The common pathway of sexual differentiation, where a productive human female has an XX chromosome pair, and a productive male has an XY pair, is relevant to the development of intersex conditions.

During fertilization, the sperm adds either an X (female) or a Y (male) chromosome to the X in the ovum. This determines the genetic sex of the embryo. During the first weeks of development, genetic male and female fetuses are "anatomically indistinguishable", with primitive gonads beginning to develop during approximately the sixth week of gestation. The gonads, in a "bipotential state", may develop into either testes (the male gonads) or ovaries (the female gonads), depending on the consequent events. Through the seventh week, genetically female and genetically male fetuses appear identical.

At around eight weeks of gestation, the gonads of an XY embryo differentiate into functional testes, secreting testosterone. Ovarian differentiation, for XX embryos, does not occur until approximately Week 12 of gestation. In normal female differentiation, the Müllerian duct system develops into the uterus, Fallopian tubes, and inner third of the vagina.

In males, the Müllerian duct-inhibiting hormone MIH causes this duct system to regress. Next, androgens cause the development of the Wolffian duct system, which develops into the vas deferens, seminal vesicles, and ejaculatory ducts.

By birth, the typical fetus has been completely "sexed" male or female, meaning that the genetic sex (XY-male or XX-female) corresponds with the phenotypical sex; that is to say, genetic sex corresponds with internal and external gonads, and external appearance of the genitals.

DSDs are medical conditions involving the way the reproductive system develops from infancy (and before birth) through young adulthood. There are several types of DSDs and their effect on the external and internal reproductive organs varies greatly.

A frequently-used social and medical adjective for people with DSDs is "intersex". Parents with DSD children and clinicians involved in DSD treatment usually try to make clear distinctions between biological sex, social gender, and sexual orientation. This helps reduce confusion about the differences between being intersex, being transgender, and being gay/lesbian.

The most common DSD is congenital adrenal hyperplasia (CAH), which results in a person with female (XX) chromosomes having genitals that look somewhat masculine. In mild cases CAH results in a slightly enlarged clitoris, while in more severe cases it can be difficult to decide (just by looking) whether a baby is male or female (this is called having ambiguous genitals). Nevertheless, if they are old enough to know the difference, most children with CAH think of themselves as girls. CAH is caused by a problem with the adrenal glands and is usually treated by taking a daily medication to replace or supplement the missing adrenal hormones. (When this adrenal problem occurs in people with male (XY) chromosomes, the result is over-masculinization and premature puberty).

Another common DSD is androgen insensitivity syndrome (AIS), which means that a person with male (XY) chromosomes does not respond to testosterone in the usual way. This results in a body that to some degree has a feminine appearance. In Complete Androgen Insensitivity Syndrome (CAIS) the result is a totally feminine appearance, including typical female breast development. Consequently, most young women with CAIS are unaware of their condition until the early teen years when they fail to menstruate. In the milder form, called Partial Androgen Insensitivity Syndrome (PAIS), the genitals can vary from mostly female to almost completely male. Some people with PAIS think of themselves as girls/women, others regard themselves as boys/men, and some consider themselves mixed-gender.

One of the more unusual DSDs is 5-alpha-reductase deficiency (5ARD). It is caused by a shortage early in life of an enzyme that activates testosterone. In this condition, a person with male (XY) chromosomes has a body that appears female before puberty. After puberty begins, other testosterone-activating enzymes become available and the body soon takes on a masculine appearance, with the scrotum and penis usually reaching typical or nearly-typical size. If 5ARD is diagnosed at a young age, the child is often raised as a boy (a 1996 Brazilian study suggested that the majority of adults with this condition consider themselves men but this has been questioned in some more recent research).

In addition to CAH, CAIS, PAIS, and 5ARD there are several rarer types of DSDs, and in some cases it is not possible to make a clear diagnosis of the underlying condition.

The penis and clitoris are essentially the same organ (differing only in size, and generically called the phallus). In typical males, the urethra is located at the tip of the penis, while in typical females the urethra is located below the base of the clitoris. When the phallus is of intermediate size, it is possible also to have a urethral opening located along the shaft; this condition is known as hypospadias.

Open-minded parenting, appropriate and conservative medical intervention, and age-appropriate child involvement in the treatment plan contribute greatly to successful outcomes for the entire range of DSDs.

