All NOS subtypes produce NO, but each may play a different biologic role in various tissues. nNOS and eNOS are considered constitutive forms because they share biochemical features: They are calcium-dependent, they require calmodulin and reduced nicotinamide adenine dinucleotide phosphate for catalytic activity, and they are competitively inhibited by arginine derivatives. nNOS is involved in the regulation of neurotransmission, and eNOS is involved in the regulation of blood flow.
"The hope," explained Dr. Swerdloff in a telephone interview, "is this will provide some clarity as to whether testosterone replacement therapy will benefit men in this older age group who clearly have abnormal testosterone and have some symptoms." He added, "We don't know whether it will be beneficial at all the endpoints we are studying, or be beneficial to some and not others. We don't know if the benefits occur at different blood levels that are attained in the individuals."

If it is determined that ED is a problem, the patient evaluation should include a detailed sexual and medical history and a physical exam. In particular, it is important to evaluate the ED within the context of ejaculatory problems. There is a strong interplay between premature ejaculation (PE) and ED, with about a third of ED patients reporting PE. The relationship between the PE and ED is bidirectional and successful treatment of one often requires treatment of the other.14
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
Patients receiving penile prostheses should be instructed in the operation of the prosthesis before surgery and again in the postoperative period. The prosthesis usually is not activated until approximately 6 weeks after surgery, so as to allow the edema and pain to subside. The prosthesis is checked in the office before the patient begins to use it. 

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]

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What you need to know about STDs Sexually transmitted diseases (STDs) are infections that are passed on from one person to another through sexual contact. There are many STDs, including chlamydia, genital warts, syphilis, and trich. This article looks at some of the most common STDs, the symptoms, and how to avoid getting or passing an STD one on. Read now
Dr. Adriane Fugh-Berman, associate professor of pharmacology and director of the industry watchdog group PharmedOut.org at Georgetown University School of Medicine, calls this kind of direct-to-consumer pharmaceutical advertising "evil." She likened the efforts to sell TRT to earlier campaigns to push hormone replacement therapy for post-menopausal women. "They stole the playbook," she said. "This hormone is being thrown around like sugar water."
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.
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.
An analysis of 14 studies involving more than 90,000 patients with ED confirmed the relation between ED and an increased risk of cardiovascular events and mortality. [56] Compared with patients without ED, those with ED had a 44% increased risk of cardiovascular events, a 25% increased risk of all-cause mortality, a 62% increased risk of MI, and a 39% increased risk of cerebrovascular events. Treatment of ED, either through lifestyle interventions or by pharmacologic means, may improve prognosis and reduce risk.
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.
"One of the reasons erectile dysfunction increases with age is that the diseases that lead to it also increase with age," notes Dr. Feloney. Evaluating the causes of erectile dysfunction starts with your doctor taking a good health history and giving you a physical exam. Common medical issues that can lead to erectile dysfunction include diabetes, high blood pressure, hardening of the arteries, low testosterone, and neurological disease. Talk to your doctor about better managing these health conditions.
Medications for erectile dysfunction don't work for everyone and may cause side effects that make a particular drug hard to take. "Work with your doctor to find the right treatment. There are still options for people who fail at medical treatment," advises Feloney. Alternatives to erectile dysfunction drugs include vacuum pump devices, medications injected into the penis, testosterone replacement if needed, and a surgical penile implant.
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TT may help you but it may have adverse (harmful) results. (See discussion of these side effects below.) The Federal Drug Administration (FDA) has said that testosterone drug labels should state that there is a risk for heart disease and stroke for some men using testosterone products. All men should be checked for heart disease and stroke before, and periodically while on, TT. The AUA however, on careful review of evidence-based peer review literature, has stated that there is no strong evidence that TT either increases or decreases the risk of cardiovascular events.
They also don't make clear how risky exposure to testosterone gel is for others—female partners, children, even pets. The gel is actually notorious for transferring to others. It can cause excess hair to grow on women's faces and arms, deepen their voices, interrupt menstruation, and make them anxious and irritable. In children, exposure to testosterone gels and creams can cause premature puberty and aggression. And in pets, it can cause aggressive behavior and enlargement of the genitalia.
The changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range and the figure rises to 50% in those aged over 80. The figures concerning free testosterone are even higher as would be expected in view of the concurrent decrease in SHBG levels (Harman et al 2001).
The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (see figure to the right).[125] When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These latter two hormones stimulate the testis to synthesize testosterone. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.
During the second trimester, androgen level is associated with sex formation.[13] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult's own levels. A mother's testosterone level during pregnancy is correlated with her daughter's sex-typical behavior as an adult, and the correlation is even stronger than with the daughter's own adult testosterone level.[14]
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.
All NOS subtypes produce NO, but each may play a different biologic role in various tissues. nNOS and eNOS are considered constitutive forms because they share biochemical features: They are calcium-dependent, they require calmodulin and reduced nicotinamide adenine dinucleotide phosphate for catalytic activity, and they are competitively inhibited by arginine derivatives. nNOS is involved in the regulation of neurotransmission, and eNOS is involved in the regulation of blood flow.
Late onset hypogonadism reflects a particular pathophysiology and it may not be appropriate to extrapolate results from studies concerning the effects of testosterone in treating hypogonadism of other etiology to aging males. For this reason, the age of men treated in clinical trials is certainly relevant. Other important factors include patient comorbidities and the preparation and route of testosterone replacement used in the study, which can affect the production of estrogen and dihydrotestosterone, testosterone’s active metabolites
CONDITIONS OF USE: The information in this database is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is sage, appropriate or effective for you or anyone else. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment.
Knowing about your history of ED will help your health provider learn if your problems are because of your desire for sex, erection function, ejaculation, or orgasm (climax). Some of these questions may seem private or even embarrassing. However, be assured that your doctor is a professional and your honest answers will help find the cause and best treatment for you.
It appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme. [24] The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.
medicines called alpha-blockers such as Hytrin (terazosin
HCl), Flomax (tamsulosin HCl), Cardura (doxazosin
mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl),
 Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin).
Alpha-blockers are sometimes prescribed for prostate
problems or high blood pressure. In some patients, the use
of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
What you need to know about STDs Sexually transmitted diseases (STDs) are infections that are passed on from one person to another through sexual contact. There are many STDs, including chlamydia, genital warts, syphilis, and trich. This article looks at some of the most common STDs, the symptoms, and how to avoid getting or passing an STD one on. Read now
The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone. More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility. 

