In the short term, alcohol relaxes muscles in the penis, letting blood to flow in (which is a good thing). However, alcohol also prevents other blood vessels from closing and trapping all the extra blood. Erections depend on trapping increased blood flow in the erectile tissue of the penis. If you don’t trap that extra blood, you don’t get an erection. In the long run, excessive alcohol consumption can cause liver scarring, high blood pressure, and can damage your blood vessels resulting in erectile dysfunction.

For best results, men with ED take these pills about an hour or two before having sex. The drugs require normal nerve function to the penis. PDE5 inhibitors improve on normal erectile responses helping blood flow into the penis. Use these drugs as directed. About 7 out of 10 men do well and have better erections. Response rates are lower for Diabetics and cancer patients.
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
Abnormally high levels of testosterone could be the result of an adrenal gland disorder, or even cancer of the testes. High levels may also occur in less serious conditions. Congenital adrenal hyperplasia, which can affect males and females, is a rare but natural cause for elevated testosterone production. Your doctor may order other tests if your levels are exceedingly high.
Erectile dysfunction is the inability to develop or maintain an erection that is rigid enough to allow penetration of the vagina, and therefore functional sexual intercourse. Generally, the term erectile dysfunction is applied if this occurs frequently (75% of the time) over a significant period if time (several weeks to months). If this is the case, the term impotence may also be used.
Clinical trials of the effect of testosterone on glucose metabolism in men have occurred in diabetic and non-diabetic populations. Data specific to aging males is not available. A series of studies investigated the effects of testosterone or dihydrotestosterone given for 6 weeks or 3 months to middle aged, non-diabetic obese men (Marin, Holmang et al 1992; Marin, Krotkiewski et al 1992; Marin et al 1993). It was found that physiological treatment doses led to improved insulin resistance, as measured by the gold standard technique using a euglycemic clamp and/or serum glucose and insulin responses during glucose tolerance test. These improvements were associated with decreased central obesity, measured by computered tomography (CT) or waist-hip ratio, without reduced total fat mass. Insulin resistance improved more with testosterone than dihydrotestosterone treatment and beneficial effects were greater in men with lower baseline testosterone levels. Increasing testosterone levels into the supraphysiological range lead to decreased glucose tolerance.
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[147] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[2][147][153][154] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[155] skin, hair follicles, and brain[156] and aromatase is highly expressed in adipose tissue, bone, and the brain.[157][158] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[148] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[159] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[160]

Erectile dysfunction in older men. Because erections primarily involve the blood vessels, it is not surprising that the most common causes in older men are conditions that block blood flow to the penis, such as atherosclerosis or diabetes. Another vascular cause may be a faulty vein, which lets blood drain too quickly from the penis. Other physical disorders, as well as hormonal imbalances and certain operations, may also result in erectile dysfunction.
Given the high risk of priapism during escalation of therapy for intracorporeal injection, it is recommended that the drugs be administered in a supervised office visit initially and that the patient be given a well-articulated plan for treatment of priapism if it occurs. Escalation guidelines for alprostadil alone vary, but a general guideline is to start at 2.5 mcg and increase by 2.5 mcg to a dose of 5 mcg and then in increments of 5 mcg to 10 mcg until an erection sufficient for penetration, not lasting more than 1 hour, is achieved. If there is no response to the initial 2.5-mcg dose, escalation dosing can be slightly more liberal.34 A European prospective trial of PGE1 alone found 91% of the 54 patients completing the 4 years of the study reported good or better tolerability and satisfaction with therapy.35

