^11,35 DHEA is produced in the adrenal glands (50%) and in small amounts by the gonads (20%), brain, placenta, and from conversion of DHEAS in the peripheral tissues.^{8,11,28,29,36}

Figure 1.

Androgen Biosynthesis in females with the classical pathway and various pathways. Abbreviations: 17-OH-Pregnenolone, 17 hydroxypregnenolone; 17 OH-Progesterone, 17 hydroxyprogesterone; DHEAS, dehydroepiandrosterone sulphate: DHEA, dehydroepiandrosterone, DHT, dihydrotestosterone; 11 OHT, 11 betahydroxytestosterone; 11KT, 11 ketotestosterone; 11OHA4, 11 betahydroxyandrostenedione; 11KA4, 11ketoandrostenedione.

Androstenedione, another pro-androgen, is produced in the adrenals (50%) and gonads (50%) and in the peripheral tissues when converted from DHEAS via DHEA.^11,28,29 Individuals who have had an oophorectomy have about a 30% reduction in androstenedione. Hypopituitarism and exogenous corticosteroids can also reduce levels.¹¹ LH stimulates androstenedione production resulting in a midcycle elevation that coincides with the peak of estradiol.^10,11 This is no coincidence as androstenedione is transported to the granulosa cells and aromatizes to estrone and further to estradiol.¹⁰ The peripheral conversion of androstenedione accounts for approximately 50% of testosterone production.²⁹ It is the primary steroid hormone secreted by the ovaries after menopause.²⁹

Testosterone (C19, H28, O2) is the second most potent androgen and has a strong affinity for the androgen receptor.¹⁰ Testosterone is the product of the ovarian theca cells (25%-33%) and adrenal cortex reticular zone (25%-33%). The other half to two-thirds of testosterone comes from the conversion of androstenedione and DHEA in peripheral tissues.^{10,14,28,32,33} It is regulated by LH and insulin.^{10,14,28,32,33} Testosterone is the most abundant ovarian androgen.³⁵ Stimulated by FSH, testosterone, which is similar in structure to estrogen, is converted to estrone and estradiol by aromatase and 17-Beta-hydroxysteroid dehydrogenase.^{10,11,27,33,37,38} About 1-2% of testosterone circulates in its free form and about 98-99% of testosterone is bound to proteins.³⁴ Approximately 33% is weakly bound to albumin and approximately 66% is bound to sex steroid hormone-binding globulin (SHBG).^{12,14,32–34}

Dihydrotestosterone (DHT) is the most potent androgen and has the highest affinity for androgen receptors (AR).^12,29,30,38 DHT is a metabolite of testosterone and androstenedione by 5 alpha reductase in the peripheral tissues.^11,17,28 With serum concentrations 14 times higher than testosterone, it is the most abundant female sex steroid.³⁴ DHT’s serum concentration level in females is 0.02 ng/mL.¹¹ Unlike testosterone, it does not aromatize into estradiol and is more active biologically.^11,17 Further androgen action results when DHT and 11-ketodihydrotestosterone (11KDHT) synthesize in the peripheral tissues.³²

Other androgen metabolites include: 11-betahydroxytestosterone (11OHT), 11-ketoandrostenedione (11KA), 11-ketotestosterone (11KT), 11-ketodihydrotestosterone (11KDHT), and 11-betahydroxyandrostenedione (11OHA).^8,28,34,37 Some androgen metabolites bind to the AR and have similar “androgenic potency” as testosterone and DHT.³⁷

Androgens have two mechanisms of action. First, they are directly biologically active in target organs when they bind to androgen receptors (AR). Second, they act indirectly by aromatization into estrogens and/or reduction to DHT and other metabolites.^8,10,30,39 It takes several minutes up to several hours for physiological actions to be mediated by aromatization or genomic effects.^8,13,40 The AR gene is located on the X chromosome.^30,41 Genomic effects occur when androgens bind to the AR receptor inducing gene transcription and expression.^8,13,40 In their inactive state, ARs are located in the cytoplasm.^8,41 Upon binding with ligands, the receptors dimerize and translocate into the nucleus where it activates transcription of target genes.^8,41 Non-genomic effects are mediated by several mechanisms including, androgen interactions with plasma membrane receptors and ion channels and through aromatization to estrogen and subsequent activation of the estrogen receptor (ER).^8,40,41 Vasodilation and muscle contraction are examples of non-genomic effects that take only seconds to minutes to act.^13,40 These rapid effects are the consequence of androgen exposure on intracellular Ca2+ which create reproducible non-genomic effects at the cellular level.⁸ In pregnant females, the of the placenta has non-genomic membrane androgen receptors and is itself a source of testosterone.⁴¹

