Just as with erectile dysfunction in men, lack of sexual function in women may be treated with hormonal patches or tablets to correct hormonal imbalances, clitoral vacuum pump devices and medication to improve blood flow, sexual sensation and arousal.

Many practitioners today treat both men and women who have SSRI-induced anorgasmia with sildenafil, more commonly known as Viagra. While this approach is known to work well in men with sexual dysfunction, it is only recently that the effectiveness of sildenafil in women with sexual dysfunction is coming to light. A recent study by H. G. Nurnberg et al. showed a complete or very significant reversal of their sexual dysfunction upon taking sildenafil one hour prior to sexual activity. In this study, eight out of the nine women required 50 mg of sildenafil while the 9th woman required 100 mg of sildenafil.

Another option for women who have SSRI-induced anorgasmia is the use of vardenafil. Vardenafil is a type 5 phosphodiesterase (PDE5) inhibitor that facilitates muscle relaxation and improves penile erection in men. However, there is much controversy about the efficiency of the drug used in the reversal of female sexual dysfunction. Vardenafil is similar to sildenafil, but vardenafil is less expensive and may be covered under some insurance plans. A study by A.K. Ashton M.D. has shown that in the case of one particular woman, the effects of vardenafil as opposed to sildenafil have not only been comparable in the effectiveness, but that vardenafil is cheaper and reversal of sexual dysfunction requires a smaller dose. So far, vardenafil has been approved by the Food and Drug administration only for use in men.

The NIH states that yohimbine hydrochloride has been shown in human studies to be possibly effective in the treatment of male impotence resulting from erectile dysfunction or SSRI usage (e.g., anorgasmia). Published reports have shown it to be effective in the treatment of orgasmic dysfunction in men.

Cabergoline, an agonist of dopamine D₂ receptors which inhibits prolactin production, was found in a small study to fully restore orgasm in one third of anorgasmic subjects, and partially restore orgasm in another third. Limited data has shown that the drug amantadine may help to relieve SSRI-induced sexual dysfunction. Cyproheptadine, buspirone, stimulants such as amphetamines (including the antidepressant bupropion), nefazodone and yohimbine have been used to treat SSRI-induced anorgasmia. Reducing the SSRI dosage may also resolve anorgasmia problems.

Treatment depends on the cause.

Exercise, particularly aerobic exercise during midlife is effective for preventing ED; exercise as a treatment is under investigation. For tobacco smokers, cessation results in a significant improvement.

Oral pharmacotherapy and vacuum erection devices are first-line treatments, followed by injections of drugs into the penis, and penile implants.

The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken orally.

A cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for erectile dysfunction.

One of the following medications maybe injected into the penis: papaverine, phentolamine, and prostaglandin E1.

Estrogens are responsible for the maintenance of collagen, elastic fibers, and vasoculature of the urogenital tract, all of which are important in maintaining vaginal structure and functional integrity; they are also important for maintaining vaginal pH and moisture levels, both of which aid in keeping the tissues lubricated and protected. Prolonged estrogen deficiency leads to atrophy, fibrosis, and reduced blood flow to the urogenital tract, which is what causes menopausal symptoms such as vaginal dryness and pain related to sexual activity and/or intercourse. It has been consistently demonstrated that women with lower sexual functioning have lower estradiol levels.

Androgen therapy for hypoactive sexual desire disorder (HSDD) has a small benefit but its safety is not known. It is not approved as a treatment in the United States. If used it is more common among women who have had an oophorectomy or who are in a postmenopausal state. However, like most treatments, this is also controversial. One study found that after a 24-week trial, those women taking androgens had higher scores of sexual desire compared to a placebo group. As with all pharmacological drugs, there are side effects in using androgens, which include hirutism, acne, ploycythaemia, increased high-density lipoproteins, cardiovascular risks, and endometrial hyperplasia is a possibility in women without hysterectomy. Alternative treatments include topical estrogen creams and gels can be applied to the vulva or vagina area to treat vaginal dryness and atrophy.