Although not proven, it is likely that erectile dysfunction can be prevented by good general health, paying particular attention to body weight, exercise, and cigarette smoking. For example, heart disease and diabetes are problems that can cause erectile dysfunction, and both are preventable through lifestyle changes such as sensible eating and regular exercise. Furthermore, early diagnosis and treatment of associated conditions like diabetes, hypertension and high cholesterol may prevent or delay erectile dysfunction, or stop the erectile dysfunction from getting more serious.
Testosterone is most commonly associated with sex drive in men. It also affects mental health, bone and muscle mass, fat storage, and red blood cell production. Abnormally low or high levels can affect a man’s mental and physical health. Your doctor can check your testosterone levels with a simple blood test. Testosterone therapy is available to treat men with low levels of testosterone. If you have low T, ask your doctor if this type of therapy might benefit you.
The doctor regularly measured my levels to be sure they were within the normal range for a male my age. In other words, I wasn’t taking ‘roids to get big; I was getting control of hormones that were not functioning well. This is how you should look at testosterone therapy – it is a gentle nudge to help you be in normal ranges, not a big push to get you huuu-yge. If you’re like me, you want “normal ranges” of a 27-year-old, not of a 60-year-old. It’s my plan to keep my testosterone where it is now (around 700) no matter what it takes. Right now, the Bulletproof Diet and the other biohacks I’ve written about do that! I’m 43.
"Bring back the younger inner you," says the Low T Center. According to its website, its president, Mr. (notably not "Dr.") Mike Sisk, "created these centers out of a need." They promise their testosterone injections "do not just help boost a low sex drive but can also boost energy, decrease body fat, irritability, and depression." They go so far as to claim that "research finds testosterone replacement can solve long-term health issues like Alzheimer's and heart disease."
Impotence, also known as erectile dysfunction or ED, is a very common problem, affecting up to half of 40-70 year old men in Australia.Treatment techniques for impotence have varied through the years, from external steel mechanical attachments, to static electricity attached to the penis and testicles, to simple aphrodisiacs such as oysters. Until as recently as 1970, erectile failure was almost always seen as being due to psychological causes and was usually treated with psychotherapy.Since then, the medical causes contributing to impotence have been recognised and the treatment of impotence has been revolutionised, providing a range of options which are far more acceptable and very much more successful.Treatment options for impotenceTreatment choices for erectile dysfunction include:medicines;self-injection therapy;devices such as vacuum pumps;penile implant surgery;hormone therapy; andcounselling.If you have erectile dysfunction, the treatment your doctor recommends will depend on the severity of symptoms and the underlying cause of your impotence.Your doctor will want to check that any conditions that could be contributing to or causing erectile dysfunction are being treated.Your doctor may also suggest that you make some lifestyle adjustments, such as:increasing the amount of physical activity you get;losing weight if you are overweight;reducing the amount of alcohol you drink;quitting smoking; andnot taking illicit drugs.These lifestyle recommendations can help improve impotence related to several causes and improve your health in general.Medicines for erectile dysfunctionThe first tablet available for erectile dysfunction, sildenafil (brand name Viagra), has been largely responsible for helping to bring the topic of erectile dysfunction out into the open. Similar medications — tadalafil (Cialis) and vardenafil ( Levitra) — are also available. These medicines all work in a similar way, although there is some difference in how long their effect lasts. Sildenafil, tadalafil and vardenafil belong to a group of medicines called phosphodiesterase type 5 (PDE5) inhibitors because they block the PDE5 enzyme.How do oral medicines help treat erectile dysfunction?PDE5 inhibitors help in the process of getting and keeping an erection by working on chemicals in the body that are involved in erections. These medicines work by stopping PDE5 from breaking down an erection-producing chemical called cyclic guanosine monophosphate (cGMP). cGMP helps to relax the smooth muscle cells in the penis's erectile tissue, allowing more blood to flow into the penis to cause an erection. When PDE5 is temporarily blocked by these medicines, it can’t break down the erection producing cGMP, so an erection can be achieved and maintained. PDE5 inhibitors can be used in the treatment of erectile dysfunction that is due to physical or psychological causes.Medications such as Viagra, Cialis and Levitra will work only if you are sexually stimulated. They are not aphrodisiacs and won’t increase your sex drive.Side effects of PDE5 inhibitorsSide effects of these medicines can include headaches, flushes, blocked nose, indigestion and dizziness.In rare situations, sildenafil and vardenafil can cause a distortion of vision or change in colour vision.Tadalafil has been associated with back pain.Who can take medicines for impotence?PDE5 inhibitors cannot be taken by all men, so your doctor will need to evaluate your suitability before prescribing either of these medications.Men taking nitrates (often used to treat angina) should never take phosphodiesterase type 5 (PDE5) inhibitors. PDE5 inhibitors should also not be taken with some medicines used to treat high blood pressure.PDE5 inhibitors may also not be suitable for men with certain heart conditions or low blood pressure. Check with your doctor to find out if this type of medication may be suitable for you.Self-injection therapySelf-injection therapy delivers a medicine called alprostadil (brand name Caverject), also known as prostaglandin E-1, to the erectile tissue of the penis. Prostaglandin E-1 occurs naturally in the body and helps increase the blood flow to the penis to cause an erection. Unlike the PDE5 inhibitors, alprostadil will cause an erection whether the penis is stimulated or not.Self-injection therapy is usually recommended if PDE5 inhibitor medicines are not suitable or have not been effective in the treatment of erectile dysfunction.How to use self-injection therapyAlprostadil is injected into either of the 2 cigar-shaped chambers of the penis known as the corpora cavernosa, which run along the length of the penis, one on either side. Your doctor or urologist (specialist in problems with male reproductive organs and the urinary tract) will give you instructions on how to do this.Alprostadil should produce an erection in 5 to 20 minutes and, generally, the erection will last for 30 to 60 minutes.You should not use alprostadil more than once in a 24-hour period, and you