Androgen receptors are found in the nervous system, skin, breast, bone, muscle, liver, kidney, blood vessels, the endometrium, vagina, urogenital tissue, male reproductive tissue, some cancer cells, the immune system, and adipose tissue.^{8,11,17,30,42} Several genetic, environmental, and biological factors such as polymorphisms, methylation status of the gene, varying enzyme activity can determine the expression of the androgen receptor in any individual.^13,31,38 For example, there are over 400 known mutations of genes that can lead to androgen insensitivity syndrome causing individuals with XY chromosomes to have a female genotype.³⁰ Almost every tissue in a female’s body has androgen receptors making the effect of androgens crucial in many aspects of female health.^8,29,42–44 Even menstrual cycle related fluctuations of estrogen and progesterone can influence the AR.¹³ In short, individuals with identical levels of androgens may have variance in the androgenic effects due to varying factors including the abundance of Ars their expression and activity, and methylation levels.¹³

Measuring testosterone

Comparing units of measurement

When measuring sex steroids, estradiol is typically measured in picograms per milliliter (pg/mL), progesterone in nanograms per milliliter (ng/mL) or nanomoles per liter (nmol/L), and testosterone in nanograms per deciliter (ng/dL) or nanomoles per liter (nmol/L). Conversion of the units is needed to make a comparison of the concentration of the different hormones in human serum (Table 1). One nanogram equals 1,000 picograms. For comparison, when nanograms or nanomoles of androgens are converted to pg/mL, approximate measures for androgens would be 5,000 pg/mL for DHEA, 2,000 pg/mL for androstenedione and 400 pg/mL for testosterone.⁸ When the units are converted, it is apparent that androgens are circulating in much higher quantities in females than estradiol or progesterone.^8,16,45 Studies have shown the quantity of androgens are five to 50 times higher than the quantity of estrogen.^{8,10,11,45,46} This is not to suggest that estrogen plays a lesser role in female physiology and health than testosterone. While both quantity and potency play a role in determining the physiologic effects of a hormone, they should not be conflated.⁴⁷ However, although the quantity of a hormone cannot alone determine the physiologic effects of that hormone, the relatively high levels of testosterone in females suggest it plays an important physiologic role that has been overlooked.⁴⁵

Table 1.

Metric units of measurement.

Prefix	Symbol	Value
Deci	d	one tenth
Centi	c	one hundredth
Milli	m	one thousandth
Micro	mc or µ	one millionth
Nano	n	one billionth
Pico	p	one trillionth

The Center for Disease Control⁴⁸ has published reference ranges for estradiol and testosterone in females and males. However, the testosterone reference ranges do not include cyclic fluctuations based on the menstrual cycle phases.

Although historically free testosterone was thought to be the active form that produces the most androgenic effects, it is easily degradable and unstable.^8,27,29 Because androgens are loosely bound to albumin with low affinity, they can easily be freed and reach target tissues.⁸ Additionally, evidence that points to free testosterone as the biologically active testosterone is lacking, and some research suggests that total testosterone should be considered the main biomarker.^{12,14,32,37,39,42,49} Additional studies propose that SHBG-bound testosterone may be capable of having an independent biological effect leading some experts to advocate for measuring total testosterone and SHBG levels.^8,27,29 Still others argue that serum testosterone levels may not be necessary at all as they cannot measure the testosterone that is synthesized in the peripheral tissues (50%) or account for individual variability.^34,35 Some testosterone that is weakly bound to albumin or synthesized in the tissues is capable of binding to the androgen receptors.^8,29 This complex system of sex steroid synthesis, referred to as intracrinology, involves the peripheral transformation of DHEA into testosterone and DHT, the aromatization of testosterone to estrogen, and many other variables.