Although there are no approved pharmaceuticals for addressing female sexual disorders, several are under investigation for their effectiveness. A vacuum device is the only approved medical device for arousal and orgasm disorders. It is designed to increase blood flow to the clitoris and external genitalia. Women experiencing pain with intercourse are often prescribed pain relievers or desensitizing agents. Others are prescribed lubricants and/or hormone therapy. Many patients with female sexual dysfunction are often also referred to a counselor or therapist for psychosocial counseling.

Many men attempt to treat themselves for premature ejaculation by trying to distract themselves, such as by trying to focus their attention away from the sexual stimulation. There is little evidence to indicate that it is effective and it tends to detract from the sexual fulfilment of both partners. Other self-treatments include thrusting more slowly, withdrawing the penis altogether, purposefully ejaculating before sexual intercourse, and using more than one condom. Using more than one condom is not recommended as the friction will often lead to breakage. Some men report these to have been helpful.

By the 21st century, most men with premature ejaculation could cure themselves, either on their own or with a partner, using self-help resources, and only those with unusually severe problems had to consult sex therapists, who cured 75 to 80 percent.

Several treatments have been tested for treating premature ejaculation. A combination of medication and non-medication treatments is often the most effective method.

The condition is sometimes classified as a psychiatric disorder. However, it can also be caused by medical problems such as diabetic neuropathy, multiple sclerosis, genital mutilation, complications from genital surgery, pelvic trauma (such as from a straddle injury caused by falling on the bars of a climbing frame, bicycle or gymnastics beam), hormonal imbalances, total hysterectomy, spinal cord injury, cauda equina syndrome, uterine embolisation, childbirth trauma (vaginal tearing through the use of forceps or suction or a large or unclosed episiotomy), vulvodynia and cardiovascular disease.

A common cause of situational anorgasmia, in both men and women, is the use of anti-depressants, particularly selective serotonin reuptake inhibitors (SSRIs). Though reporting of anorgasmia as a side effect of SSRIs is not precise, studies have found that 17–41% of users of such medications are affected by some form of sexual dysfunction.

Another cause of anorgasmia is opiate addiction, particularly to heroin.

About 15% of women report difficulties with orgasm, and as many as 10% of women in the United States have never climaxed. Only 29% of women always have orgasms with their partner.

Although erections are not necessary for satisfying sexual encounters, many men see them as important, and treating erectile dysfunction improves their relationships and quality of life. Whatever treatment is used, it works best in combination with talk-oriented therapy to help integrate it into the sex life.

Oral medications and mechanical devices are the first choice in treatment because they are less invasive, are often effective, and are well tolerated. Oral medications include sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra).

Penis pumps induce erections without the need for drugs or invasive treatments. To use a pump, the man inserts his penis into a cylinder, then pumps it to create a vacuum which draws blood into the penis, making it erect. He then slides a ring from the outside of the cylinder onto the base of the penis to hold the blood in and maintain the erection. A man who is able to get an erection but has trouble maintaining it for long enough can use a ring by itself. The ring cannot be left on for more than 30 minutes and cannot be used at the same time as anticoagulant medications.

If oral medications and mechanical treatments fail, the second choice is local injections: medications such as papaverine and prostaglandin that alter the blood flow and trigger erection are injected into the penis. This method is preferred for its effectiveness, but can cause pain and scarring.

Another option is to insert a small pellet of medication into the urethra, but this requires higher doses than injections and may not be as effective. Topical medications to dilate the blood vessels have been used, but are not very effective or well tolerated. Electrical stimulation of efferent nerves at the S2 level can be used to trigger an erection that lasts as long as the stimulation does.

Surgical implants, either of flexible rods or inflatable tubes, are reserved for when other methods fail because of the potential for serious complications, which occur in as many as 10% of cases. They carry the risk of eroding penile tissue (breaking through the skin). Although satisfaction among men who use them is high, if they do need to be removed implants make other methods such as injections and vacuum devices unusable due to tissue damage.