should use it no more than 3 times a week.Don’t try to use more than the recommended dose of alprostadil, as your erection may last longer than is medically safe.Who can use self-injection therapy?You should ask your doctor if alprostadil is suitable for you. Your doctor will also be able to tell you how much alprostadil to use, depending on your condition and whether or not you are taking any other medications, and also how to use alprostadil properly.People with certain illnesses, such as leukaemia and sickle cell anaemia, or who have a penile implant or Peyronie’s disease, where the penis may be scarred and produces erections that are not straight, should not use alprostadil.Men for whom sexual activity is not advised should not use alprostadil.Side effects of injection therapyThe most common side effects of alprostadil include pain in the penis or bruising in the penis at the site of injection. Fibrosis (the development of fibrous tissue) can also develop following injections into the penis.The most serious side effect is priapism (a persistent erection), which is a medical emergency. Your doctor will inform you of what to do if you have an erection that persists for 2 hours or more. It is very important that you follow your doctor’s instructions and inform them that you have experienced this side effect.Vacuum erection devicesVacuum erection devices work by creating a vacuum, which increases blood flow to the penis, producing an erection.The penis is lubricated and placed inside a hollow plastic chamber. Air is pumped out of the chamber, either manually or by a battery powered pump. This creates a vacuum which pulls blood into the penis to cause an erection. This takes about 5 minutes.Once the penis is erect, the man fits a rubber ring around the base of his penis to keep the blood trapped inside the penis when the cylinder is removed. After intercourse, the ring can be removed to return the penis to a limp state.Vacuum erection devices avoid surgery and can be used as often as required. However, they may be difficult to use, and many men and their partners feel they take much of the pleasure and spontaneity away from sexual activities. Vacuum pumps are not suitable for men who have problems with blood clotting, or blood disorders such as leukaemia.Penile implant surgery for impotencePenile implant surgery is not a common procedure but in some cases it may be the most appropriate treatment for erectile dysfunction.The procedure involves placing an implant inside the penis, along its length, so that it can become erect. The implant may be a pair of semi-rigid rods or a pair of inflatable cylinders.The inflatable implants allow the penis to look and feel limp (flaccid) or erect, depending on how much the cylinders are inflated. The cylinders in an inflatable implant are hollow, and the man gets an erection by squeezing a pump located in his scrotum to fill the cylinders with salt water (saline) stored in a reservoir implanted in his lower abdomen. A release valve drains the saline out of the cylinders and back into the reservoir.With the semi-rigid, malleable rod type of implant, the rods run along the length of the penis and can be bent upwards to produce an erect penis, or downwards when an erect penis is not required.Like all surgery, there are some risks, such as infection or bleeding. If you have had surgery and have severe pain, fever, swelling or excessive bleeding, you should contact your doctor as soon as possible.Vascular surgery for erectile dysfunctionIn cases where a man’s anatomy prevents blood flow into or out of the penis, vascular surgery may be an option. This treatment option is rarely recommended, and is usually only successful in younger men.If there is a blockage that prevents blood from flowing into the penis, a doctor may recommend an operation that bypasses the blocked blood vessels, using a length of vein or manufactured tubing, to allow more blood to flow into the penis and help produce an erection.If the problem is that blood leaks back out of the penis, this can be corrected by tying off the major veins that drain the penis, a procedure known as venous ligation.Hormone treatments for impotenceIn a small number of men, blood tests may show abnormally low levels of testosterone, the male sex hormone. In such cases your doctor might prescribe a course of testosterone injections or a testosterone implant. The supplements can help boost sex drive as well as increasing the ability to have erections. Testosterone gel or patches, applied daily to the skin, are another option.Complementary medicines for erectile dysfunctionThere is a lack of scientific evidence supporting the effectiveness of complementary therapies for the treatment of impotence.Always check with your doctor before taking any herbal medicines or supplements for impotence. These formulations may contain ingredients that can interact with other medicines or cause dangerous side effects.Counselling for men with impotenceErectile dysfunction often has physical causes, but sometimes there is a psychological basis for erection problems. Often this is a form of performance anxiety. A man may have had an episode of erectile dysfunction due to some passing cause like fatigue, stress, relationship difficulty or intoxication. This may have led to embarrassment or a feeling of failure. Even if the physical cause does not remain, future attempts to have sex may trigger memories of this embarrassment and acute anxiety that it will happen again. This anxiety itself is capable of causing erectile dysfunction, and so a man may get trapped in a self-reinforcing cycle of anxiety and erectile dysfunction. In these instances, seeing a GP, counsellor or psychologist can be very helpful.Stress, anxiety, depression and low self-esteem, in fact, almost all significant emotional problems, can have a major effect on sexuality. So do many chronic physical illnesses, even if they don't directly affect genital function. Counsellors and psychologists can assist with these and a wide range of other sexual and relationship problems and can also help female partners suffering from sexual problems. They are particularly skilled in helping patients to overcome guilt or anxiety relating to sexual abuse, and in helping couples to sort out relationship difficulties. Simple problems can be dealt with in a few visits, but more complex problems may require several months or even years of therapy.Your doctor may be able to recommend a psychologist or counsellor who specialises in sexual and relationship problems. Last Reviewed: 12 December 2016
If a young man's low testosterone is a problem for a couple trying to get pregnant, gonadotropin injections may be an option in some cases. These are hormones that signal the body to produce more testosterone. This may increase the sperm count. Hedges also describes implantable testosterone pellets, a relatively new form of treatment in which several pellets are placed under the skin of the buttocks, where they release testosterone over the course of about three to four months. Injections and nasal gels may be other options for some men.