According to the UN Office of the High Commissioner for Human Rights:

In biological terms, sex may be determined by a number of factors present at birth, including:

- the number and type of sex chromosomes;

- the type of gonads—ovaries or testicles;

- the sex hormones;

- the internal reproductive anatomy (such as the uterus in females); and

- the external genitalia.

People whose characteristics are not either all typically male or all typically female at birth are intersex.

Some intersex traits are not always visible at birth; some babies may be born with ambiguous genitals, while others may have ambiguous internal organs (testes and ovaries). Others will not become aware that they are intersex unless they receive genetic testing, because it does not manifest in their phenotype.

Disorders of sex development (DSD), sometimes referred to as disorders of sex differentiation or differences of sex development, are medical conditions involving the reproductive system. More specifically, these terms refer to "congenital conditions in which development of chromosomal, gonadal, or anatomical sex is atypical."

The term has been controversial, and research has shown that affected people experience a negative impact, with the terminology impacting choice and utilization of health care providers. The World Health Organization and many medical journals still reference DSDs as intersex traits or conditions. The Council of Europe, and Inter-American Commission on Human Rights have called for a review of medical classifications that unnecessarily medicalize intersex traits.

Sex determination and differentiation is generalized with chromosomal sex during fertilization. At early stages, phenotypic sex does not match chromosomal sex—until later during intrauterine development, sexual maturation is reached. During intrauterine development, females change to male with the testes moving down from a blind vaginal pouch with a developing scrotum, as well as a penis which initially resembled a clitoris. What seems like a female phenotype is altered by increased testosterone levels secretion.

Mutations affecting the androgen receptor (AR) gene may cause either complete or partial androgen insensitivity syndrome. Androgen, a hormone used to describe a group of sex steroid hormones, is responsible for affecting male pseudohermaphroditism. The differentiation of the fetus as male takes place during the sixth or seventh week of gestation. The development is directed by the testicular determining factor: the gene SRY (sex determining region on Y chromosome). Throughout 9th to 13th week, the development of a male genitalia is dependent upon the conversion of testosterone to the more potent androgen by the action of 5α-reductase within the target tissues of the genitalia. A type of internal male pseudohermaphroditism is Persistent Müllerian duct syndrome, which is developed through synthesis of Müllerian-inhibiting factor defects. In such instances, duct derivatives are now in 46XY males—this includes the uterus, fallopian tubes, and upper vagina. These individuals with a hernia sac and bowel loops were found with duct derivatives as well as testes.

A study on a male pseudohermaphrodite kitten showed there was a combination of gastrointestinal and urogenital congenital abnormalities. It was confirmed to have type II atresia ani and rectovaginal fistula that is associated with male pseudohermaphroditism.

Surgery is sometimes performed to alter the appearance of the genitals. However many surgeries performed on intersex people lack clear evidence of necessity, can be considered as mutilating, and are widely considered to be human rights violations when performed without the informed consent of the recipient.

Approximately 1 in 20,000 individuals with a male appearance have 46,XX testicular disorder.

In about 80 percent of individuals with 46,XX testicular disorder of sex development, the condition results from an abnormal exchange of genetic material between chromosomes (translocation). This exchange occurs as a random event during the formation of sperm cells in the affected person's father. The translocation causes the SRY gene to be misplaced, almost always onto an X chromosome. If a fetus is conceived from a sperm cell with an X chromosome bearing the SRY gene, it will develop as a male despite not having a Y chromosome. This form of the condition is called SRY-positive 46,XX testicular disorder of sex development.

About 20 percent of those with 46 XX testicular disorder of sex development do not have the SRY gene. This form of the condition is called SRY-negative 46,XX testicular disorder of sex development. The cause of the disorder in these individuals is often unknown, although changes affecting other genes have been identified. Individuals with SRY-negative 46,XX testicular disorder of sex development are more likely to have ambiguous genitalia than are people with the SRY-positive form.

Treatment includes androgen (testosterone) supplementation to artificially initiate puberty, testicular prosthetic implantation, and psychological support. Gender Dysphoria may result in anorchic individuals who are assigned male at birth and raised as male despite lacking the necessary masculinizing hormones during prenatal, childhood, and adolescent development. Anorchic individuals who have a female identity may be administered estrogen alone in place of testosterone as no androgen blockers are necessary due to the lack of gonads.

The 2006 Consensus statement on the management of intersex disorders states that individuals with 17β-hydroxysteroid dehydrogenase III deficiency have an intermediate risk of germ cell malignancy, at 28%, recommending that gonads be monitored. A 2010 review put the risk of germ cell tumors at 17%.