It is also possible for erectile dysfunction to exist not as a direct result of SCI but due to factors such as major depression, diabetes, or drugs such as those taken for spasticity. Finding and treating the root cause may alleviate the problem. For example, men who experience erectile problems as the result of a testosterone deficiency can receive androgen replacement therapy.

Compared with the options available for treating sexual dysfunction in men (for whom results are concretely observable), those available for women are limited. For example, PDE5 inhibitors, oral medications for treating erectile dysfunction in men, have been tested for their ability to increase sexual responses such as arousal and orgasm in women—but no controlled trials have been done in women with SCI, and trials in other women yielded only inconclusive results. In theory, women's sexual response could be improved using a vacuum device made to draw blood into the clitoris, but few studies on treatments for sexual function in women with SCI have been carried out. There is a particular paucity of information outside the area of reproduction.

The FDA has approved one medication for the treatment of disorders of female libido, flibanserin.

The 5α-reductase inhibitors finasteride and dutasteride may also be used in men with BPH. These medications inhibit the 5α-reductase enzyme, which, in turn, inhibits production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers, no benefit was reported in short-term trials, but in a longer term study (3–4 years) there was a greater reduction in BPH progression to acute urinary retention and surgery than with either agent alone, especially in patients were more severe symptoms and larger prostates. Other trials have confirmed reductions in symptoms, within 6 months in one trial, an effect that was maintained after withdrawal of the alpha blocker. Side effects include decreased libido and ejaculatory or erectile dysfunction. The 5α-reductase inhibitors are contraindicated in pregnant women because of their teratogenicity due to interference with fetal testosterone metabolism, and as a precaution, pregnant women should not handle crushed or broken tablets.

There is no standard method of treating or managing POIS. Patients need to be thoroughly examined in an attempt to find the causes of their POIS symptoms, which are often difficult to determine, and which vary across patients. Once a cause is hypothesized, an appropriate treatment can be attempted. At times, more than one treatment is attempted, until one that works is found.

Affected individuals typically avoid sexual activity, especially ejaculation, or schedule it for times when they can rest and recover for several days afterwards. In case post-coital tristesse (PCT) is suspected, patients could be treated with selective serotonin reuptake inhibitors.

Another patient, in whom POIS was suspected to be caused by cytokine release, was successfully treated with nonsteroidal anti-inflammatory drugs (NSAIDs) just prior to and for a day or two after ejaculation. The patient took diclofenac 75 mg 1 to 2 hours prior to sexual activity with orgasm, and continued twice daily for 24 to 48 hours.

One POIS patient with erectile dysfunction and premature ejaculation had much lower severity of symptoms on those occasions when he was able to maintain penile erection long enough to achieve vaginal penetration and ejaculate inside his partner. The patient took tadalafil to treat his erectile dysfunction and premature ejaculation. This increased the number of occasions on which he was able to ejaculate inside his partner, and decreased the number of occasions on which he experienced POIS symptoms. This patient is thought to have Dhat syndrome rather than true POIS.

In one patient, the POIS symptoms were so severe, that he decided to undergo castration in order to relieve them. The POIS symptoms were cured by the castration.

Two patients, in whom POIS was suspected to be caused by auto-immune reaction to their own semen, were successfully treated by allergen immunotherapy with their own autologous semen. They were given multiple subcutaneous injections of their own semen for three years. Treatment with autologous semen "might take 3 to 5 years before any clinically relevant symptom reduction would become manifest".

Treatments are not always successful, especially when the cause of POIS in a particular patient has not been determined. In one patient, all of whose routine laboratory tests were normal, the following were attempted, all without success: ibuprofen, 400 mg on demand; tramadol 50 mg one hour pre-coitally; and escitalopram 10 mg daily at bedtime for 3 months.

Antimuscarinics such as tolterodine may also be used, especially in combination with alpha blockers. They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control symptoms of an overactive bladder.