Camacho EM1, Huhtaniemi IT, O'Neill TW, Finn JD, Pye SR, Lee DM, Tajar A, Bartfai G, Boonen S, Casanueva FF, Forti G, Giwercman A, Han TS, Kula K, Keevil B, Lean ME, Pendleton N, Punab M, Vanderschueren D, Wu FC; EMAS Group. “Age-associated changes in hypothalamic-pituitary-testicular function in middle-aged and older men are modified by weight change and lifestyle factors: longitudinal results from the European Male Ageing Study.” Eur J Endocrinol. 2013 Feb 20;168(3):445-55. doi: 10.1530/EJE-12-0890. Print 2013 Mar.
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Some self-administered measures may be useful in the primary care setting to screen for and evaluate the degree of ED.12 The most commonly used instrument is the International Index of Erectile Function, a 15-item questionnaire that has been validated in many populations and is considered the gold standard to evaluate patients for ED.13 The Sexual Health Inventory for Men is a short-form, 5-item questionnaire developed to monitor treatment progress.12 It is important to recognize that short-form questionnaire does not evaluate specific areas of the sexual cycle, such as sexual desire, ejaculation, and orgasm; however, it may be useful in discussing ED with patients and evaluating treatment results over time.
After bombarding consumers with advertising, and massaging physicians with free meals and medical "information," the stage is set to seal the deal. "The fat guy has been seeing the ads on TV," said Fugh-Berman. "The doc has just come from a medical meeting where they were talking about how using testosterone can fight depression, etc., and they are being primed in a different way."
Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
Erectile dysfunction or disorder (ED) is the inability to develop and maintain an erection for satisfactory sexual intercourse or activity. Erectile dysfunction or erectile disorder are the preferred terms as opposed to impotence. There are no uniform criteria defining how consistent the problem has to be and for what duration it must be present to considered ED. The Diagnostic and Statistical Manual of Mental Disorder-5 specifies a duration of at least 6 months in its definition of ED.1
Many clinical studies have looked at the effect of testosterone treatment on body composition in hypogonadal men or men with borderline low testosterone levels. Some of these studies specifically examine these changes in older men (Tenover 1992; Morley et al 1993; Urban et al 1995; Sih et al 1997; Snyder et al 1999; Kenny et al 2001; Ferrando et al 2002; Steidle et al 2003; Page et al 2005). The data from studies, on patients from all age groups, are consistent in showing an increase in fat free mass and decrease in fat mass or visceral adiposity with testosterone treatment. A recent meta-analysis of 16 randomized controlled trials of testosterone treatment effects on body composition confirms this pattern (Isidori et al 2005). There have been less consistent results with regard to the effects of testosterone treatment of muscle strength. Some studies have shown an increase in muscle strength (Ferrando et al 2002; Page et al 2005) with testosterone whilst others have not (Snyder et al 1999). Within the same trial some muscle group strengths may improve whilst others do not (Ly et al 2001). It is likely that the differences are partly due to the methodological variations in assessing strength, but it also possible that testosterone has different effects on the various muscle groups. The meta-analysis found trends toward significant improvements in dominant knee and hand grip strength only (Isidori et al 2005).
Tests such as the bulbocavernosus reflex test are used to determine if there is sufficient nerve sensation in the penis. The physician squeezes the glans (head) of the penis, which immediately causes the anus to contract if nerve function is normal. A physician measures the latency between squeeze and contraction by observing the anal sphincter or by feeling it with a gloved finger inserted past the anus.
“Although having sex at 70 is not the same as having sex at 20, erectile dysfunction is not a normal part of aging,” according to Michael Feloney, MD, urologic surgeon and expert on sexual dysfunction issues at the Nebraska Medical Center in Omaha. “You should still be able to have a satisfying sex life as you age." If you are experiencing erectile dysfunction, these 10 dos and don'ts may help.
Some self-administered measures may be useful in the primary care setting to screen for and evaluate the degree of ED.12 The most commonly used instrument is the International Index of Erectile Function, a 15-item questionnaire that has been validated in many populations and is considered the gold standard to evaluate patients for ED.13 The Sexual Health Inventory for Men is a short-form, 5-item questionnaire developed to monitor treatment progress.12 It is important to recognize that short-form questionnaire does not evaluate specific areas of the sexual cycle, such as sexual desire, ejaculation, and orgasm; however, it may be useful in discussing ED with patients and evaluating treatment results over time.
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone. 
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.