Techniques for measuring testosterone

The gold standard for measuring testosterone is via liquid chromatography–tandem mass spectrometry (LC-MS/MS).^12,14,39 It is highly sensitive and useful for measuring small molecules.²¹ Equilibrium dialysis is also considered a reference method.¹⁷ Unfortunately, these methods are not widely used due to expense and required expertise.^14,17,21 The more affordable and widely used method for measuring steroid hormones is with commercial immunoassays (IAs).²¹ Types of immunoassays include: radioimmunoassays (RIA), Enzyme immunoassay (ELISA), flourescentimmunoassays (FIA), and chemiluminescent compound (CLIA).¹⁴ At the low levels of testosterone found in females (<300 ng/dL), they lack sensitivity and specificity and have substantial variability.^{8,14,17,20,32,39,49} There was a two-to-six-fold variation in results of blinded samples of human serum plasma measured with IAs and processed by different laboratories.¹⁴

The Center for Disease Control⁵⁰ created the Hormone Standardization Program for Testosterone (HoSt) in 2007, and the standards of this program have been adopted by labs globally. Laboratories can be awarded certification if they accurately measure total testosterone in human serum to ± 6.4% mean bias when compared to a reference measurement.⁵¹ Prior to 2022, only three studies reported menstrual phase-specific reference limits for females using LC-MS/MS.^17,19–21 In 2015, the CDC⁴⁸ published a 10% to 90% reference range of total testosterone in females to be 7.1 to 49.8 ng/dL, based on the LC-MS/MS method. The normal range for total testosterone in serum remains undefined as it is variable for many reasons including circadian rhythm, menstrual cycle, BMI, age, sex, disease status, alcohol consumption, and exercise.^10,14,49 Considering the physiology of androgen biosynthesis and that at least 50% of testosterone is made in the peripheral tissues through intracellular metabolism, serum concentrations do not reflect tissue exposure to testosterone or androgen receptor sensitivity.¹⁰ For this reason, many believe that checking serum testosterone in females is arbitrary and may not inform clinical decision making.^12,32

Enodgenous testosterone and female physiology

Normal testosterone levels in females

Testosterone levels vary throughout the lifespan.^12,17,43 In humans, androgen levels are low until approximately age six when they begin to increase through adrenal production leading to the stage of development called adrenarche.^12,29,35 This process continues until the age of eight and leads to pubarche, the stimulation of pubic and axillary hair production and adult body odor.^29,35 At puberty, androgens are produced in the ovaries and testosterone is converted into estradiol; ovulation is dependent upon these levels.⁸ Insufficient testosterone or overproduction of testosterone can lead to anovulation.⁸ Testosterone is higher in adolescents experiencing an anovulatory menstrual cycle.²⁰

Contributing to the difficulty in defining “normal” androgen levels in females, research demonstrates that testosterone levels change significantly throughout the menstrual cycle.^8,14,30,49 Testosterone in the follicular phase is largely produced by the adrenal precursors.²⁹ In one 2022 review, eight studies showed testosterone higher in the follicular phase while nine studies showed testosterone higher in the luteal phase of the menstrual cycle.^{8,10,13,20,29,32,51} During the LH surge associated with ovulation, testosterone synthesis increases in the ovarian theca cells.^10,29 Despite the mid-cycle peak described in most studies, the high day-to-day variation in any one individual does not appear to be dependent on the menstrual cycle.^8,18 The nadir of testosterone is found just prior to menstruation.¹⁰ The vast variation in results between studies can be attributed to many variables including: study design, sample choice (saliva or serum), the testosterone assessment technique (LC-MS/MS, equilibrium dialysis, or assay), form of testosterone measured (free or total), the frequency in which samples were taken, how “healthy female” was defined, the time of day of sample collection, the phase of the menstrual cycle, BMI, age, use of contraceptives, and many more.^{8,10,12,28,37,52} Another important variable is that SHBG binds testosterone and is highly dependent on estrogen levels and insulin resistance.²¹ It is also helpful to remember the function of intracrinology and that serum testosterone concentrations do not account for the testosterone found in the peripheral tissues.^8,53