Phosphodiesterase-5 inhibitors such as sildenafil citrate show some symptomatic relief, suggesting a possible common cause with erectile dysfunction. Tadalafil was considered then rejected by NICE in the UK for the treatment of symptoms associated with BPH. In 2011, the U.S. Food and Drug Administration approved tadalafil to treat the signs and symptoms of benign prostatic hyperplasia, and for the treatment of BPH and erectile dysfunction (ED), when the conditions occur simultaneously.

Female sexual arousal disorder (FSAD) is a disorder characterized by a persistent or recurrent inability to attain sexual arousal or to maintain arousal until the completion of a sexual activity. The diagnosis can also refer to an inadequate lubrication-swelling response normally present during arousal and sexual activity. The condition should be distinguished from a general loss of interest in sexual activity and from other sexual dysfunctions, such as the orgasmic disorder (anorgasmia) and hypoactive sexual desire disorder, which is characterized as a lack or absence of sexual fantasies and desire for sexual activity for some period of time.

Although female sexual dysfunction is currently a contested diagnostic, it has become more common in recent years to use testosterone-based drugs off-label to treat FSAD. While drug companies are technically not allowed to market these drugs for off-label uses, sharing the information with doctors at CME conferences has proved to be an effective way to navigate around the FDA approval process.

It is possible that a similar disease exists in women, though, as of 2016, there is only one documented female patient.

Because bicalutamide blocks the , like all antiandrogens, it can interfere with the androgen-mediated sexual differentiation of the genitalia (and brain) during prenatal development. In pregnant rats given bicalutamide at a dosage of 10 mg/kg/day (resulting in circulating drug levels approximately equivalent to two-thirds of human therapeutic concentrations) and above, feminization of male offspring, such as reduced anogenital distance and hypospadias, as well as impotence, were observed. No other teratogenic effects were observed in rats or rabbits receiving up to very high dosages of bicalutamide (that corresponded to up to approximately two times human therapeutic levels), and no teratogenic effects of any sort were observed in female rat offspring at any dosage. As such, bicalutamide is a selective reproductive teratogen in males, and may have the potential to produce undervirilization/sexually ambiguous genitalia in male fetuses.

A case report of male breast cancer subsequent to bicalutamide-induced gynecomastia has been published. According to the authors, "this is the second confirmed case of breast cancer in association with bicalutamide-induced gynaecomastia (correspondence AstraZeneca)." It is notable, however, that gynecomastia does not seem to increase the risk of breast cancer in men. Moreover, the lifetime incidence of breast cancer in men is approximately 0.1%, the average age of diagnosis of prostate cancer and male breast cancer are similar (around 70 years), and millions of men have been treated with bicalutamide for prostate cancer, all of which are potentially in support of the notion of chance co-occurrences. In accordance, the authors concluded that "causality cannot be established" and that it was "probable that the association is entirely coincidental and sporadic."

Testosterone has been used to successfully treat undervirilization in some but not all men with PAIS, despite having supraphysiological levels of testosterone to start with. Treatment options include transdermal gels or patches, oral or injectable testosterone undecanoate, other injectable testosterone esters, testosterone pellets, or buccal testosterone systems. Supraphysiological doses may be required to achieve the desired physiological effect, which may be difficult to achieve using non-injectable testosterone preparations. Exogenous testosterone supplementation in unaffected men can produce various unwanted side effects, including prostatic hypertrophy, polycythemia, gynecomastia, hair loss, acne, and the suppression of the hypothalamic-pituitary-gonadal axis, resulting in the reduction of gonadotropins (i.e., luteinizing hormone and follicle-stimulating hormone) and spermatogenic defect. These effects may not manifest at all in men with AIS, or might only manifest at a much higher concentration of testosterone, depending on the degree of androgen insensitivity. Those undergoing high dose androgen therapy should be monitored for safety and efficacy of treatment, possibly including regular breast and prostate examinations. Some individuals with PAIS have a sufficiently high sperm count to father children; at least one case report has been published that describes fertile men who fit the criteria for grade 2 PAIS (micropenis, penile hypospadias, and gynecomastia). Several publications have indicated that testosterone treatment can correct low sperm counts in men with MAIS. At least one case report has been published that documents the efficacy of treating a low sperm-count with tamoxifen in an individual with PAIS.