Erectile dysfunction can be embarrassing and difficult to talk about for some men. Many men may feel like they need to hide their diagnosis from their partner. "Failure to communicate openly about erectile dysfunction can result in both partners drawing away from the relationship," warns Feloney. Remember that your partner is also affected by your problem; being open and honest is the best way to decrease fear and anxiety. Discuss options for achieving sexual satisfaction together, and be positive — most erectile dysfunction problems can be treated.
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).

This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the person's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
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 symptoms of erectile dysfunction include difficulty achieving an erection, trouble maintaining an erection, and a reduced interest in sex. Because male sexual arousal is a fairly complex process, it can sometimes be difficult to identify a specific cause. Arousal starts in the brain but it also involves the nerves, muscles, and blood vessels and can be impacted by hormones and emotions. If a problem develops with any of these things, erectile dysfunction could be the consequence.

For people who are worried about low or high testosterone, a doctor may perform a blood test to measure the amount of the hormone in the patient's blood. When doctors find low-T, they may prescribe testosterone therapy, in which the patient takes an artificial version of the hormone. This is available in the following forms: a gel to be applied to the upper arms, shoulders or abdomen daily; a skin patch put on the body or scrotum twice a day; a solution applied to the armpit; injections every two or three weeks; a patch put on the gums twice a day; or implants that last four to six months.
The mechanisms by which testosterone plays a role in erectile function are not completely understood. A study evaluating the effect of testosterone on erections in surgically castrated rabbits and control animals, in which the rabbits’ intracavernosal pressures were compared after cavernosal nerve stimulation, determined that castrated rabbits had much lower pressures after stimulation than control rabbits did. [21] Notably, the pressures increased when castrated rabbits received exogenous testosterone replacement.
Vascular damage may result from radiation therapy to the pelvis and prostate in the treatment of prostate cancer. [36] Both the blood vessels and the nerves to the penis may be affected. Radiation damage to the crura of the penis, which are highly susceptible to radiation damage, can induce ED. Data indicate that 50% of men undergoing radiation therapy lose erectile function within 5 years after completing therapy; fortunately, some respond to one of the PDE5 inhibitors.
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]
Her remark was entirely destructive of poetry, since it was to the effect that poetry had nothing whatever to do with her; all her friends spent their lives in making up phrases, she said; all his feeling was an illusion, and next moment, as if to taunt him with his impotence, she had sunk into one of those dreamy states which took no account whatever of his existence.
Surgical intervention for a number of conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply.[8] Erectile dysfunction is a common complication of treatments for prostate cancer, including prostatectomy and destruction of the prostate by external beam radiation, although the prostate gland itself is not necessary to achieve an erection. As far as inguinal hernia surgery is concerned, in most cases, and in the absence of postoperative complications, the operative repair can lead to a recovery of the sexual life of people with preoperative sexual dysfunction, while, in most cases, it does not affect people with a preoperative normal sexual life.[13]
Can apple cider vinegar treat erectile dysfunction? Apple cider vinegar is thought to have many health benefits, but can it help treat erectile dysfunction (ED)? ED can result from cardiovascular problems, diabetes, and other factors. Apple cider vinegar may help improve symptoms of conditions related to ED. Find out how it may help, and how to use it safely. Read now