The management of 17β-hydroxysteroid dehydrogenase III deficiency can consist, according to one source, of the elimination of gonads prior to puberty, in turn halting masculinization.

Hewitt and Warne state that, children with 17β-hydroxysteroid dehydrogenase III deficiency who are raised as girls often later identify as male, describing a "well known, spontaneous change of gender identity from female to male" that "occurs after the onset of puberty." A 2005 systematic review of gender role change identified the rate of gender role change as occurring in 39–64% of individuals with 17β-hydroxysteroid dehydrogenase III deficiency raised as girls.

Estimates for the incidence of androgen insensitivity syndrome are based on a relatively small population size, thus are known to be imprecise. CAIS is estimated to occur in one of every 20,400 46,XY births. A nationwide survey in the Netherlands based on patients with genetic confirmation of the diagnosis estimates that the minimal incidence of CAIS is one in 99,000. The incidence of PAIS is estimated to be one in 130,000. Due to its subtle presentation, MAIS is not typically investigated except in the case of male infertility, thus its true prevalence is unknown.

Low sexual desire alone is not equivalent to HSDD because of the requirement in HSDD that the low sexual desire causes marked distress and interpersonal difficulty and because of the requirement that the low desire is not better accounted for by another disorder in the DSM or by a general medical problem. It is therefore difficult to say exactly what causes HSDD. It is easier to describe, instead, some of the causes of low sexual desire.

In men, though there are theoretically more types of HSDD/low sexual desire, typically men are only diagnosed with one of three subtypes.

- Lifelong/generalised: The man has little or no desire for sexual stimulation (with a partner or alone) and never had.

- Acquired/generalised: The man previously had sexual interest in his present partner, but lacks interest in sexual activity, partnered or solitary.

- Acquired/situational: The man was previously sexually interested in his present partner but now lacks sexual interest in this partner but has desire for sexual stimulation (i.e. alone or with someone other than his present partner.)

Though it can sometimes be difficult to distinguish between these types, they do not necessarily have the same cause. The cause of lifelong/generalized HSDD is unknown. In the case of acquired/generalized low sexual desire, possible causes include various medical/health problems, psychiatric problems, low levels of testosterone or high levels of prolactin. One theory suggests that sexual desire is controlled by a balance between inhibitory and excitatory factors. This is thought to be expressed via neurotransmitters in selective brain areas. A decrease in sexual desire may therefore be due to an imbalance between neurotransmitters with excitatory activity like dopamine and norepinephrine and neurotransmitters with inhibitory activity, like serotonin. The, New York-based, "New View Campaign" organization has expressed skepticism about too much emphasis on explanations based on neurotransmitters because emphasis on such explanations have been made largely by "educational" efforts funded by Boehringer-Ingelheim while it was attempting to get the FDA to approve a drug affecting neurotransmitters for treatment for HSDD. Low sexual desire can also be a side effect of various medications. In the case of acquired/situational HSDD, possible causes include intimacy difficulty, relationship problems, sexual addiction, and chronic illness of the man’s partner. The evidence for these is somewhat in question. Some claimed causes of low sexual desire are based on empirical evidence. However, some are based merely on clinical observation. In many cases, the cause of HSDD is simply unknown.

There are some factors that are believed to be possible causes of HSDD in women. As with men, various medical problems, psychiatric problems (such as mood disorders), or increased amounts of prolactin can cause HSDD. Other hormones are believed to be involved as well. Additionally, factors such as relationship problems or stress are believed to be possible causes of reduced sexual desire in women. According to one recent study examining the affective responses and attentional capture of sexual stimuli in women with and without HSDD, women with HSDD do not appear to have a negative association to sexual stimuli, but rather a weaker positive association than women without HSDD

Anorchia (or anorchism) is an XY disorder of sex development in which individuals have both testes absent at birth. Within a few weeks of fertilization, the embryo develops rudimentary gonads (testes), which produce hormones responsible for the development of the reproductive system. If the testes fail to develop within eight weeks, the baby will develop female genitalia (see Swyer syndrome). If the testes begin to develop but are lost or cease to function between eight and 10 weeks, the baby will have ambiguous genitalia when it is born. However, if the testes are lost after 14 weeks, the baby will have partial male genitalia with the notable absence of gonads.