Gonadectomy at time of diagnosis is the current recommendation for PAIS if presenting with cryptorchidism, due to the high (50%) risk of germ cell malignancy. The risk of malignancy when testes are located intrascrotally is unknown; the current recommendation is to biopsy the testes at puberty, allowing investigation of at least 30 seminiferous tubules, with diagnosis preferably based on OCT3/4 immunohistochemistry, followed by regular examinations. Hormone replacement therapy is required after gonadectomy, and should be modulated over time to replicate the hormone levels naturally present in the body during the various stages of puberty. Artificially induced puberty results in the same, normal development of secondary sexual characteristics, growth spurt, and bone mineral accumulation. Women with PAIS may have a tendency towards bone mineralization deficiency, although this increase is thought to be less than is typically seen in CAIS, and is similarly managed.

Dr. Mahmood Bhutta, an otorhinolaryngologist at John Radcliffe Hospital, states that sexually induced sneezing may be genetically determined, and may result from the way the central nervous system is wired:

"[T]his reflex demonstrates evolutionary relics in the wiring of a part of the nervous system called the autonomic nervous system. [...] This is the part beyond our control, and which controls things like our heart rate and the amount of light let in by our pupils. [...] Sometimes the signals in this system get crossed, and I think this may be why some people sneeze when they think about sex."

Another possible explanation concerns the existence of erectile tissue in the nose, which may become engorged during sexual arousal, triggering a sneeze.

The person experiences sneezing as a result of sexual thoughts, arousal, intercourse, or orgasm. Sneezing occurs independent of external nasal stimuli or allergens, and may occur at any point during a sexual experience. Both men and women are affected by the phenomenon.

Phallophobia in its narrower sense is a fear of the erect penis and in a broader sense an excessive aversion to masculinity.

Transurethral needle ablation of the prostate (TUNA) has been shown to be ineffective in trials.

In a preliminary 2005 open label study of 16 treatment-recalcitrant CPPS patients, controversial entities known as nanobacteria were proposed as a cause of prostatic calcification and symptoms found in CPPS. Patients were treated with EDTA (to dissolve the calcifications) and 3 months of tetracycline (a calcium-leaching antibiotic with anti-inflammatory effects, used here to kill the "pathogens"), and half had significant improvement in symptoms. Scientists have expressed strong doubts about whether nanobacteria are living organisms. Research in 2008 showed that "nanobacteria" are merely tiny lumps of abiotic limestone.

Phytotherapeutics such as quercetin and flower pollen extract have been studied in small clinical trials; the evidence is insufficient to judge safety or efficacy.

The evidence supporting a viral cause of prostatitis and chronic pelvic pain syndrome is weak. Single case reports have implicated herpes simplex virus (HSV) and cytomegalovirus (CMV) but a study using PCR failed to demonstrate the presence of viral DNA in patients with chronic pelvic pain syndrome undergoing radical prostatectomy for localized prostate cancer. The reports implicating CMV must be interpreted with caution because in "all" cases the patients were immunocompromised. For HSV the evidence is weaker still and there is only one reported case and the causative role of the virus was not proven, and there are no reports of successful treatments using antiviral drugs such as aciclovir.

Due to the concomitant presence of bladder disorders, gastrointestinal disorders, and mood disorders, research has been conducted to understand whether CP/CPPS might be caused by problems with the hypothetical bladder-gut-brain axis.

Research has been conducted to understand how chronic bladder pain affects the brain, using techniques like MRI and functional MRI; as of 2016 it appeared that people with CP/CPPS have increased grey matter in the primary somatosensory cortex, the Insular cortex, the insular cortex, and the anterior cingulate cortex, and in the central nucleus of the amygdala; studies in rodents have shown that blocking the metabotropic glutamate receptor 5 which is expressed in the central nucleus of the amygdala, can block bladder pain.