To fully understand the levels of hormones in the menstrual cycle, a standard unit of measurement should be used. This involves converting all units of measurement to the chosen standard unit. In Table 2, reference ranges for estrogen and testosterone were converted to pg/mL to match the common unit of measurement for estrogens. Most images of the menstrual cycle do not include a unit of measurement on the y axis. Illustrations without a unit of measurement fail to accurately compare the quantity and fluctuation of hormone levels in the normal physiology of the menstrual cycle. When the normal reference ranges of testosterone and estrogens are shown together in an illustration with a unit of measurement on the y axis, the abundance of testosterone in comparison to estrogen is apparent (see Figure 2). Because normal testosterone ranges during the menstrual cycle have yet to be established, Figure 2 does not show a continuous line to estimate testosterone levels. There is, however, a general consensus about when the peak (750 pg/mL) and nadir (150 pg/mL) of testosterone occur. Therefore, only the peak and nadir are represented with symbols on the graph.

Table 2.

Reference Ranges of Estrogen and Testosterone in the Menstrual Cycle in pg/mL.

Menstrual cycle phase	Estrogen^a	Total testosterone^b
Early Follicular	20-50	150-750
Late Follicular	40-350
Midcycle/ovulation	150-750
Luteal Phase	30-450
Postmenopausal	≤20

^aEstrogen ranges from.⁴⁸

^bThere are no standard menstrual-phase reference ranges for testosterone.⁴⁸

Figure 2.

Ranges of Estrogen and Total Testosterone During the Menstrual Cycle in pg/mL.

During the reproductive years and prior to menopause, androgen levels decrease considerably between the ages of 20 and 45.^{8,29,31,32,39} Toward the end of the reproductive years, female cycles are increasingly anovulatory and therefore, no mid-cycle surge of LH occurs.^33,49 The result is decreased stimulation on the ovarian theca cells to produce testosterone.⁴⁹ In the years following the last menstrual cycle, the ovaries produce relatively more testosterone than in the late reproductive or premenopausal years.²⁹ This is due in part to the elevation of LH that stimulates ovarian testosterone production after depletion of ovarian follicles.^29,49 Another contributing factor to the relative increase in free testosterone is the post-menopausal fall in circulating SHBG and estradiol.^11,28 When LH then drops after menopause, testosterone slowly decreases.^8,12 Overall, despite this short-term postmenopausal increase in ovarian testosterone production, median serum testosterone levels are similar to levels in the late reproductive years.^11,49 Due to the large range of serum testosterone levels at the individual level, serum testosterone levels alone cannot differentiate between a female in the late reproductive years and one who is postmenopausal.⁴⁹

The ovaries continue to produce testosterone after menopause, but total testosterone levels decrease due to decreased androgen precursors, specifically androstenedione.^8,11,29 During menopause, androgen receptor expression decreases in all areas of the body.⁵⁴ Ovaries in postmenopausal females can produce a small amount of testosterone while females who have undergone surgical menopause demonstrate lower testosterone levels than those with naturally occurring menopause.⁴⁹ The testosterone nadir appears to occur at around age 62 and may show a slight increase in later years.^8,29 The cause of the increase is unknown.¹² After menopause, most androgens are produced in the adrenals and females may commonly have insufficient levels of androgens.^21,32 Oral exogenous estrogen therapy, either for contraception or hormone replacement therapy, increases SHBG levels and further contributes to a fall in free testosterone concentrations.¹¹

Effects of endogenous androgens in females

Examining the abundance of androgens in female circulation as well as the presence of AR in almost every tissue contributes to understanding the role these androgens play in female physiology.²⁹ Many studies demonstrate the physiological effects of endogenous testosterone in females (Table 3). This data highlights the many ways androgens contribute to the overall health and well-being of females.

Table 3.

Effects of endogenous androgens in females.

