Secondary anorgasmia is close to 50% among males undergoing prostatectomy; 80% among radical prostatectomies. This is a serious adverse result because radical prostatectomies are usually given to younger males who are expected to live more than 10 years. At more advanced ages, the prostate is less likely to grow during that person's remaining lifetime. This is generally caused by damage to the primary nerves serving the penile area, which pass near the prostate gland. Removal of the prostate frequently damages or even completely removes these nerves, making sexual response unreasonably difficult.

People who are orgasmic in some situations may not be in others. A person may have an orgasm from one type of stimulation but not from another, achieve orgasm with one partner but not another, or have an orgasm only under certain conditions or only with a certain type or amount of foreplay. These common variations are within the range of normal sexual expression and should not be considered problematic.

A person who is troubled by experiencing situational anorgasmia should be encouraged to explore alone and with his or her partner those factors that may affect whether or not he or she is orgasmic, such as fatigue, emotional concerns, feeling pressured to have sex when he or she is not interested, or a partner's sexual dysfunction. In the relatively common case of female situational anorgasmia during penile-vaginal intercourse, some sex therapists recommend that couples incorporate manual or vibrator stimulation during intercourse, or using the female-above position as it may allow for greater stimulation of the clitoris by the penis or pubic symphysis or both, and it allows the woman better control of movement.

Medical conditions that can cause delayed ejaculation include hypogonadism, thyroid disorders, pituitary disorders such as Cushing's disease, prostate surgery outcome, and drug and alcohol use. Difficulty in achieving orgasm can also result from pelvic surgery that involved trauma to pelvic nerves responsible for orgasm. Some men report a lack of sensation in the nerves of the glans penis, which may or may not be related to external factors, including a history of circumcision.

Delayed ejaculation is a possible side effect of certain medications, including selective serotonin reuptake inhibitors (SSRIs), opiates such as morphine, methadone, or oxycodone, many benzodiazepines such as Valium, certain antipsychotics, and antihypertensives.

Psychological and lifestyle factors have been discussed as potential contributors, including insufficient sleep, distraction due to worry, distraction from the environment, anxiety about pleasing their partner and anxiety about relationship problems.

One proposed cause of delayed ejaculation is adaptation to a certain masturbatory technique. The sensations a man feels when masturbating may bear little resemblance to the sensations he experiences during intercourse. Factors such as pressure, angle and grip during masturbation can make for an experience so different from sex with a partner that the ability to ejaculate is reduced or eliminated.

On the same note, it may be the visual factor present in masturbation that may delay vaginal ejaculation. As the sensation during masturbation is intrinsically linked with the visual input of a sexual model, be it male or female, the diminished view during sex may result in the loss of that link, and as such, delay ejaculation in the man. A possible cure for this may be a better view of the partner during intercourse.

The causes of premature ejaculation are unclear. Many theories have been suggested, including that PE was the result of masturbating quickly during adolescence to avoid being caught, of performance anxiety, of an unresolved Oedipal conflict, of passive-aggressiveness, and having too little sex; but there is little evidence to support any of these theories.

Several physiological mechanisms have been hypothesized to contribute to causing premature ejaculation including serotonin receptors, a genetic predisposition, elevated penile sensitivity, and nerve conduction atypicalities.

The nucleus paragigantocellularis of the brain has been identified as having involvement in ejaculatory control. Scientists have long suspected a genetic link to certain forms of premature ejaculation. In one study, 91 percent of men who have had premature ejaculation for their entire lives also had a first-relative with lifelong premature ejaculation. Other researchers have noted that men who have premature ejaculation have a faster neurological response in the pelvic muscles.

PE may be caused by prostatitis or as a drug side effect.

Premature ejaculation is a prevalent sexual dysfunction in men; however, because of the variability in time required to ejaculate and in partners' desired duration of sex, exact prevalence rates of PE are difficult to determine. In the "Sex in America" surveys (1999 and 2008), University of Chicago researchers found that between adolescence and age 59, approximately 30% of men reported having experienced PE at least once during the previous 12 months, whereas about 10 percent reported erectile dysfunction (ED). Although ED is men's most prevalent sex problem after age 60, and may be more prevalent than PE overall according to some estimates, premature ejaculation remains a significant issue that, according to the survey, affects 28 percent of men age 65–74, and 22 percent of men age 75–85. Other studies report PE prevalence ranging from 3 percent to 41 percent of men over 18, but the great majority estimate a prevalence of 20 to 30 percent—making PE a very common sex problem.

