It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.
When stimulated by the nerves, the spongy tissue arranges itself in such a way that more blood can be stored in the penis. The veins running through the outer sheath of the penis then compress which stops the blood from leaving the penis. As the blood is stopped from flowing out, the penis fills with blood and stretches within the outer casing, giving an erection.
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[48] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[49] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[50]
Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer's type,[100][101][102][103] a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,[104] where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.

Men who produce more testosterone are more likely to engage in extramarital sex.[55] Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.[54] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[59]
However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. [48]
Important future developments will include selective androgen receptor modulators (SARMs). These drugs will be able to produce isolated effects of testosterone at androgen receptors. They are likely to become useful clinical drugs, but their initial worth may lie in facilitating research into the relative importance of testosterone’s action at the androgen receptor compared to at other sites or after conversion to other hormones. Testosterone will remain the treatment of choice for late onset hypogonadism for some time to come.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][147] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][147] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][147] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[149][150] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[148]
Effective treatment for erectile dysfunction is available, and for most men will allow the return to a fulfilling sex life. The side effects of the treatment for erectile dysfunction vary depending on the treatment that is used. Some may interrupt the spontaneity of sexual activity. For example, PDE-5 inhibitors typically need to be taken one hour before sex. Side effects may include headaches, indigestion, vasodilation, diarrhoea and blue tinge to vision. Other treatments such as penile injections may cause pain at the injection site, or an erection that will not go down. Treatment options need to be carefully discussed with your doctor to determine which one is best suited to you.
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005). 
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