The intensity of sexual desire in healthy men and women differs from one person to the other. Hypoactive desire, which affects millions of people worldwide, is probably the most underestimated, neglected, undefined, difficult to evaluate and treat, and frustrating sexual disorder. Health care providers are faced with a plethora of clinical studies on various other sexual disturbances but with a dearth of evidence regarding the proper diagnosis and management of low sexual desire, no objective tools to assess or measure it, and plenty of misconceptions and ignorance about it. Diminished desire or low libido in men is commonly, and erroneously, misdiagnosed and treated as erectile disorder (ED) — with very poor results in most cases.
Furthermore, all the commonly used so-called aphrodisiac foods, herbs, potions, and concoctions, such as ginseng, Spanish fly, cantharidin, caviar, oysters, chocolate, strawberries, spicy foods, Ginkgo biloba, and moderate amounts of alcohol, have not been proven particularly effective. It was suggested recently that nuts could increase sexual desire; however, this claim needs to be substantiated by further scientific studies. In cases when some of the aforementioned substances are successful for increasing libido in some men, perhaps it is because they may block mental sexual inhibitions or work on a motivational or other psychological level.
With the availability and success of the phosphodiesterase type 5 inhibitors in restoring normal sexual functioning, millions of men with erectile dysfunction (ED) can achieve firm, lasting erections allowing satisfactory intercourse. But those medications cannot heighten libido — so, ironically, a large group of men is capable of producing erection, but they have little or no real desire to do so. Some of them would rather play golf or watch television; many others, however, are frustrated by their low desire and would very much like to experience the ultimate joy of sex once again. Viagravation is a term that was proposed to describe the deep aggravation experienced by men who are willing and able to use an ED medication to achieve erection but lack the physiological or psychological motivation to engage in sex — with the resulting deep frustration experienced by their sexual partners.
The complex cerebral phenomenon of sexual desire is poorly understood, despite various theories of its mechanism. Masters and Johnson (1970) originally proposed the linear theory, which stipulates that “sexual thoughts and fantasies and an innate urge to experience sexual tensions and release are markers of desire.” They emphasized that “the personal experience of lustful desire in both sexual partners should precede any initiation of sexuality” (Meuleman EJH, Van Lankveld JDM 2004).
Real life, however, demonstrates universal differences between partners’ experiences of sexual desire, for example, in timing and frequency of sexual activity. In addition, couples engage in sexual activity not only because of an intrinsic urge, but also for non-sexual motives such as pleasing the partner, distracting from boredom or gloom, material rewards, or other conjugal or personal reasons; this is termed “receptive sexual desire,” as opposed to “active desire.” The oversimplified linear model soon gave way to multifactorial or circular hypotheses of interrelationship among sexual desire, arousal, and performance, influenced by unconscious and conscious motives.
Janssen et al.’s (2000) theory of sexual desire presents a two-stage information processing model. In the first stage, subliminal sexual stimuli, such as subconscious fantasies and thoughts, prepare the sexual system for arousal by rendering it receptive to the perception of additional erotic stimuli such as touch, sight, sound, and odor. Following this primary motivational engagement, the man can become aware of a desire to proceed with the enjoyment of a sexual experience. Thus, Janssen et al. propose that an arousal phase precedes and motivates desire.
The mental sexual arousal then modulates the chemicals in the brain’s limbic centers, leading to secretion of the facilitating neurotransmitter oxytocin and blocking the inhibiting neurotransmitter serotonin. This process, by activating the sex center in the sacral spinal cord, stimulates the pelvic and penile nerves to produce penile engorgement and erection, which is gratifying and reinforces or increases the man’s desire and arousal (Meuleman EJH, Van Lankveld JDM 2004). But during this second stage, it is also possible for inhibitory stimuli, such as mental preoccupation, anxiety, anger, fear of failure, and nonsexual thoughts, to derail the process.
In the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (American Psychiatric Association 1994), hypoactive sexual desire disorder (HSDD) is defined as “the persistent or recurrent absence or deficit of sexual fantasies and desire for sexual activity, accounting for factors that affect sexual function, e.g., age, sex, and life context.” It is extremely difficult to assess HSSD’s true prevalence, which ranges from zero to 15% in population-based studies—this is certainly an underestimation, especially as most men do not reveal sexual problems unless explicitly questioned by their physicians.
Assessment of a libido problem is based on direct and unambiguous questions, posed by the physician to the patient, regarding sexual motivation and desire. Additional helpful information can be obtained from the patient’s partner or by using questionnaires such as the Sexual Desire Inventory or the Golombock-Rust Inventory of Sexual Satisfaction.
