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.
Failure to achieve an erection is not uncommon for most men and may be considered normal even if it happens as often as 20 percent of the time. There is a wide range of normal when it comes to sexual functioning and sexual relationships. "Generally if a couple feels comfortable with their sex life and they enjoy intimacy together, erectile dysfunction may not be much of an issue. But if erectile dysfunction is causing stress in a relationship, then help is available," says Feloney.
With sex therapy, your counselor looks at the sexual problems you and your partner are having. Sex therapy works with problems such as performance anxiety, which means that you worry so much about whether you will be able to have sex that you are not able to. It also helps when you have erection problems that are not due to physical or drug problems, or premature ejaculation (you come too quickly). It may help you to reach orgasm or to learn to relax enough to avoid pain during sex. Counseling can help you to adjust to the treatment you and your doctor choose.
Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer,[10] and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[170] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[171]
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]
Some men report being helped by an oral medication called yohimbine, which comes from the bark of a tree that grows in India and Africa. This drug, which needs to be taken every day, has been reported to help about 20 to 25 percent of the men taking it. A relatively new but widely used oral medication called Viagra requires a careful medical evaluation by your doctor.
Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.[2] In addition, testosterone is involved in health and well-being,[3] and the prevention of osteoporosis.[4] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
Testosterone is a sex hormone that plays important roles in the body. In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm. A small amount of circulating testosterone is converted to estradiol, a form of estrogen. As men age, they often make less testosterone, and so they produce less estradiol as well. Thus, changes often attributed to testosterone deficiency might be partly or entirely due to the accompanying decline in estradiol.
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.
The Massachusetts Male Aging Study (MMAS) documented an inverse correlation between ED risk and high-density lipoprotein (HDL) cholesterol levels but did not identify any effect from elevated total cholesterol levels. [15] Another study involving male subjects aged 45-54 years found a correlation with abnormal HDL cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS included a preponderance of older men.
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.

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."


Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
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.
Stress is your body responding to your environment. And it’s a good thing—in limited doses. When you get stressed out your body makes chemicals like adrenaline that make you stronger, faster, fitter, and even able to think more clearly. Most people call this reaction the “fight-or-flight” response, and it’s a life-saver in dangerous situations. In a very real sense, adrenaline makes you a part-time superhero. The problems happen when your body deals with constant stress.
Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date. [4] Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process. 

Testosterone is the primary male sex hormone and an anabolic steroid. In male humans, testosterone plays a key role in the development of male reproductive tissues such as testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle and bone mass, and the growth of body hair.[2] In addition, testosterone is involved in health and well-being,[3] and the prevention of osteoporosis.[4] Insufficient levels of testosterone in men may lead to abnormalities including frailty and bone loss.
"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 .
If you have unstable heart disease of any kind, heart failure or unstable, what we call angina, contraindication to using the medications. All right? So if you’re in an unstable medical state, these medications are not a good idea. Now, there are relative issues. If you may be taking a blood pressure medicine or a medicine for your prostate which dilates your blood vessel a little bit– you know, the typical ones are what we call the alpha blockers– you may have an additive effect from the medication. But for the most part, the medicines are incredibly safe.
Treatment involves addressing the underlying causes, lifestyle modifications, and addressing psychosocial issues.[1] In many cases, a trial of pharmacological therapy with a PDE5 inhibitor, such as sildenafil, can be attempted. In some cases, treatment can involve inserting prostaglandin pellets into the urethra, injecting smooth muscle relaxants and vasodilators into the penis, a penile prosthesis, a penis pump, or vascular reconstructive surgery.[1][2] It is the most common sexual problem in men.[3]
NO is produced by the enzyme NO synthase (NOS). [13] NOS plays many roles, ranging from homeostasis to immune system regulation. To date, 3 subtypes have been identified: nNOS, iNOS, and eNOS, which are produced by the genes NOS1, NOS2, and NOS3, respectively. This nomenclature is derived from the sources of the original isolates: neuronal tissue (nNOS), immunoactivated macrophage cell lines (iNOS), and vascular endothelium (eNOS). The subtypes are not, however, limited to the tissues from which they were first isolated.

There have been case reports of development of prostate cancer in patients during treatment with testosterone, including one case series of twenty patients (Gaylis et al 2005). It is not known whether this reflects an increase in incidence, as prostate cancer is very common and because the monitoring for cancer in patients treated with testosterone is greater. Randomized controlled trials of testosterone treatment have found a low incidence of prostate cancer and they do not provide evidence of a link between testosterone treatment and the development of prostate cancer (Rhoden and Morgentaler 2004). More large scale clinical trials of longer durations of testosterone replacement are required to confirm that testosterone treatment does not cause prostate cancer. Overall, it is not known whether testosterone treatment of aging males with hypogonadism increases the risk of prostate cancer, but monitoring for the condition is clearly vital. This should take the form of PSA blood test and rectal examination every three months for the first year of treatment and yearly thereafter (Nieschlag et al 2005). Age adjusted PSA reference ranges should be used to identify men who require further assessment. The concept of PSA velocity is also important and refers to the rate of increase in PSA per year. Patients with abnormal rectal examination suggestive of prostate cancer, PSA above the age specific reference range or a PSA velocity greater than 0.75 ng/ml/yr should be referred to a urologist for consideration of prostate biopsy.


In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
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