Osteoporosis refers to pathological loss of bone density and strength. It is an important condition due to its prevalence and association with bone fractures; most commonly of the hip, vertebra and forearm. Men are relatively protected from the development of osteoporosis by a higher peak bone mass compared with women (Campion and Maricic 2003). Furthermore, women lose bone at an accelerated rate immediately following the menopause. Nevertheless, men start to lose bone mass during early adult life and experience an increase in the rate of bone loss with age (Scopacasa et al 2002). Women of a given age have a higher prevalence of osteoporosis in comparison to men but the prevalence increases with age in both sexes. As a result, men have a lower incidence of osteoporotic fractures than women of a given age but the gap between the sexes narrows with advancing age (Chang et al 2004) and there is evidence that hip fractures in men are associated with greater mortality than in women (Campion and Maricic 2003).
There's the rub, so to speak. Recalling the cautionary lessons learned about sex steroid hormone therapy in postmenopausal women from theWomen's Health Initiative, Dr. Brad Anawalt wrote in the Journal of Clinical Endocrinology and Metabolism, "We are threatened with a reprise of promiscuous prescription of sex steroid hormone therapy in aging men, obese men, diabetic men, and other groups of men with a high prevalence of low serum androgen levels. We are threatened with a mad 'T' party."
Mood disturbance and dysthymia are part of the clinical syndrome of hypogonadism. Epidemiological studies have found a positive association between testosterone levels and mood, and depressed aging males have lower testosterone levels than controls (Barrett-Connor, Von Muhlen et al 1999). Furthermore, induction of a hypogonadal state during treatment of men for prostate cancer leads to an increase in depression scores (Almeida et al 2004). Trials of testosterone treatment effects on mood have varied in outcome. Data on the effects on men with depression are conflicting (Seidman et al 2001; Pope et al 2003) but there is evidence that testosterone treatment of older hypogonadal men does result in improvements in mood (Wang et al 1996) and that this may occur through changes in regional brain perfusion (Azad et al 2003).
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
Obesity and metabolic syndrome can cause changes in blood pressure, body composition, and cholesterol which may lead to ED. Other conditions that may contribute to erectile dysfunction include Parkinson’s, multiple sclerosis, Peyronie’s disease, sleep disorders, alcoholism, and drug abuse. Taking certain medications can also increase your risk for ED.
If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[176] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).
Although vardenafil does not seem to produce significant clinical QT prolongation, it has been suggested that it be avoided in patients who have congenital QT prolongation abnormalities and in patients using class I antiarrhythmic drugs, such as quinidine and procainamide. It is also best to avoid the use of vardenafil with class III antiarrhythmic drugs, such as amiodarone or sotalol.