There is a common misconception that younger men are more likely to suffer premature ejaculation and that its frequency decreases with age. Prevalence studies have indicated, however, that rates of PE are constant across age groups.

The female sexual response system is complex and even today, not fully understood. The most prevalent of female sexual dysfunctions that have been linked to menopause include lack of desire and libido; these are predominantly associated with hormonal physiology. Specifically, it is the decline in serum estrogens that causes these changes in sexual functioning. Androgen depletion may also play a role, but currently this is less clear. The hormonal changes that take place during the menopausal transition have been suggested to affect women's sexual response through several mechanisms, some more conclusive than others.

Erectile dysfunction from vascular disease is usually seen only amongst elderly individuals who have atherosclerosis. Vascular disease is common in individuals who have diabetes, peripheral vascular disease, hypertension and those who smoke. Any time blood flow to the penis is impaired, erectile dysfunction is the end result.

Hormone deficiency is a relatively rare cause of erectile dysfunction. In individuals with testicular failure like in Klinefelter syndrome, or those who have had radiation therapy, chemotherapy or childhood exposure to mumps virus, the testes may fail and not produce testosterone. Other hormonal causes of erectile failure include brain tumors, hyperthyroidism, hypothyroidism or disorders of the adrenal gland.

Structural abnormalities of the penis like Peyronie's disease can make sexual intercourse difficult. The disease is characterized by thick fibrous bands in the penis which leads to a deformed-looking penis.

Drugs are also a cause of erectile dysfunction. Individuals who take drugs to lower blood pressure, uses antipsychotics, antidepressants, sedatives, narcotics, antacids or alcohol can have problems with sexual function and loss of libido.

Priapism is a painful erection that occurs for several hours and occurs in the absence of sexual stimulation. This condition develops when blood gets trapped in the penis and is unable to drain out. If the condition is not promptly treated, it can lead to severe scarring and permanent loss of erectile function. The disorder occurs in young men and children. Individuals with sickle-cell disease and those who abuse certain medications can often develop this disorder.

Therapy usually involves homework assignments and exercises intended to help a man get used to having orgasms through insertional intercourse, vaginal, anal, or oral, that is through the way to which he is not accustomed. Commonly, the couple is advised to go through three stages. At the first stage, a man masturbates in the presence of his partner. Sometimes, this is not an easy matter as a man may be used to having orgasms alone. After a man learns to ejaculate in the presence of his partner, the man's hand is replaced with the hand of his partner. In the final stage, the receptive partner inserts the insertive partner's penis into the partner's vagina, anus, or mouth as soon as the ejaculation is felt to be imminent. Thus, a man gradually learns to ejaculate inside the desired orifice by an incremental process.

A number of studies have explored the factors that contribute to female sexual arousal disorder and female orgasmic disorder. These factors include both psychological and physical factors. Psychologically, possible causes of the disorder include the impact of childhood and adolescence experiences and current events – both within the individual and within the current relationship.

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.

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.

Estimates of the percentage of female sexual dysfunction attributable to physical factors have ranged from 30% to 80%. The disorders most likely to result in sexual dysfunction are those that lead to problems in circulatory or neurological function. These factors have been more extensively explored in men than in women. Physical etiologies such as neurological and cardiovascular illnesses have been directly implicated in both premature and retarded ejaculation as well as in erectile disorder, but the contribution of physiological factors to female sexual dysfunction is not so clear. However, recent literature does suggest that there may be an impairment in the arousal phase among diabetic women. Given that diabetic women show a significant variability in their response to this medical disorder, it is not surprising that the disease’s influence on arousal is also highly variable. In fact, the lack of a clear association between medical disorders and sexual functioning suggests that psychological factors play a significant part in the impact of these disorders on sexual functioning.