Targeted cells	Life phase	Endogenous effects
Bone	Postmenopausal	Promotes bone density, growth, and maintenance^55–58
	Reproductive	Increases trabecular bone density^8,12,27,59
	Postmenopausal	Promotes increased bone mineral density of the hip and lumbar bones in ages 67-94¹²
	Postmenopausal	Fewer occurrences of hip fractures⁶⁰
Brain	All ages	Neuroprotective^29,61
	All ages	Controls neuroplasticity⁶²
	All ages	Organizes the brain to maintain mental and physical health⁸
	Postmenopausal	Antidepressive properties especially postmenopausal^63,64
	Perimenopause	Maintains memory and cognition^49,58,65
	All ages	Protective for dementia and Alzheimer’s Disease (incidence and development^61,62
	All ages	Positively effects endothelial function and acts as a vasodilator in the brain⁴⁹
	All ages	Protective against oxidative stress⁴⁹
Breasts	All ages	Androgen receptors inhibit estrogen receptor activity on breast cancer cells⁶⁶
Cardiovascular	All ages	Possible inverse relationship between testosterone and cardiovascular disease^12,13,67
	Postmenopausal	Potent vasodilator on vascular endometrium^8,35,68
	Postmenopausal	Positively associated with brachial artery flow-mediated dilatation⁶⁸
	Reproductive	Favorable results on vasomotor tone, endothelial function, and peripheral vascular resistance^12,29
Endometrium	Postmenopausal	Induces endometrial atrophy for postmenopausal women taking estrogen alone⁶⁹
Immune System	All ages	Immunosuppressive action responsible for decreased autoimmune processes, decreased inflammatory markers, infection, and tumor formation⁷⁰
Kidney	All ages	Possibly increases production of EPO^8,71
Liver	Postmenopausal	Higher testosterone levels are associated with lower triglycerides and higher HDL⁷²
Muscles and Body Composition	All ages	Increases muscle mass and strength⁸
	Reproductive	Associated with greater lean muscle mass^12,61
	Reproductive	Better competitive performance⁷³
Ovary/Ovulation	Reproductive	Essential for recruitment of follicles and ovulation^10,74
	Reproductive	Aids FSH in initiating follicular and granulosa cell growth proliferation⁷⁴
	Reproductive	Aids in regulation of all phases of ovarian function by controlling follicular atresia ensuring a dominant follicle is prepared for ovulation⁷⁴
Pregnancy	Reproductive	Essential for endometrial preparation for pregnancy^8,29,69
Pregnancy	Reproductive	Controls the decidualization process to help regulate the onset of pregnancy⁷⁴
Sex/Libido	All ages	Increases sexual desire^58,75–77
	Reproductive	Sexual desire correlates with mid-cycle, ovulation phase associated with increase in mid-cycle androgen increase^10,77
	All ages	Free testosterone and androstenedione have a significant positive influence on sexual desire^34,78
	Reproductive	Stimulates blood flow increasing orgasm ability³⁴
Skin	Reproductive	Regulates hair growth and wound healing⁷⁹
Skin	All ages	Increase sebum production and acts on sebaceous and apocrine glands⁸
Vagina	Reproductive	Promotes proliferation of epithelial cells of the vagina⁷⁸

Endogenous androgen insufficiency and androgen excess in females

The benefits of androgens on disease prevention and biological function depend on the levels of excretion and androgen receptor activity.⁸ Lack or excess of androgens can cause pathology.³² Endogenous androgen excess, or hyperandrogenism in females, is characterized by excessive secretion of androgens leading to side effects such as hirsutism, acne, alopecia, and menstrual disorders.³⁸ Individuals with hyperandrogenism are also at increased risk for cardiovascular disease, Type 2 diabetes, dyslipidemia, metabolic syndrome and hypertension.⁸⁰ The diagnostic criteria for hyperandrogenism are the elevation of testosterone, free or total, higher than the normal female level.³⁸ Clinically, testosterone levels above 50 ng/mL are congruent with acne and/or hirsutism.^21,38 However, many studies have shown that testosterone levels up to 75 ng/dL and higher are typical in females, especially at mid-cycle.⁸ Differential diagnoses for hyperandrogenism include: physiologic or idiopathic hyperandrogenism of puberty, PCOS, Cushing’s syndrome, ovarian or adrenal neoplasms, or hyperprolactinemia.^8,20,38 Positive effects of hyperandrogenism are seen in elite athletes with PCOS exhibiting increased lean muscle mass, higher maximum oxygen intake, increased competitiveness, and increased muscle strength.⁷³