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.
Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
Overall, few patients have a compelling contraindication to testosterone treatment. The majority of men with late onset hypogonadism can be safely treated with testosterone but all will require monitoring of prostate parameters HDL cholesterol, hematocrit and psychological state. It is also wise to monitor symptoms of sleep apnea. Other specific concerns may be raised by the mode of delivery such as local side effects from transdermal testosterone.

There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
Another effect that can limit treatment is polycythemia, which occurs due to various stimulatory effects of testosterone on erythropoiesis (Zitzmann and Nieschlag 2004). Polycythemia is known to produce increased rates of cerebral ischemia and there have been reports of stroke during testosterone induced polycythaemia (Krauss et al 1991). It is necessary to monitor hematocrit during testosterone treatment, and hematocrit greater than 50% should prompt either a reduction of dose if testosterone levels are high or high-normal, or cessation of treatment if levels are low-normal. On the other hand, late onset hypogonadism frequently results in anemia which will then normalize during physiological testosterone replacement.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group[183] was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry",[184] and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[185]
Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[10] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[10] Women and children who are exposed may develop virilization.[10] It is recommended that individuals with prostate cancer not use the medication.[10] It can cause harm if used during pregnancy or breastfeeding.[10]
Sleep apnea is another frequently listed contraindication to testosterone treatment. There have been a few reports of the development, or worsening, of sleep apnea during testosterone therapy (Matsumoto et al 1985) but sleep apnea is actually associated with lower serum testosterone levels (Luboshitzky et al 2002). The reduction in fat mass during treatment with testosterone could potentially be beneficial for sleep apnea, so many specialists will still consider patients for treatment with appropriate monitoring. It is wise to take a clinical history for sleep apnea during testosterone treatment in all men and perform sleep studies in those who develop symptoms.