Kenneth Maravilla, Professor of Radiology and Neurological Surgery and Director of MRI Research Laboratory at the University of Washington, Seattle, presented research findings based on neuro-imaging of women's sexual function. In a small pilot study of four women with female sexual arousal disorder, Maravilla reported there was less brain activation seen in this group, including very little activation in the amygdala. These women also showed increased activation in the temporal areas, in contrast to women without sexual difficulties, who showed deactivation in similar areas. This may suggest an increased level of inhibition with an arousal stimulus in this small group of women with FSAD.

Several types of medications, including selective serotonin reuptake inhibitors (SSRIs), can cause sexual dysfunction and in the case of SSRI and SNRI, these dysfunctions may become permanent after the end of the treatment.

In certain cultures, deliberately inducing retrograde ejaculation by squeezing the urethra at the base or applying pressure to the perineum is done as a form of primitive male birth control ("coitus saxonicus"). An example is the practices of the Oneida Community. However, it is not considered a reliable method when compared to most modern types of birth control. Besides the common risks of pregnancy from pre-ejaculate and lack of protection from STDs, the technique itself can be hard to execute correctly during the act of coitus, especially if the male does not fully understand the anatomy involved.

Many doctors also do not recommend coitus saxonicus due to the risk of putting pressure on the pudendal nerve, which can cause numbness in the penis.

It can depend on one or more of several causes, including:

- Sexual inhibition

- Pharmacological inhibition. They include mostly antidepressant and antipsychotic medication, and the patients experiencing that tend to quit them

- Autonomic nervous system

- Prostatectomy - surgical removal of the prostate.

- Ejaculatory duct obstruction

- Spinal cord injury causes sexual dysfunction including anejaculation. The rate of being able to ejaculate varies with the type of lesion, as detailed in the table at right.

- old age

Anejaculation, especially the "orgasmic" variant, is usually indistinguishable from retrograde ejaculation. However, a negative urinalysis measuring no abnormal presence of spermatozoa in the urine will eliminate a retrograde ejaculation diagnosis.

Thus, if the affected man has the sensations and involuntary muscle-contractions of an orgasm but no or very low-volume semen, ejaculatory duct obstruction is another possible underlying pathology of anejaculation.

The first-line method for sperm retrieval in men with spinal cord injury is "penile vibratory stimulation" (PVS). The penile vibratory stimulator is a plier-like device that is placed around glans penis to stimulate it by vibration. In case of failure with PVS, spermatozoa are sometimes collected by electroejaculation, or surgically by per cutaneous epididymal sperm aspiration (PESA) or testicular sperm extraction (TESE).

If a couple is experiencing infertility as a result of retrograde ejaculation and medications are not helping, the male's ejaculate may be centrifuged and the isolated sperm injected directly into the woman through the use of intrauterine insemination. In more severe cases, in-vitro fertilization with intracytoplasmic sperm injection may be used.

The human breast cancer susceptibility gene 2 (BRCA2) is employed in homologous recombinational repair of DNA damages during meiosis. A common single-nucleotide polymorphism of BRCA2 is associated with severe oligospermia.

Men with mild oligospermia (semen concentration of 15 million to 20 million sperm/ml) were studied for an association of sperm DNA damage with life style factors. A significant association was found between sperm DNA damage and factors such as age, obesity and occupational stress.

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

Pre-testicular factors refer to conditions that impede adequate support of the testes and include situations of poor hormonal support and poor general health including:

- Hypogonadotropic hypogonadism due to various causes

- Obesity increases the risk of hypogonadotropic hypogonadism. Animal models indicate that obesity causes leptin insensitivity in the hypothalamus, leading to decreased Kiss1 expression, which, in turn, alters the release of gonadotropin-releasing hormone (GnRH).

- Undiagnosed and untreated coeliac disease (CD). Coeliac men may have reversible infertility. Nevertheless, CD can present with several non-gastrointestinal symptoms that can involve nearly any organ system, even in the absence of gastrointestinal symptoms. Thus, the diagnosis may be missed, leading to a risk of long-term complications. In men, CD can reduce semen quality and cause immature secondary sex characteristics, hypogonadism and hyperprolactinaemia, which causes impotence and loss of libido. The giving of gluten free diet and correction of deficient dietary elements can lead to a return of fertility. It is likely that an effective evaluation for infertility would best include assessment for underlying celiac disease, both in men and women.

