Hyperandrogenism, especially high levels of testosterone, can cause serious adverse effects on women’s bodies if left untreated. High testosterone levels have been seen to be associated with obesity, hypertension, amenorrhea(stop of menstrual cycles), and ovulatory dysfunction, which can lead to infertility. The more prominent signs of hyperandrogenism are hirsutism (unwanted growth of hair especially in the abdominal region and places on the back), acne after adolescence, deepening of voice, and alopecia(balding). Hyperandrogenism has also been seen to cause individuals to have a high tolerance to insulin, which can lead to type two diabetes, and dyslipidemia, such as high cholesterol. These effects have also been seen to have a large psychological impact on the individual, sometimes often leading to societal anxiety and depression, especially in adolescent girls and young women. Paired with obesity and hirsutism, it can cause the individual to have low self-esteem, and a poor view of oneself.

Hyperandrogenism affects 5-10% of females of reproductive age. Hyperandrogenism can affect both males and females, but is more noticeable in females due to the fact that elevated levels of androgens in females often facilitates virilization. Due to the fact that hyperandrogenism is characterized by the elevation of male sex hormone levels, symptoms of hyperandrogenism in men are often negligible. Hyperandrogenism in females is typically diagnosed in late adolescence with a medical evaluation. The medical evaluation tends to consist of a pelvic exam, observation of external symptoms, and a blood test measuring androgen levels.

Symptoms of the condition in males consist of loss of libido, impotence, infertility, shrinkage of the testicles, penis, and prostate, diminished masculinization (e.g., decreased facial and body hair growth), low muscle mass, anxiety, depression, fatigue, vasomotor symptoms (hot flashes), insomnia, headaches, and osteoporosis. In addition, symptoms of hyperestrogenism, such as gynecomastia and feminization, may be concurrently present in males.

In females, hypoandrogenism consist of loss of libido, decreased body hair growth, depression, fatigue, vaginal vasocongestion (which can result in cramps), vasomotor symptoms (e.g., hot flashes and palpitations), insomnia, headaches, osteoporosis and reduced muscle mass. Symptoms of hypoestrogenism may be present in both sexes in cases of severe androgen deficiency (as estrogens are synthesized from androgens).

Common signs and symptoms of PCOS include the following:

- Menstrual disorders: PCOS mostly produces oligomenorrhea (fewer than nine menstrual periods in a year) or amenorrhea (no menstrual periods for three or more consecutive months), but other types of menstrual disorders may also occur.

- Infertility: This generally results directly from chronic anovulation (lack of ovulation).

- High levels of masculinizing hormones: Known as hyperandrogenism, the most common signs are acne and hirsutism (male pattern of hair growth, such as on the chin or chest), but it may produce hypermenorrhea (heavy and prolonged menstrual periods), androgenic alopecia (increased hair thinning or diffuse hair loss), or other symptoms. Approximately three-quarters of women with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of hyperandrogenemia.

- Metabolic syndrome: This appears as a tendency towards central obesity and other symptoms associated with insulin resistance. Serum insulin, insulin resistance, and homocysteine levels are higher in women with PCOS.

Asians affected by PCOS are less likely to develop hirsutism than those of other ethnic backgrounds.

Women with hypogonadism do not begin menstruating and it may affect their height and breast development. Onset in women after puberty causes cessation of menstruation, lowered libido, loss of body hair and hot flashes. In boys it causes impaired muscle and beard development and reduced height. In men it can cause reduced body hair and beard, enlarged breasts, loss of muscle, and sexual difficulties. A brain tumor (central hypogonadism) may involve headaches, impaired vision, milky discharge from the breast and symptoms caused by other hormone problems.

The symptoms of hypogonadotrophic hypogonadism, a subtype of hypogonadism, include late, incomplete or lack of development at puberty, and sometimes short stature or the inability to smell; in females, a lack of breasts and menstrual periods, and in males a lack of sexual development, e.g., facial hair, penis and testes enlargement, deepening voice.

Hypoandrogenism is caused primarily by either dysfunction, failure, or absence of the gonads ("hypergonadotropic") or impairment of the hypothalamus or pituitary gland ("hypogonadotropic"), which in turn can be caused by a multitude of different stimuli, including genetic conditions (e.g., GnRH/gonadotropin insensitivity and enzymatic defects of steroidogenesis), tumors, trauma, surgery, autoimmunity, radiation, infections, toxins, drugs, and many others. Alternatively, it may be the result of conditions such as androgen insensitivity syndrome or hyperestrogenism. More simply, old age may also be a factor in the development of hypoandrogenism, as androgen levels decline with age.