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).


Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[31]
Transdermal preparations of testosterone utilize the fact that the skin readily absorbs steroid hormones. Initial transdermal preparations took the form of scrotal patches with testosterone loaded on to a membranous patch. Absorption from the scrotal skin was particularly good and physiological levels of testosterone with diurnal variation were reliably attained. The scrotal patches are now rarely used because they require regular shaving or clipping of scrotal hair and because they produce rather high levels of dihydrotestosterone compared to testosterone (Behre et al 1999). Subsequently, non-scrotal patches were developed but the absorptive capacity of non-scrotal skin is much lower, so these patches contain additional chemicals which enhance absorption. The non-scrotal skin patches produce physiological testosterone levels without supraphysiological dihydrotestosterone levels. Unfortunately, the patches produce a high rate of local skin reactions often leading to discontinuation (Parker and Armitage 1999). In the last few years, transdermal testosterone gel preparations have become available. These require daily application by patients and produce steady state physiological testosterone levels within a few days in most patients (Swerdloff et al 2000; Steidle et al 2003). The advantages compared with testosterone patches include invisibility, reduced skin irritation and the ability to adjust dosage, but concerns about transfer to women and children on close skin contact necessitate showering after application or coverage with clothes.
Alprostadil (also known as prostaglandin E1 [PGE1]) is the prominent known smooth-muscle dilator of the corpus cavernosum. Its mechanism of action is believed to be the promotion of intracellular accumulation of cyclic adenosine monophosphate, thereby causing decreased intracellular accumulation of calcium and resulting smooth muscle relaxation. Alprostadil can be delivered to the erectile tissue either via an intraurethral suppository that is massaged and then absorbed across the corpus spongiosum of the urethra to the corpora cavernosa, or directly injected into the corpora cavernosa. When administered urethrally, doses are substantially higher than when directly injected (typical dosing is 500 mcg to 1 mg intraurethral compared with 2.5 mcg to 20 mcg intracavernosal).
The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids. Behavioural changes (such as increased irritability) may also be observed. Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
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.
Men with medical conditions that may cause a sustained erection, such as sickle cell anemia, leukemia, or multiple myeloma, or a man who has an abnormally-shaped penis, may not benefit from these medications. Also, men with liver diseases or a disease of the retina, such as macular degeneration or retinitis pigmentosa, may not be able to take these medications, or may need to take the lowest dosage.
Replacement therapy may produce desired results, such as greater muscle mass and a stronger sex drive. However, the treatment does carry some side effects. Oily skin and fluid retention are common. The testicles may also shrink, and sperm production could decrease significantly. Some studies have found no greater risk of prostate cancer with testosterone replacement therapy, but it continues to be a topic of ongoing research.
The physical side effects of chemotherapy are usually temporary and resolve within one to two weeks after stopping the chemotherapy. However, chemotherapy agents, such as Ciplatin or Vincristine, may interfere with the nerves that control erection leading to possible impotence. Make sure you discuss potential side effects of cancer chemotherapy with your doctor or healthcare provider.
It is essential to discuss erectile dysfunction with your doctor, so any serious underlying causes can be excluded and treatment options can be discussed. Many men are embarrassed discussing this issue with their doctor, or even their partner. Open communication with your doctor, and in your relationship, is important for effectively managing this common problem.
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.

Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[46] This may be linked to the ovulatory shift hypothesis,[47] where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.


A team led by Dr. Joel Finkelstein at Massachusetts General Hospital investigated testosterone and estradiol levels in 400 healthy men, 20 to 50 years of age. To control hormone levels, the researchers first gave the participants injections of a drug that suppressed their normal testosterone and estradiol production. The men were randomly assigned to 5 groups that received different amounts (from 0 to 10 grams) of a topical 1% testosterone gel daily for 16 weeks. Half of the participants were also given a drug to block testosterone from being converted to estradiol.
Can apple cider vinegar treat erectile dysfunction? Apple cider vinegar is thought to have many health benefits, but can it help treat erectile dysfunction (ED)? ED can result from cardiovascular problems, diabetes, and other factors. Apple cider vinegar may help improve symptoms of conditions related to ED. Find out how it may help, and how to use it safely. Read now
Many experts believe that atrophy, a partial or complete wasting away of tissue, and fibrosis, the growth of excess tissue, of the smooth muscle tissue in the body of the penis (cavernous smooth muscle) triggers problems with being able to maintain a firm erection. Poor ability to maintain an erection is often an early symptom of erectile dysfunction. Although the condition is called venous leak, the real problem is not with the veins but malfunction of the smooth muscle that surrounds the veins. The end result is difficulty with maintain a firm erection (losing an erection too quickly) that is now believe to be an early manifestation of atherosclerosis and vascular disease.
Low-intensity extracorporeal shock wave therapy has been proposed as a new non-invasive treatment for erectile dysfunction caused by problems with blood vessels. Shock wave therapy machines are now available in some medical practices in Australia. Although there is some evidence that it may help a proportion of men with erectile dysfunction, more research is needed before clear recommendations on its use can be made.
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).
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]
"The hard part," said Dr. Anawalt, "is the man who is 50 pounds overweight and sedentary, who sees a TV ad and goes to see his doctor. Let's say he has a thoughtful doctor who does the right test, at the right time of day (morning), and the test comes back low. Many of these guys will have low or slightly low testosterone. We have no evidence for whether or not it's a benefit to give these guys testosterone." He added that concern about their testosterone level could be a good thing if it spurs men to lose weight and exercise. "A low testosterone level can be a marker of poor health," he said.
Associated morbidity may include various other male sexual dysfunctions, such as premature (early) ejaculation and male hypoactive sexual desire disorder. The NHSLS found that 28.5% of men aged 18-59 years reported premature ejaculation, and 15.8% lacked sexual interest during the past year. An additional 17% reported anxiety about sexual performance, and 8.1% had a lack of pleasure in sex. [51]
It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.
For people who are worried about low or high testosterone, a doctor may perform a blood test to measure the amount of the hormone in the patient's blood. When doctors find low-T, they may prescribe testosterone therapy, in which the patient takes an artificial version of the hormone. This is available in the following forms: a gel to be applied to the upper arms, shoulders or abdomen daily; a skin patch put on the body or scrotum twice a day; a solution applied to the armpit; injections every two or three weeks; a patch put on the gums twice a day; or implants that last four to six months.
Erectile dysfunction, also known as ED or impotence, is the inability to attain or maintain an erection of the penis adequate for the sexual satisfaction of both partners. It can be devastating to the self-esteem of a man and of his partner. As many as 30 million American men are afflicted on a continuing basis, and transient episodes affect nearly all adult males. But nearly all men who seek treatment find some measure of relief.
The prevalence of biochemical testosterone deficiency increases with age. This is partly due to decreasing testosterone levels associated with illness or debility but there is also convincing epidemiological data to show that serum free and total testosterone levels also fall with normal aging (Harman et al 2001; Feldman et al 2002). The symptoms of aging include tiredness, lack of energy, reduced strength, frailty, loss of libido, decreased sexual performance depression and mood change. Men with hypogonadism experience similar symptoms. This raises the question of whether some symptoms of aging could be due to relative androgen deficiency. On the other hand, similarities between normal aging and the symptoms of mild androgen deficiency make the clinical diagnosis of hypogonadism in aging men more challenging.
In men with hypogonadism, a low level of testosterone is produced due to a problem in the testicles or the pituitary gland. According to Harvard Medical School, determining exactly what constitutes a low testosterone level is a controversial matter. Levels of this hormone fluctuate wildly and even vary according to the time of day. However, generally physicians only decide to treat a patient for hypogonadism if the blood testosterone level is below 300 ng/dL and the following symptoms outlined by The National Institutes of Health are present.    
"The hope," explained Dr. Swerdloff in a telephone interview, "is this will provide some clarity as to whether testosterone replacement therapy will benefit men in this older age group who clearly have abnormal testosterone and have some symptoms." He added, "We don't know whether it will be beneficial at all the endpoints we are studying, or be beneficial to some and not others. We don't know if the benefits occur at different blood levels that are attained in the individuals."
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.
In summary, low testosterone levels are linked to the presence of numerous cardiovascular risk factors. Testosterone treatment acts to improve some of these factors, but effects may vary according to pre- and post-treatment testosterone levels, as well as other factors. There is little data from trials specific to aging males. Appropriately-powered randomized controlled trials, with cardiovascular disease primary endpoints, are needed to clarify the situation, but in the meantime the balance of evidence is that testosterone has either neutral or beneficial effects on the risk of cardiovascular disease in men. It is particularly important to define the effect of testosterone treatment on cardiovascular disease in view of its potential use as an anti-anginal agent.
ED can also occur among younger men. A 2013 study found that one in four men seeking their first treatment for ED were under the age of 40. The researchers found a stronger correlation between smoking and illicit drug use and ED in men under 40 than among older men. That suggests that lifestyle choices may be a main contributing factor for ED in younger men.

