Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.
Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge. Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.
You may find this hard to believe, but some common breakfast foods like Kellogg’s corn flakes and Graham crackers were invented 100 years ago to lower male libido. Kellogg and Graham believed that male sexual desire was the root of society’s problems, so they set out to make bland foods that would take away libido (this is absolutely true; look it up). That low fat, grain-based thing absolutely works wonders for lowering testosterone.
Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.
Hypogonadism (as well as age-related low testosterone) is diagnosed with blood tests that measure the level of testosterone in the body. The Endocrine Society recommends testing for suspected low T with a total testosterone test. It may be performed in the morning when testosterone levels tend to be highest in young men, although this isn't necessarily the case in older men. The test may be repeated on another day if the results show a low T level. (5)
The hormone also plays a role in sex drive, sperm production, fat distribution, red cell production, and maintenance of muscle strength and mass, according to the Mayo Clinic. For these reasons, testosterone is associated with overall health and well-being in men. One 2008 study published in the journal Frontiers of Hormone Research even linked testosterone to the prevention of osteoporosis in men.
In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6. 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations. The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism. In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites. Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.
In a randomized double-blind, parallel, placebo-controlled trial, sildenafil plus testosterone was not superior to sildenafil plus placebo in improving erectile function in men with ED and low testosterone levels.  The objective of the study was to determine whether the addition of testosterone to sildenafil therapy improves erectile response in men with ED and low testosterone levels.
Erectile dysfunction - (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. A penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis.
The first period occurs between 4 and 6 weeks of the gestation. Examples include genital virilisation such as midline fusion, phallic urethra, scrotal thinning and rugation, and phallic enlargement; although the role of testosterone is far smaller than that of dihydrotestosterone. There is also development of the prostate gland and seminal vesicles.
ICI therapy often produces a reliable erection, which comes down after 20-30 minutes or with climax. Since the ICI erection is not regulated by your penile nerves, you should not be surprised if the erection lasts after orgasm. The most common side effect of ICI therapy is a prolonged erection. Prolonged erections (>1 hour) can be reversed by a second injection (antidote) in the office.
ED usually has a multifactorial etiology. Organic, physiologic, endocrine, and psychogenic factors are involved in the ability to obtain and maintain erections. In general, ED is divided into 2 broad categories, organic and psychogenic. Although most ED was once attributed to psychological factors, pure psychogenic ED is in fact uncommon; however, many men with organic etiologies may also have an associated psychogenic component.
But if a man with sleep apnea is diagnosed with low testosterone alone, taking the supplemental hormone can worsen sleep apnea. That's why it's crucial for men with low testosterone to get a thorough workup by an endocrinologist so underlying conditions that can cause low testosterone, such as sleep apnea or pituitary-gland tumors, don't go undiagnosed, Dr. Goodman says.
Erections occur in response to tactile, olfactory, and visual stimuli. The ability to achieve and maintain a full erection depends not only on the penile portion of the process but also on the status of the peripheral nerves, the integrity of the vascular supply, and biochemical events within the corpora. The autonomic nervous system is involved in erection, orgasm, and tumescence. The parasympathetic nervous system is primarily involved in sustaining and maintaining an erection, which is derived from S2-S4 nerve roots.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.