Hypoactive desire results from a wide variety of biological and psychological factors, including aging and chronic medical conditions such as coronary artery disease (CAD), heart failure, AIDS, and renal failure. Some bodybuilders and men with eating disorders are also subject to low desire. The psychiatric conditions most commonly associated with low libido include depression, anxiety, anger, and relationship disorders (Morales A 2003, Wyllie MG 2003, Meuleman EJH, Van Lankveld JDM 2004, Wyllie MG 2005).
Although it has long been accepted that desire in both genders depends on psychological and hormonal factors, no definitive scientific proof has supported this theory. But a study recently published in Molecular Psychiatry (Ebstein RP 2006), by examining the DNA of 148 healthy male and female university students, demonstrated that self-reported low sexual desire was correlated with genetic differences, namely, “the variants in a gene called the D4 receptor” (Ebstein RP 2006). This may mean that low sexual desire can be considered a normal biological, rather than psychological, condition. Of course, this interesting finding requires confirmation by additional multicenter studies before its acceptance by the medical community.
Hormonal underpinnings of decreased sexual desire are complex. It has long been medically accepted that low serum levels of the male hormone testosterone may result in absent or hypoactive desire in older men, as well as in postmenopausal women. In males, this hormone is produced when the brain’s hypothalamus secretes gonadotropin-releasing hormone (GnRH), stimulating the pituitary gland to produce two hormones: follicular stimulating hormone (FSH), which contributes to sperm production, and luteinizing hormone (LH), which stimulates the testicles to secrete testosterone. (Most testosterone is produced by the testicles, and some by the adrenal glands.)
Testosterone plays major roles in spermatogenesis, embryonic sexual differentiation, pubertal maturation, and pituitary gonadotropin secretion. It also affects the body’s secretion of erythropoietin (a hormone from the adult kidneys that stimulates bone marrow to produce red blood cells), muscle growth and strength, insulin secretion and sensitivity, serum lipid profile, and blood pressure. It also regulates the formation of cyclic guanosine monophosphate through nitric oxide synthase, which is essential for the development and maintenance of a hard erection. This could explain the poor response to phosphodiesterase type 5 inhibitors in cases of hypogonadism (Morelli A et al. 2007).
In the newborn male, concentrations of serum FSH, LH, and testosterone are low but then rise for several months after birth and decline again by 9-12 months. From six to eight years of age until the completion of puberty, LH and FSH progressively increase, along with a steep rise in testosterone at age 12-14 secondary to the nighttime hypersecretion of LH during midpuberty. Men produce about 5 milligrams of testosterone per day.
Testosterone secretion can be impaired, however, by congenital or pathological lesions in the testicles, pituitary, or hypothalamus. Interference with the hypothalamus or pituitary by elevated blood levels of testosterone, estradiol, or prolactin may also lead to hypoactive or absent sexual desire.
To summarize, the involved endocrine organs and their hormones are as follows:
Hypothalamus: GnRH, other hormones Pituitary gland: prolactin, secreted by specialized lactotroph cells; LH; FSH; other gonadotropins; human gonadotropin hormone.
Testicles: most testosterone (about 90%), secreted by specialized Leydig cells Adrenal glands: a little testosterone (about 10%), adrenaline, other hormones.
Sexual differentiation in the fetus occurs after the sixth week of gestation and under the influence of multiple genes, especially the SRY gene on the sex-determining region of the Y chromosome. At this time, the primitive testicles form Leydig cells, Sertoli cells (these provide support, nutrition, and protection to developing sperms), and Mullerian inhibiting substance (MIS). MIS causes regression of the fetal paramesonephric ducts, which would otherwise — in the female, who doesn’t produce MIS — form the fallopian tubes, uterus, and upper two-thirds of the vagina.
The formation of testosterone from cholesterol is responsible for development of the male genital ducts, including the vas deferens, epididymis, and seminal vesicles from the fetal mesonephric ducts. Placental luteinizing hormone (LH) prompts the initial secretion of testosterone from the new Leydig cells. Concomitantly in early gestation, the fetal pituitary gland in both males and females begins to synthesize and store its own LH and follicular stimulating hormone and secretes them in high concentrations, contributing to the secretion of testosterone. Starting in the fourth month of gestation, the male external genitalia (penis and scrotum) develop under the influence of dihydrotestosterone, which is converted from testosterone by the enzyme 5-alpha reductase.
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