Tests include observable lack of testes, low testosterone levels (typical female levels), elevated follicle stimulating hormone and luteinizing hormone levels, XY karyotype, ultrasound or magnetic resonance imaging showing absent gonadal tissue, low bone density, low anti-Müllerian hormone levels, and surgical exploration for evidence of male gonadal tissue.

Androgen insensitivity syndrome (AIS) is an intersex condition in which there is a partial or complete inability of many cells in the affected genetic male to respond to androgenic hormones. This can prevent or impair the masculinization of male genitalia in the developing genetic male (chromosomal XY) fetus, as well as the development of male secondary sexual characteristics at puberty. Clinical phenotypes range from a normal male habitus with mild spermatogenic defect or reduced secondary terminal hair; to a full female habitus despite the presence of a Y-chromosome. Women (chromosomal XX) who are heterozygous for the AR gene have normal primary and secondary sexual characteristics; this female carrier will pass the affected AR gene to any child she has with 50% likelihood. AIS is the largest single entity that leads to 46,XY undermasculinized genitalia.

The androgen receptor (AR), which is defective due to a mutation in most of these syndromes, is a type of nuclear receptor that is activated by binding to either of the androgenic hormones (testosterone or dihydrotestosterone) in the cytoplasm, and then translocates into the nucleus where it binds to DNA, provided androgen response elements and coactivators are present. This combination functions as a transcription complex to turn on androgen gene expression. Thus the AR activates these genes to mediate the effects of androgens in the human body, including the development and maintenance of the male sexual phenotype and generalized anabolic effects. Over 400 AR mutations have been reported.

AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitivity syndrome (CAIS) is indicated when the external genitalia are that of a normal female; mild androgen insensitivity syndrome (MAIS) is indicated when the external genitalia are that of a normal male, and partial androgen insensitivity syndrome (PAIS) is indicated when the external genitalia are partially, but not fully, masculinized.

Management of AIS is currently limited to symptomatic management; no method is currently available to correct the malfunctioning androgen receptor proteins produced by "AR" gene mutations. Areas of management include sex assignment, genitoplasty, gonadectomy in relation to tumor risk, hormone replacement therapy, genetic counseling, and psychological counseling.

A problem for people with penile agenesis is the absence of a urinary outlet. Before genital metamorphosis, the urethra runs down the anal wall, to be pulled away by the genital tubercle during male development. Without male development this does not occur. The urethra can be surgically redirected to the rim of the anus immediately after birth to enable urination and avoid consequent internal irritation from urea concentrate. In such cases, the perineum may be left devoid of any genitalia, male or female.

A working penis transplant on to an agenetic patient has never been successful. Only one major penis graft was successfully completed. This occurred in China and the patient shortly rejected it on psychological grounds. However a full female or agenetic to male transplant is not yet facilitated to fulfil full reproductive functions.

On March 18, 2013, it was announced that Andrew Wardle, a British man born without a penis, was going to receive a pioneering surgery to create a penis for him. The surgeons hope to "fold a large flap of skin from his arm — complete with its blood vessels and nerves — into a tube to graft onto his pubic area." If the surgery goes well, the odds of starting a family are very good.

In an embryo, the conversion of the gonads into testicles in males-to-be and into ovaries in females-to-be is the function of Leydig cells. In testicular agenesis, this process fails. Penile agenesis can be caused by testicular agenesis. Testes are the sole producer of 5-alpha dihydrotestosterone (5aDHT) in the male body. Where the gonads fail to metamorphose into testes, there is no 5aDHT. Therefore, the masculising process that builds the genital tubercle, the precursor to the penis, is stillborn. When this happens, the child is born with both penile and testicular agenesis and is known by the slang term "nullo". This combination of both conditions is estimated to occur in between 20-30 million male births.

Penile agenesis can exist independently after full testicular development; in this case its cause is unknown.

During embryogenesis, without any external influences for or against, the human reproductive system is intrinsically conditioned to give rise to a female reproductive organisation.

As a result, if a gonad cannot express its sexual identity via its hormones—as in gonadal dysgenesis—then the affected person, no matter whether their chromosomes are XY or XX, will develop external female genitalia. Internal female genitalia, primarily the uterus, may or may not be present depending on the cause of the disorder.

In both sexes, the commencement and progression of puberty require functional gonads that will work in harmony with the hypothalamic and pituitary glands to produce adequate hormones.

