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).

ICI Alprostadil may be used as a mixture with two other drugs to treat ED. This combination therapy called "bimix or trimix" is stronger than alprostadil alone and has become standard treatment for ED. Only the Alprostadil ingredient is FDA approved for ED. The amount of each drug used can be changed based on the severity of your ED, by an experienced health professional. You will be trained by your health professional on how to inject, how much to inject and how to safely raise the drug's dosage if necessary.
However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, nearly half showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:
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
Exercise and lifestyle modifications may improve erectile function. Weight loss may help by decreasing inflammation, increasing testosterone, and improving self-esteem. Patients should be educated to increase activity, reduce weight, and stop smoking, as these efforts can improve or restore erectile function in men without comorbidities. Precise glycemic control in diabetic patients and pharmacologic treatment of hypertension may be important in preventing or reducing sexual dysfunction. [49]
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. 

The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[122] In the testes, testosterone is produced by the Leydig cells.[123] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).

Long-term predictions based on an aging population and an increase in risk factors (eg, hypertension, diabetes, vascular disease, pelvic and prostate surgery, benign prostatic hyperplasia, and lower urinary tract symptoms) suggest a large increase in the number of men with ED. In addition, the prevalence of ED is underestimated because physicians frequently do not question their patients about this disorder.
Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.
If you’re experiencing psychological ED, you may benefit from talk therapy. Therapy can help you manage your mental health. You’ll likely work with your therapist over several sessions, and your therapist will address things like major stress or anxiety factors, feelings around sex, or subconscious conflicts that could be affecting your sexual well-being. 

Erectile dysfunction can cause strain on a couple. Many times, men will avoid sexual situations due to the emotional pain associated with ED, causing their partner to feel rejected or inadequate. It is important to communicate openly with your partner. Some couples consider seeking treatment for ED together, while other men prefer to seek treatment without their partner's knowledge. A lack of communication is the primary barrier for seeking treatment and can prolong the suffering. The loss of erectile capacity can have a profound effect on a man. The good news is that ED can usually be treated safely and effectively.
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
Treatment depends on the underlying cause. In general, exercise, particularly of the aerobic type, is effective for preventing ED during midlife. Exercise as a treatment is under investigation.[22]:6, 18–19 For tobacco smokers, cessation often results in a significant improvement.[23] Oral pharmacotherapy and vacuum erection devices are first-line treatments,[22]:20, 24 followed by injections of drugs into the penis, as well as penile implants.[22]:25–26 Vascular reconstructive surgeries are beneficial in certain groups.[24]

A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
These "disease-awareness" campaigns—ostensibly a public service intended to educate those potentially at risk about a condition they may not even have heard of but "could" have—are subtle, even insidious. They may not mention a specific product, but a bit of sleuthing reveals that their sponsors are usually pharmaceutical companies that "just happen" to manufacture products used to treat the real (or at least alleged) condition.
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.
The first step in treating the patient with ED is to take a thorough sexual, medical, and psychosocial history. Questionnaires are available to assist clinicians in obtaining important patient data. (See Presentation.) Successful treatment of sexual dysfunction has been demonstrated to improve sexual intimacy and satisfaction, improve sexual aspects of quality of life, improve overall quality of life, and relieve symptoms of depression. (See Treatment.)

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.
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
The Food and Drug Administration (FDA) does not recommend alternative therapies to treat sexual dysfunction.[27] Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of ED, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products.[28][29][30][31][32] The FDA has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant.[33]
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.

Long-term predictions based on an aging population and an increase in risk factors (eg, hypertension, diabetes, vascular disease, pelvic and prostate surgery, benign prostatic hyperplasia, and lower urinary tract symptoms) suggest a large increase in the number of men with ED. In addition, the prevalence of ED is underestimated because physicians frequently do not question their patients about this disorder.

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.
Most men may not openly talk about their erection problems, but erectile dysfunction — when a man cannot achieve or maintain an erection well enough or long enough to have satisfying sex — is very common. According to the National Institutes of Health, 5 percent of 40-year-olds and 15 to 25 percent of 65-years old have ED. But while ED is more likely to occur as a man gets older, it doesn’t come automatically with age.
Cavernosography measurement of the vascular pressure in the corpus cavernosum. Saline is infused under pressure into the corpus cavernosum with a butterfly needle, and the flow rate needed to maintain an erection indicates the degree of venous leakage. The leaking veins responsible may be visualized by infusing a mixture of saline and x-ray contrast medium and performing a cavernosogram.[21] In Digital Subtraction Angiography (DSA), the images are acquired digitally.
The rise in testosterone levels during competition predicted aggression in males but not in females.[86] Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression.[87] Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations.[88] Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence.[89] Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli.[90] Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.[91]
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.
In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.[124]
Overall, it seems that both estrogen and testosterone are important for normal bone growth and maintenance. Deficiency or failure of action of the sex hormones is associated with osteoporosis and minimal trauma fractures. Estrogen in males is produced via metabolism of testosterone by aromatase and it is therefore important that androgens used for the treatment of hypogonadism be amenable to the action of aromatase to yield maximal positive effects on bone. There is data showing that testosterone treatment increases bone mineral density in aging males but that these benefits are confined to hypogonadal men. The magnitude of this improvement is greater in the spine than in the hip and further studies are warranted to confirm or refute any differential effects of testosterone at these important sites. Improvements seen in randomized controlled trials to date may underestimate true positive effects due to relatively short duration and/or baseline characteristics of the patients involved. There is no data as yet to confirm that the improvement in bone density with testosterone treatment reduces fractures in men and this is an important area for future study.
Conditions associated with reduced nerve and endothelium function (eg, aging, hypertension, smoking, hypercholesterolemia, and diabetes) alter the balance between contraction and relaxation factors (see Pathophysiology). These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.

 5. Medline Plus. US National Library of Medicine. NIH National Institutes of Health. Drugs that may cause impotence (updated 21 Jan 2015). http://www.nlm.nih.gov/medlineplus/ency/article/004024.htm (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence treatmentsIf you have impotence (erectile dysfunction), the treatment your doctor recommends will depend on thErectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotenceGum disease linked to erectile dysfunctionAdvanced gum disease (periodontitis) has been linked to an increased risk of erectile dysfunction, wPeyronie's diseasePeyronie’s disease is condition where a band of scar tissue forms in the penis, causing aAdvertisement

show that total testosterone levels increase after exercising, especially after resistance training. Low testosterone levels can affect your sex drive and your mood. The good news is that exercise improves mood and stimulates brain chemicals to help you feel happier and more confident. Exercise also boosts energy and endurance, and helps you to sleep better. Fitness experts recommend 30 minutes of exercise every day.
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