Observed physiological abnormalities of the condition include a dramatic overexpression of aromatase and, accordingly, excessive levels of estrogens including estrone and estradiol and a very high rate of peripheral conversion of androgens to estrogens. In one study, cellular aromatase mRNA expression was found to be at least 10 times higher in a female patient compared to the control, and the estradiol/testosterone ratio after an injection of testosterone in a male patient was found to be 100 times greater than the control. Additionally, in another study, androstenedione, testosterone, and dihydrotestosterone (DHT) were found to be either low or normal in males, and follicle-stimulating hormone (FSH) levels were very low (likely due to suppression by estrogen, which has antigonadotropic effects as a form of negative feedback inhibition on sex steroid production in sufficiently high amounts), whereas luteinizing hormone (LH) levels were normal.

According to a recent review, estrone levels have been elevated in 17 of 18 patients (94%), while estradiol levels have been elevated only in 13 of 27 patients (48%). As such, estrone is the main estrogen elevated in the condition. In more than half of patients, circulating androstenedione and testosterone levels are low to subnormal. The ratio of circulating estradiol to testosterone is >10 in 75% of cases. FSH levels are said to be consistently low in the condition, while LH levels are in the low to normal range.

It is notable that gynecomastia has been observed in patients in whom estradiol levels are within the normal range. This has been suggested to be due to "in situ" conversion of adrenal androgens into estrone and then estradiol (via local 17β-HSD) in breast tissue (where aromatase activity may be particularly high).

The symptoms of AES, in males, include heterosexual precocity (precocious puberty with phenotypically-inappropriate secondary sexual characteristics; i.e., a fully or mostly feminized appearance), severe prepubertal or peripubertal gynecomastia (development of breasts in males before or around puberty), high-pitched voice, sparse facial hair, hypogonadism (dysfunctional gonads), oligozoospermia (low sperm count), small testes, micropenis (an ususually small penis), advanced bone maturation, an earlier peak height velocity (an accelerated rate of growth in regards to height), and short final stature due to early epiphyseal closure. The incidence of gynecomastia appears to be 100%, with 20 of 30 male cases opting for mastectomy according to a review.

In females, symptoms of AES include isosexual precocity (precocious puberty with phenotypically-appropriate secondary sexual characteristics), macromastia (excessively large breasts), an enlarged uterus, menstrual irregularities, and, similarly to males, accelerated bone maturation and short final height. Of seven females described in one report, three had macromastia (rate of ~43%). A 10-year-old girl with gigantomastia has subsequently also been described.

Fertility, though usually affected to one degree or another—especially in males—is not always impaired significantly enough to prevent sexual reproduction, as evidenced by vertical transmission of the condition by both sexes.

Examples of symptoms of hypogonadism with underdevelopment of the Gonads (testicles and ovaries) include delayed, reduced, or absent puberty, low libido, and infertility.

Polycystic ovary syndrome (PCOS) is a set of symptoms due to elevated androgens (male hormones) in women. Signs and symptoms of PCOS include irregular or no menstrual periods, heavy periods, excess body and facial hair, acne, pelvic pain, difficulty getting pregnant, and patches of thick, darker, velvety skin. Associated conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer.

PCOS is due to a combination of genetic and environmental factors. Risk factors include obesity, not enough physical exercise, and a family history of someone with the condition. Diagnosis is based on two of the following three findings: no ovulation, high androgen levels, and ovarian cysts. Cysts may be detectable by ultrasound. Other conditions that produce similar symptoms include adrenal hyperplasia, hypothyroidism, and hyperprolactinemia.

PCOS has no cure. Treatment may involve lifestyle changes such as weight loss and exercise. Birth control pills may help with improving the regularity of periods, excess hair growth, and acne. Metformin and anti-androgens may also help. Other typical acne treatments and hair removal techniques may be used. Efforts to improve fertility include weight loss, clomiphene, or metformin. In vitro fertilization is used by some in whom other measures are not effective.

PCOS is the most common endocrine disorder among women between the ages of 18 and 44. It affects approximately 2% to 20% of this age group depending on how it is defined. It is one of the leading causes of poor fertility. The earliest known description of what is now recognized as PCOS dates from 1721 in Italy.

The classic feature of gynecomastia is male breast enlargement with soft, compressible, and mobile subcutaneous chest tissue palpated under the areola of the nipple in contrast to softer fatty tissue. This enlargement may occur on one side or both. Dimpling of the skin and nipple retraction are not typical features of gynecomastia. Milky discharge from the nipple is also not a typical finding, but may be seen in a gynecomastic individual with a prolactin secreting tumor. An increase in the diameter of the areola and asymmetry of chest tissue are other possible signs of gynecomastia.

Males with gynecomastia may appear anxious or stressed due to concerns about the possibility of having breast cancer.

