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.

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.

Whether or not aging directly affects women's sexual functioning during menopause is another area of controversy. However, many studies, including Hayes and Dennerstein's critical review, have demonstrated that aging has a powerful impact on sexual function and dysfunction in women, specifically in the areas of desire, sexual interest, and frequency of orgasm. In addition, Dennerstien and colleagues found that the primary predictor of sexual response throughout menopause is prior sexual functioning. This means that it is important to understand how the physiological changes in men and women can affect their sexual desire. Despite the seemingly negative impact that menopause can have on sexuality and sexual functioning, sexual confidence and well-being can improve with age and menopausal status. Furthermore, the impact that a relationship status can have on quality of life is often underestimated.

Testosterone, along with its metabolite dihydrotestosterone, is extremely important to normal sexual functioning in men and women. Dihydrotestosterone is the most prevalent androgen in both men and women. Testosterone levels in women at age 60 are, on average, about half of what they were before the women were 40. Although this decline is gradual for most women, those who’ve undergone bilateral oophorectomy experience a sudden drop in testosterone levels; this is because the ovaries produce 40% of the body's circulating testosterone.

Sexual desire has been related to three separate components: drive, beliefs and values, and motivation. Particularly in postmenopausal women, drive fades and is no longer the initial step in a woman's sexual response (if it ever was).

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.

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.

Freudian theory postulated that rapid ejaculation was a symptom of underlying neurosis. It stated that the man suffers unconscious hostility toward women, so he ejaculates rapidly, which satisfies him but frustrates his lover, who is unlikely to experience orgasm that quickly. Freudians claimed that premature ejaculation could be cured using psychoanalysis. But even years of psychoanalysis accomplished little, if anything, in curing premature ejaculation.

There is no evidence that men with premature ejaculation harbor unusual hostility toward women.

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.

There has been little investigation of the impact of individual factors on female sexual dysfunction. Such factors include stress, levels of fatigue, gender identity, health, and other individual attributes and experiences, such as dysfunctional sexual beliefs that may affect sexual desire or response. Over exposure to pornography-style media is also thought to lead to poor body image, self-consciousness and lowered self-esteem. An individual's sexual activity is disrupted by overwhelming emotional distress resulting in inability to attain sexual pleasure. Sexual dysfunction can also occur secondary to major psychiatric disorders, including depression.

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

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.

SPD can be first apparent in childhood and adolescence with solitariness, poor peer relationships, and underachievement in school. This may mark these children as different and make them subject to teasing.

Being a personality disorder, which are usually chronic and long-lasting mental conditions, schizoid personality disorder is not expected to improve with time without treatment; however, much remains unknown because it is rarely encountered in clinical settings.

Some evidence suggests the Cluster A personality disorders have shared genetic and environmental risk factors and there is an increased prevalence of schizoid personality disorder in relatives of people with schizophrenia and schizotypal personality disorder. Twin studies with schizoid personality disorder traits (e.g. low sociability and low warmth) suggest these are inherited. Besides this indirect evidence, the direct heritability estimates of SPD range from 50-59%. To Sula Wolff, who did extensive research and clinical work with children and teenagers with schizoid symptoms, "schizoid personality has a constitutional, probably genetic, basis." The link between SPD and being underweight may also point to the involvement of biological factors.

In general, prenatal caloric malnutrition, premature birth and a low birth weight are risk factors for being afflicted by mental disorders and may contribute to the development of schizoid personality disorder as well. Those who have experienced traumatic brain injury may be also at risk of developing features reflective of schizoid personality disorder.

Other researchers had hypothesized excessively perfectionist, unloving or neglectful parenting could play a role.

Globally diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of the population).

Diabetes is the leading known cause of neuropathy in developed countries, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetes. It is estimated that neuropathy affects 25% of people with diabetes. Diabetic neuropathy is implicated in 50–75% of nontraumatic amputations.

The main risk factor for diabetic neuropathy is hyperglycemia. In the DCCT (Diabetes Control and Complications Trial, 1995) study, the annual incidence of neuropathy was 2% per year but dropped to 0.56% with intensive treatment of Type 1 diabetics. The progression of neuropathy is dependent on the degree of glycemic control in both Type 1 and Type 2 diabetes. Duration of diabetes, age, cigarette smoking, hypertension, height, and hyperlipidemia are also risk factors for diabetic neuropathy.

The mechanisms of diabetic neuropathy are poorly understood. At present, treatment alleviates pain and can control some associated symptoms, but the process is generally progressive.

As a complication, there is an increased risk of injury to the feet because of loss of sensation (see diabetic foot). Small infections can progress to ulceration and this may require amputation.