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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]
Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
Erectile dysfunction (previously called impotence) is the inability to get or maintain an erection that is sufficient to ensure satisfactory sex for both partners. This problem can cause significant distress for couples. Fortunately more and more men of all ages are seeking help, and treatment for ED has advanced rapidly. The enormous demand for “anti-impotence” drugs suggests that erection problems may be more common than was previously thought. Find out more about the causes and treatment of erectile dysfunction here.

The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids. Behavioural changes (such as increased irritability) may also be observed. Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.
A common and important cause of ED is vasculogenic. Many men with ED have comorbid conditions such as hyperlipidemia, hypercholesterolemia, tobacco abuse, diabetes mellitus, or coronary artery disease (CAD). [6] The Princeton III Consensus recommends screening men who present with ED for cardiovascular risk factors; ED may be the earliest presentation of atherosclerosis and vascular disease. [7]
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
In the U.S., where millions watch the Super Bowl simply to see the clever and costly commercials, and where pharmaceuticals with potentially deadly side effects are pushed on the public at every turn, it's probably not surprising that ads for "Low T" are now splayed across billboards in Florida, with its huge number of older residents, or that a chain of "Low T Centers" has sprung up in Texas and around the heartland.
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
There are risks to prosthetic surgery and patients are counselled before the procedure. If there is a post-operative infection, the implant will likely be removed. The devices are reliable, but in the case of mechanical malfunction, the device or a part of the device will need to be replaced surgically. If a penile prosthesis is removed, other non-surgical treatments may no longer work.
Oral/buccal (by mouth). The buccal dose comes in a patch that you place above your incisor (canine or "eyetooth"). The medication looks like a tablet but you should not chew or swallow it. The drug is released over 12 hours. This method has fewer harmful side effects on the liver than if the drug is swallowed, but it may cause headaches or cause irritation where you place it.
Penile erection is managed by two mechanisms: the reflex erection, which is achieved by directly touching the penile shaft, and the psychogenic erection, which is achieved by erotic or emotional stimuli. The former uses the peripheral nerves and the lower parts of the spinal cord, whereas the latter uses the limbic system of the brain. In both cases, an intact neural system is required for a successful and complete erection. Stimulation of the penile shaft by the nervous system leads to the secretion of nitric oxide (NO), which causes the relaxation of smooth muscles of corpora cavernosa (the main erectile tissue of penis), and subsequently penile erection. Additionally, adequate levels of testosterone (produced by the testes) and an intact pituitary gland are required for the development of a healthy erectile system. As can be understood from the mechanisms of a normal erection, impotence may develop due to hormonal deficiency, disorders of the neural system, lack of adequate penile blood supply or psychological problems.[18] Spinal cord injury causes sexual dysfunction including ED. Restriction of blood flow can arise from impaired endothelial function due to the usual causes associated with coronary artery disease, but can also be caused by prolonged exposure to bright light.
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.
It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.