FSH insensitivity presents itself in females as two clusters of symptoms: 1) hypergonadotropic hypogonadism or hypoestrogenism, resulting in a delayed, reduced, or fully absent puberty and associated sexual infantilism (if left untreated), reduced uterine volume, and osteoporosis; and 2) ovarian dysgenesis or failure, resulting in primary or secondary amenorrhea, infertility, and normal sized to slightly enlarged ovaries. Males on the other hand are significantly less affected, presenting merely with partial or complete infertility, reduced testicular volume, and oligozoospermia (reduced spermatogenesis).

The deficiency causes the virilization of XX fetuses. Although they will have normal female internal genitalia, clitoromegaly often results from the high androgen levels in utero, along with ambiguous external genitalia upon birth.

Testosterone may be normal or elevated.

Later, the lack of estrogen results in the presentation of primary amenorrhea and tall stature. The taller than expected height occurs because estrogen normally causes fusion of the epiphyseal growth plates in the bones, and in its absence, the girl will keep growing longer. The gonadotropins LH and FSH will both be elevated and patients present with polycystic ovaries. Furthermore, the low estrogen will predispose those with the condition to osteoporosis.

Aromatase deficiency in the baby can also affect the mother during gestation, with cystic acne, hirsutism, deepening of the voice, and clitoromegaly. Increased circulating testosterone levels are the cause. The mother's symptoms resolve after she gives birth.

Follicle-stimulating hormone (FSH) insensitivity, or ovarian insensitivity to FSH in females, also referable to as ovarian follicle hypoplasia or granulosa cell hypoplasia in females, is a rare autosomal recessive genetic and endocrine syndrome affecting both females and males, with the former presenting with much greater severity of symptomatology. It is characterized by a resistance or complete insensitivity to the effects of follicle-stimulating hormone (FSH), a gonadotropin which is normally responsible for the stimulation of estrogen production by the ovaries in females and maintenance of fertility in both sexes. The condition manifests itself as hypergonadotropic hypogonadism (decreased or lack of production of sex steroids by the gonads despite high circulating levels of gonadotropins), reduced or absent puberty (lack of development of secondary sexual characteristics, resulting in sexual infantilism if left untreated), amenorrhea (lack of menstruation), and infertility in females, whereas males present merely with varying degrees of infertility and associated symptoms (e.g., decreased sperm production).

A related condition is luteinizing hormone (LH) insensitivity (termed Leydig cell hypoplasia when it occurs in males), which presents with similar symptoms to those of FSH insensitivity but with the symptoms in the respective sexes reversed (i.e., hypogonadism and sexual infantilism in males and merely problems with fertility in females); however, males also present with feminized or ambiguous genitalia (also known as pseudohermaphroditism), whereas ambiguous genitalia does not occur in females with FSH insensitivity. Despite their similar causes, LH insensitivity is considerably more common in comparison to FSH insensitivity.

Hirsutism is excessive body hair in men and women on parts of the body where hair is normally absent or minimal, such as on the chin or chest in particular, or the face or body in general. It may refer to a male pattern of hair growth that may be a sign of a more serious medical condition, especially if it develops well after puberty. It can be caused by increased levels of androgen hormones. The amount and location of the hair is measured by a Ferriman-Gallwey score. It is different than hypertrichosis, which is excessive hair growth anywhere on the body.

Hirsutism is usually the result of an underlying endocrine imbalance, which may be adrenal, ovarian, or central. Hirsutism is a commonly presenting symptom in dermatology, endocrinology, and gynecology clinics, and one that is considered to be the cause of much psychological distress and social difficulty. Facial hirsutism often leads to the avoidance of social situations and to symptoms of anxiety and depression.

Hirsutism affects between 5–15% of all women across all ethnic backgrounds. Depending on the definition and the underlying data, estimates indicate that approximately 40% of women have some degree of unwanted facial hair.

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Hirsutism affects members of any gender, since rising androgen levels can cause excessive body hair, particularly in locations where women normally do not develop terminal hair during puberty (chest, abdomen, back, and face). The medical term for excessive hair growth that affects any gender is hypertrichosis.

Hypogonadotropic hypogonadism (HH), also known as secondary or central hypogonadism, as well as gonadotropin-releasing hormone deficiency or gonadotropin deficiency (GD), is a condition which is characterized by hypogonadism due to an impaired secretion of gonadotropins, including follicle-stimulating hormone (FSH) and luteinizing hormone (LH), by the pituitary gland in the brain, and in turn decreased gonadotropin levels and a resultant lack of sex steroid production.