- Drugs, alcohol

- Strenuous riding (bicycle riding, horseback riding)

- Medications, including those that affect spermatogenesis such as chemotherapy, anabolic steroids, cimetidine, spironolactone; those that decrease FSH levels such as phenytoin; those that decrease sperm motility such as sulfasalazine and nitrofurantoin

- Genetic abnormalities such as a Robertsonian translocation

There is increasing evidence that the harmful products of tobacco smoking may damage the testicles and kill sperm, but their effect on male fertility is not clear. Some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes.

In about 30% of infertile men no causative factor is found for their decrease in sperm concentration or quality by common clinical, instrumental, or laboratory means, and the condition is termed "idiopathic" (unexplained). A number of factors may be involved in the genesis of this condition, including age, infectious agents ( such as "Chlamydia trachomatis"), Y chromosome microdeletions, mitochondrial changes, environmental pollutants, and "subtle" hormonal changes.

A review in 2013 came to the result that oligospermia and azoospermia are significantly associated with being overweight (odds ratio 1.1), obese (odds ratio 1.3) and morbidly obese (odds ratio 2.0), but the cause of this is unknown. It found no significant relation between oligospermia and being underweight.

There is not enough known about persistent genital arousal disorder to definitively pinpoint a cause. Medical professionals think it is caused by an irregularity in sensory nerves, and note that the disorder has a tendency to strike post-menopausal women, or those who have undergone hormonal treatment.

Some drugs such as trazodone may cause priapism as a side effect, in which case discontinuing the medication may give relief. Additionally, the condition can sometimes start only after the discontinuation of SSRIs. In some recorded cases, the syndrome was caused by or can cause a pelvic arterial-venous malformation with arterial branches to the penis or clitoris; surgical treatment was effective in this case.

In other situations where the cause is unknown or less easily treatable, the symptoms can sometimes be reduced by the use of antidepressants, antiandrogenic agents, and anaesthetising gels. Psychotherapy with cognitive reframing of the arousal as a healthy response may also be used.

More recently, the symptoms of the condition have also been linked with pudendal nerve entrapment. Regional nerve blocks and less common surgical intervention have demonstrated varying degrees of success in most cases. There is, however, no evidence for the long-term efficacy of surgical intervention.

In one recent case, serendipitous relief of symptoms was noted from treatment with varenicline, a treatment for nicotine addiction.

In the DSM-5, male hypoactive sexual desire disorder is characterized by "persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and desire for sexual activity", as judged by a clinician with consideration for the patient's age and cultural context. Female sexual interest/arousal disorder is defined as a "lack of, or significantly reduced, sexual interest/arousal", manifesting as at least three of the following symptoms: no or little interest in sexual activity, no or few sexual thoughts, no or few attempts to initiate sexual activity or respond to partner's initiation, no or little sexual pleasure/excitement in 75%-100% of sexual experiences, no or little sexual interest in internal or external erotic stimuli, and no or few genital/nongenital sensations in 75%-100% of sexual experiences.

For both diagnoses, symptoms must persist for at least six months, cause clinically significant distress, and not be better explained by another condition. Simply having lower desire than one's partner is not sufficient for a diagnosis. Self-identification of a lifelong lack of sexual desire as asexuality precludes diagnosis.

Aspermia is the complete lack of semen with ejaculation (not to be confused with azoospermia, the lack of sperm cells in the semen). It is associated with infertility.

One of the causes of aspermia is retrograde ejaculation, which can be brought on by excessive drug use, or as a result of prostate surgery. It can also be caused by alpha blockers such as tamsulosin and silodosin.

Another cause of aspermia is ejaculatory duct obstruction, which may result in a complete lack of or a very low-concentration semen (oligospermia), in which the semen contains only the secretion of accessory prostate glands downstream to the orifice of the ejaculatory ducts.

Aspermia can be caused by androgen deficiency. This can be the result of absence of puberty, in which the prostate gland and seminal vesicles (which are the main sources of semen) remain small due to lack of androgen exposure and do not produce seminal fluid, or of treatment for prostate cancer, such as maximal androgen blockade.