PCOS accounts for 80 to 85% of females hyperandrogenism.^8,20,38 Of those individuals with PCOS, 65-90% have a hyperandrogenic PCOS phenotype with increased androstenedione, total testosterone and DHEAS.⁸¹ Estimated prevalence of insulin resistance in those with PCOS is 65-95% and can occur in both normal and overweight individuals; however, PCOS and obesity does increase the risk of insulin resistance.⁸⁰ Insulin inhibits SHBG levels causing increased levels of free testosterone.⁸⁰ Furthermore, increased levels of insulin cause increased secretion of androgens from the ovary; this combination of elevated androgens and insulin resistance causes an increased risk of endothelial dysfunction and cardiovascular disease in those with PCOS.⁸¹ PCOS has been associated with increased blood pressure; however, it is unclear if this effect is due to elevated androgens or other associated cardiovascular risks seen in PCOS.⁸¹ One study showed that individuals with PCOS were more likely to have elevated blood pressure compared to a control group, and individuals with PCOS who exhibited elevated blood pressure were more likely to have increased waist circumference and hypercholesterolemia.⁸² This study showed that total testosterone levels were not associated with elevated blood pressures in study participants.⁸² More research is needed to determine the cause of cardiovascular disease in those with PCOS.

Endogenous androgen insufficiency, or hypoandrogenism in females, can be caused by lack of ovarian follicle maturation, oophorectomy, exogenous corticosteroid use, hypopituitarism, estrogen replacement therapy, or contraception use, or primary hypogonadism.^8,49 Ethinyl estradiol increases SHBG leading to less free testosterone.³⁸ Other common causes of hypoandrogenism are aging, ovarian or adrenal insufficiency, panhypopituitarism, hyperprolactinemia, hypothalamic amenorrhea, eating disorders, and other pathology.^35,39 Hypoandrogenism causes symptoms of decreased sexual motivation, fatigue, lack of sense of well-being, thinning of pubic hair, decreased lean muscle mass, mood disorders, insomnia, and hot flashes.^58,83,84 Androgen insufficiency has been associated with inflammation and increased inflammatory markers, such as C-reactive protein, and increased incidences of obesity, metabolic syndrome, cancer, cardiovascular disease, osteoporosis, systemic lupus erythematosus, rheumatoid arthritis, type 2 diabetes, and Alzheimer’s Disease.^{10,12,42,56,62,83,84} No concrete criteria to aid in diagnosing androgen deficiency is available and low levels of androgens do not guarantee a person to be symptomatic.^29,35

Conclusion

There is scant quality research on the physiological effects of testosterone using female animals, female cell models, or female human participants. Research pursuing the development of more specific and sensitive assays to measure testosterone would greatly improve our understanding of the role of testosterone in females.⁴⁹ A menstrual phase specific reference range for testosterone is needed to better understand the clinical implications of hypoandrogenism and hyperandrogenism in females.¹⁷ Ultimately, more research is needed on the role and benefits of endogenous testosterone in females.^8,39,49 Additional sex-specific research could strengthen the existing evidence for the importance of testosterone in cardiovascular, neurologic, psychologic, skeletal, muscular, reproductive, sexual, and dermatologic health of females.^6,31,39,49 Health care providers and their patients would benefit from understanding natural female physiology, and further research of sex-specific factors is key to optimal health outcomes. We are hopeful that in the near future, this health disparity for females will be rectified through research, clinical trials, and education.

Limitations

Although this narrative review aims to provide a comprehensive overview of the available literature on the physiologic function of testosterone in females, it is not a systemic review, leaving open the potential of selection bias. This review is also limited by the scarcity of data on the role of testosterone in female health due to the inconsistent methodologies used in the studies available, and the small number of subjects included in research, particularly as relates to testosterone and the menstrual cycle. Lastly, studies published in languages other than English were excluded, potentially resulting in missed information from non-English speaking researchers.

Footnotes

Acknowledgements

The authors would like to thank Caroline Taylor, Senior Graphic Designer and Multimedia Specialist, at Vanderbilt University School of Nursing for her graphic design work.

ORCID iDs

Kendra Faucett

L. Amy Giles

Erin Sing

Consent for publication

Not applicable. There were no patients, participants, or guardians involved in this review article.

Author contributions

(will be replaced by CRediT author contribution information)

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The authors do not have participant data or materials to share as this was a review article without human participants.*

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