Aromatase excess syndrome (AES or AEXS), also sometimes referred to as familial hyperestrogenism or familial gynecomastia, is a rare genetic and endocrine syndrome which is characterized by an overexpression of aromatase, the enzyme responsible for the biosynthesis of the estrogen sex hormones from the androgens, in turn resulting in excessive levels of circulating estrogens and, accordingly, symptoms of hyperestrogenism. It affects both sexes, manifesting itself in males as marked or complete phenotypical feminization (with the exception of the genitalia; i.e., no pseudohermaphroditism) and in females as hyperfeminization.

To date, 30 males and 8 females with AES among 15 and 7 families, respectively, have been described in the medical literature.

In the majority of young women, hyperandrogenism leads to oily skin, acne, hirutism, menstrual irregularities and, in some cases, androgenic alopecia, clitorimegaly, changes in muscle mass and deepening of the voice. Insulin resistance can be present in different forms; some persons have high concentrations of insulin but normal levels of glucose, while others have glucose measurements in the diabetic range. A history of diabetic symptoms such as polydipsia, polyuria and weight loss may sometimes, but not always, be present. Other related symptoms to HAIR-AN syndrome include enlarged clitoris, increased libido, glucose intolerance, irregular menstruation, increased blood pressure, infertility. Obesity is also one such symptoms in some women, and is also marked in women affected by PCOS, hirsutism, acanthosis nigricans.

Hyperthecosis (or ovarian hyperthecosis) is hyperplasia of the theca interna of the ovary. Hyperthecosis occurs when an area of luteinization occurs along with stromal hyperplasia. The luteinized cells produce androgens, which may lead to hirsutism and virilization (or masculinization) in affected women.

The term hyperthecosis refers to the presence of nests of luteinized theca cells in the ovarian stroma due to differentiation of the ovarian interstitial cells into steroidogenically active luteinized stromal cells. These nests or islands of luteinized theca cells are scattered throughout the stroma of the ovary, rather than being confined to areas around cystic follicles as in polycystic ovary syndrome (PCOS). These luteinized theca cells result is greater production of androgens.

Seen as a severe form of PCOS, the clinical features of hyperthecosis are similar to those of PCOS. Women with hyperthecosis often have more markedly elevated testosterone, more hirsutism, and are much more likely to be virilized. While elevated androgens in postmenopausal women is rare, hyperthecosis can present in both premenopausal or postmenopausal women. Women with hyperthecosis may or may not have always had underlying PCOS.

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either "congenital" or "acquired", but the majority of cases are of the former nature.

Gynecomastia is an endocrine system disorder in which there is a non-cancerous increase in the size of male breast tissue. Psychological distress may occur.

The development of gynecomastia is usually associated with benign pubertal changes. However, 75% of pubertal gynecomastia cases resolve within two years of onset without treatment. In rare cases, gynecomastia has been known to occur in association with certain disease states. The pathologic causes of gynecomastia are diverse and may include Klinefelter syndrome, certain cancers, endocrine disorders, metabolic dysfunction, various medications, or may occur due to a natural decline in testosterone production. Disturbances in the endocrine system that lead to an increase in the ratio of estrogens/androgens are thought to be responsible for the development of gynecomastia. This may occur even if the levels of estrogens and androgens are both appropriate but the ratio is altered. Diagnosis is based on signs and symptoms.

Conservative management of gynecomastia is often appropriate as the condition commonly resolves on its own. Medical treatment of gynecomastia that has persisted beyond two years is often ineffective. Medications such as aromatase inhibitors have been found to be effective in rare cases of gynecomastia from disorders such as aromatase excess syndrome or Peutz–Jeghers syndrome, but surgical removal of the excess tissue is usually required.

Gynecomastia is common. Physiologic gynecomastia develops in up to 70% of adolescent boys. Newborns and adolescent males often experience temporary gynecomastia due to the influence of maternal hormones and hormonal changes during puberty, respectively.

The symptoms of isolated 17,20-lyase deficiency, in males, include pseudohermaphroditism (i.e., feminized, ambiguous, or mildly underdeveloped (e.g., micropenis, perineal hypospadias, and/or cryptorchidism (undescended testes)) external genitalia), female gender identity, and, in non-complete cases of deficiency where partial virilization occurs, gynecomastia up to Tanner stage V (due to low androgen levels, which results in a lack of suppression of estrogen); in females, amenorrhoea or, in cases of only partial deficiency, merely irregular menses, and enlarged cystic ovaries (due to excessive stimulation by high levels of gonadotropins); and in both sexes, hypergonadotropic hypogonadism (hypogonadism despite high levels of gonadotropins), delayed, impaired, or fully absent adrenarche and puberty with an associated reduction in or complete lack of development of secondary sexual characteristics (sexual infantilism), impaired fertility or complete sterility, tall stature (due to delayed epiphyseal closure), eunuchoid skeletal proportions, delayed or absent bone maturation, and osteoporosis.