For this reason, in gonadal dysgenesis the accompanying hormonal failure also prevents the development of secondary sex characteristics in either sex, resulting in a sexually infantile female appearance and infertility.

Gynandromorphism has been observed in numerous animal species, e.g., crustaceans such as lobsters and crabs, many bird species. A clear example in birds involves gynandromorphic zebra finch. These birds have lateralised brain structures in the face of a common steroid signal, providing strong evidence for a non-hormonal primary sex mechanism regulating brain differentiation.

The numbers of women with SCI giving birth and having healthy babies are increasing. Around a half to two-thirds of women with SCI report they might want to have children, and 14–20% do get pregnant at least once. Although female fertility is not usually permanently reduced by SCI, there is a stress response that can happen immediately post-injury that alters levels of fertility-related hormones in the body. In about half of women, menstruation stops after the injury but then returns within an average of five months—it returns within a year for a large majority. After menstruation returns, women with SCI become pregnant at a rate close to that of the rest of the population.

Pregnancy is associated with greater-than-normal risks in women with SCI, among them increased risk of deep vein thrombosis, respiratory infection, and urinary tract infection. Considerations exist such as maintaining proper positioning in a wheelchair, prevention of pressure sores, and increased difficulty moving due to weight gain and changes in center of balance. Assistive devices may need to be altered and medications changed.

For women with injuries above T6, a risk during labor and delivery that threatens both mother and fetus is autonomic dysreflexia, in which the blood pressure increases to dangerous levels high enough to cause potentially deadly stroke. Drugs such as nifedipine and captopril can be used to manage an episode if it occurs, and epidural anesthesia helps although it is not very reliable in women with SCI. Anesthesia is used for labor and delivery even for women without sensation, who may only experience contractions as abdominal discomfort, increased spasticity, and episodes of autonomic dysreflexia. Reduced sensation in the pelvic area means women with SCI usually have less painful delivery; in fact, they may fail to realize when they go into labor. If there are deformities in the pelvis or spine caesarian section may be necessary. Babies of women with SCI are more likely to be born prematurely, and, premature or not, they are more likely to be small for their gestational time.

Hypoactive sexual desire disorder (HSDD) or inhibited sexual desire (ISD) is considered a sexual dysfunction and is characterized as a lack or absence of sexual fantasies and desire for sexual activity, as judged by a clinician. For this to be regarded as a disorder, it must cause marked distress or interpersonal difficulties and not be better accounted for by another mental disorder, a drug (legal or illegal), some other medical condition, or asexuality. A person with ISD will not start, or respond to their partner's desire for, sexual activity.

There are various subtypes. HSDD can be general (general lack of sexual desire) or situational (still has sexual desire, but lacks sexual desire for current partner), and it can be acquired (HSDD started after a period of normal sexual functioning) or lifelong (the person has always had no/low sexual desire.)

HSDD has garnered much criticism, primarily by asexual activists. They point out that HSDD puts asexuality in the same position homosexuality was from 1974-1987. The DSM at that time recognised 'ego-dystonic homosexuality' as a disorder, defined as sexual interest in the same sex that caused significant distress. The DSM itself officially recognized this as unnecessarily pathologizing homosexuality and removed it as a disorder in 1987.

A gynandromorph can have bilateral asymmetry—one side female and one side male. Alternatively, the distribution of male and female tissue can be more haphazard.

Bilateral gynandromorphy arises very early in development, typically when the organism has between 8 and 64 cells. Later stages produce a more random pattern.

Men with SCI rank the ability to father children among their highest concerns relating to sexuality. Male fertility is reduced after SCI, due to a combination of problems with erections, ejaculation, and quality of the semen. As with other types of sexual response, ejaculation can be psychogenic or reflexogenic, and the level of injury affects a man's ability to experience each type. As many as 95% of men with SCI have problems with ejaculation (anejaculation), possibly due to impaired coordination of input from different parts of the nervous system. Erection, orgasm, and ejaculation can each occur independently, although the ability to ejaculate seems linked to the quality of the erection, and the ability to orgasm is linked to the ejaculation facility. Even men with complete injuries may be able to ejaculate, because other nerves involved in ejaculation can effect the response without input from the spinal cord. In general, the higher the level of injury, the more physical stimulation the man needs to ejaculate. Conversely, premature or spontaneous ejaculation can be a problem for men with injuries at levels T12–L1. It can be severe enough that ejaculation is provoked by thinking a sexual thought, or for no reason at all, and is not accompanied by orgasm.