Testosterone is only one of many factors that influence aggression and the effects of previous experience and environmental stimuli have been found to correlate more strongly. A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression.[66][67][68][69] Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.[70]
"I am very cautious about committing someone for life to medication," said Dr. Kathleen L. Wyne, who directs research on diabetes and metabolism at Houston's Methodist Hospital Research Institute and serves on the Sex Hormone and Reproductive Endocrinology Scientific Committee for the American Association of Clinical Endocrinologists. "That does frustrate patients because they have heard about [Low T] from TV and friends."
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.
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[138] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[139] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[140][141][142] Licorice can decrease the production of testosterone and this effect is greater in females.[143]
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.

"By expanding the boundaries of this disease to common symptoms in aging males, such as fatigue and reduced libido, drug companies seek to increase their markets and boost their sales," wrote Barbara Mintzes, an assistant professor at the University of British Columbia School of Public Health, and Agnes Vitry, a senior research fellow at the University of South Australia, in a 2012 article in the Medical Journal of Australia .
Sexual stimulation causes the release of neurotransmitters from cavernosal nerve endings and relaxation factors from endothelial cells lining the sinusoids. NOS produces NO from L-arginine, and this, in turn, produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP), which work via calcium channel and protein kinase mechanisms (see the image below). This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow.
Performance anxiety can be another cause of impotence. If a person wasn’t able to achieve an erection in the past, he may fear he won’t be able to achieve an erection in the future. A person may also find he can’t achieve an erection with a certain partner. Someone with ED related to performance anxiety may be able to have full erections when masturbating or when sleeping, yet he isn’t able to maintain an erection during intercourse.
If PDE-5 inhibitors are not suitable or don’t work, other therapies include injections into the base of the penis, which cause flow of blood into the penis and a fairly immediate erection that lasts around an hour. The drugs injected are alprostadil (Caverject and Erectile dysfunctionex) and Invicorp (VIP and phentolamine). Alprostadil may also be inserted as a gel into the opening of the penis. This is not suitable if your partner is pregnant.
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age.[15][16] The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body.[17] The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.[18]
Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.

Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.

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It seems that adequate testosterone levels are an important influence on sexual symptoms in the aging male and also influence the response of men to PDE-5 inhibitors, the first line treatment for erectile dysfunction in men. Many would now suggest screening for testosterone deficiency in all men presenting with erectile dysfunction (Gore and Rajfer 2004; Shabsigh 2005). This would seem appropriate because, in addition to benefits on sexual function, identification and treatment of hypogonadal men with testosterone could improve other symptoms of hypogonadism and protect against other conditions such as osteoporosis.

Alcohol is a depressant, not an aphrodisiac or a libido enhancer. Excessive consumption can interfere with the ability to achieve an erection at any age, and even occasional drinking can make erectile dysfunction worse in older men. Feloney advises using alcohol in moderation: "In small amounts, alcohol can relieve anxiety and may help with erectile dysfunction, but if you drink too much, it can cause erectile dysfunction or make the problem worse."

Hacking your testosterone influences everything from body composition to energy levels to mood. It’s easy to eat more butter; it’s hard to visit a doctor and get tested, but that’s what I recommend: know your levels. If you’re 25, you’ll know what your target is when you’re 35. By the time you’ve noticed symptoms of low testosterone, it’s too late to get your “normal” measurements!
Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.
Clinical trials of the effect of testosterone on glucose metabolism in men have occurred in diabetic and non-diabetic populations. Data specific to aging males is not available. A series of studies investigated the effects of testosterone or dihydrotestosterone given for 6 weeks or 3 months to middle aged, non-diabetic obese men (Marin, Holmang et al 1992; Marin, Krotkiewski et al 1992; Marin et al 1993). It was found that physiological treatment doses led to improved insulin resistance, as measured by the gold standard technique using a euglycemic clamp and/or serum glucose and insulin responses during glucose tolerance test. These improvements were associated with decreased central obesity, measured by computered tomography (CT) or waist-hip ratio, without reduced total fat mass. Insulin resistance improved more with testosterone than dihydrotestosterone treatment and beneficial effects were greater in men with lower baseline testosterone levels. Increasing testosterone levels into the supraphysiological range lead to decreased glucose tolerance.

Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[6] As the metabolism of testosterone in males is greater, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]
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