Most men have a normal sperm count, but a high proportion of sperm are abnormal; they are less motile and do not survive as well. The reason for these abnormalities is not known, but research points to dysfunction of the seminal vesicles and prostate, which concentrate substances that are toxic to sperm. Cytokines, immune proteins which promote an inflammatory response, are present at higher concentrations in semen of men with SCI, as is platelet-activating factor acetylhydrolase; both are harmful to sperm. Another immune-related response to SCI is the presence of a higher number of white blood cells in the semen.

The prevalence of pedophilia in the general population is not known, but is estimated to be lower than 5% among adult men. Less is known about the prevalence of pedophilia in women, but there are case reports of women with strong sexual fantasies and urges towards children. Most sexual offenders against children are male. Females may account for 0.4% to 4% of convicted sexual offenders, and one study estimates a 10 to 1 ratio of male-to-female child molesters. The true number of female child molesters may be underrepresented by available estimates, for reasons including a "societal tendency to dismiss the negative impact of sexual relationships between young boys and adult women, as well as women's greater access to very young children who cannot report their abuse", among other explanations.

The term "pedophile" is commonly used by the public to describe all child sexual abuse offenders. This usage is considered problematic by researchers, because many child molesters do not have a strong sexual interest in prepubescent children, and are consequently not pedophiles. There are motives for child sexual abuse that are unrelated to pedophilia, such as stress, marital problems, the unavailability of an adult partner, general anti-social tendencies, high sex drive, or alcohol use. As child sexual abuse is not automatically an indicator that its perpetrator is a pedophile, offenders can be separated into two types: pedophilic and non-pedophilic (or preferential and situational). Estimates for the rate of pedophilia in detected child molesters generally range between 25% and 50%. A 2006 study found that 35% of its sample of child molesters were pedophilic. Pedophilia appears to be less common in incest offenders, especially fathers and step-fathers. According to a U.S. study on 2429 adult male sex offenders who were categorized as "pedophiles", only 7% identified themselves as exclusive; indicating that many or most child sexual abusers may fall into the non-exclusive category.

Some pedophiles do not molest children. Little is known about this population because most studies of pedophilia use criminal or clinical samples, which may not be representative of pedophiles in general. Researcher Michael Seto suggests that pedophiles who commit child sexual abuse do so because of other anti-social traits in addition to their sexual attraction. He states that pedophiles who are "reflective, sensitive to the feelings of others, averse to risk, abstain from alcohol or drug use, and endorse attitudes and beliefs supportive of norms and the laws" may be unlikely to abuse children. A 2015 study indicates that pedophiles who molested children are neurologically distinct from non-offending pedophiles. The pedophilic molesters had neurological deficits suggestive of disruptions in inhibitory regions of the brain, while non-offending pedophiles had no such deficits.

According to Abel, Mittleman, and Becker (1985) and Ward "et al." (1995), there are generally large distinctions between the characteristics of pedophilic and non-pedophilic molesters. They state that non-pedophilic offenders tend to offend at times of stress; have a later onset of offending; and have fewer, often familial, victims, while pedophilic offenders often start offending at an early age; often have a larger number of victims who are frequently extrafamilial; are more inwardly driven to offend; and have values or beliefs that strongly support an offense lifestyle. One study found that pedophilic molesters had a median of 1.3 victims for those with girl victims and 4.4 for those with boy victims. Child molesters, pedophilic or not, employ a variety of methods to gain sexual access to children. Some groom their victims into compliance with attention and gifts, while others use threats, alcohol or drugs, or physical force.

Psychosexual disorders can vary greatly in severity and treatability. Medical professionals and licensed therapists are necessary in diagnosis and treatment plans. Treatment can vary from therapy to prescription medication. Sex therapy, behavioral therapy, and group therapy may be helpful to those suffering distress from sexual dysfunction. More serious sexual perversions may be treated with androgen blockers or selective serotonin reuptake inhibitors (SSRIs) to help restore hormonal and neurochemical balances.

The condition may be due to:

- Turner syndrome, and its variations (i.e. mosaicism)

- XX gonadal dysgenesis, also pure gonadal dysgenesis, 46,XX

- Swyer syndrome, also pure gonadal dysgenesis, 46,XY

- Perrault syndrome, XX gonadal dysgenesis + sensorineural hearing loss

- Mixed gonadal dysgenesis

- Exposure to environmental endocrine disruptors