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]


However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
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).
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.
Patients at high cardiovascular risk should not be treated for ED until their cardiac condition is stabilize. These conditions include unstable or refractory angina, myocardial infarction or cerebrovascular accident within the past 2 weeks, uncontrolled hypertension, New York Heart Association (NYHA) Functional Classification III-IV congestive heart failure, high-risk arrhythmias, hypertrophic obstructive cardiomyopathies, and moderate-to-severe valvular disease.25 This class of drugs is also contraindicated in patients who use nitroglycerin or nitrate-containing compounds.26, 27
Hormone deficiency or hypogonadism, whether primary or secondary, has been thought to impact erectile function. Approximately a third of men in the European Male Aging Study demonstrated low testosterone, suggesting that hypogonadism is overrepresented among men with ED.11 Hormone deficiency, however, is less frequently the cause of ED than diabetes or vascular disease. Many entities with a strong relationship to ED also diminish bioavailable testosterone, including obesity, diabetes, and opioid use. Other hormones involved in testosterone metabolism or availability, like thyroid stimulating hormone and gonadotropins, also may impact erectile quality, presumably through regulating bioavailable testosterone. Understanding the relationship between testosterone and ED has been impaired by a lack of standardized measurement of this hormone and the cyclic nature of its release and consumption.
Tests such as the bulbocavernosus reflex test are used to determine if there is sufficient nerve sensation in the penis. The physician squeezes the glans (head) of the penis, which immediately causes the anus to contract if nerve function is normal. A physician measures the latency between squeeze and contraction by observing the anal sphincter or by feeling it with a gloved finger inserted past the anus.
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.
A previous meta-analysis has confirmed that treatment of hypogonadal patients with testosterone improves erections compared to placebo (Jain et al 2000). A number of studies have investigated the effect of testosterone levels on erectile dysfunction in normal young men by inducing a hypogonadal state, for example by using a GnRH analogue, and then replacing testosterone at varying doses to produce levels ranging from low-normal to high (Buena et al 1993; Hirshkowitz et al 1997). These studies have shown no significant effects of testosterone on erectile function. These findings contrast with a similar study conducted in healthy men aged 60–75, showing that free testosterone levels achieved with treatment during the study correlate with overall sexual function, including morning erections, spontaneous erections and libido (Gray et al 2005). This suggests that the men in this older age group are particularly likely to suffer sexual symptoms if their testosterone is low. Furthermore, the severity of erectile dysfunction positively correlates with lower testosterone levels in men with type 2 diabetes (Kapoor, Clarke et al 2007).

Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[60] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals,[61] While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels[62] as well as temporary fluctuations. For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant[63].
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.[53] However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this change in testosterone levels is no longer apparent.[53] Men who produce less testosterone are more likely to be in a relationship[54] or married,[55] and men who produce more testosterone are more likely to divorce;[55] however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels.[56] Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts.[57] Married men who engage in bond-maintenance activities such as spending the day with their spouse/and or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.[58]
Erectile dysfunction (ED) is the inability to get an erection or to keep one that's firm enough or that lasts long enough for a man to have a satisfying sexual experience. Occasional bouts of ED aren't unusual. In fact, as many as one in five men deal with erectile dysfunction to some degree. Symptoms, of course, are rather obvious. And while age can be a risk factor, so can medication use, health conditions, lifestyle factors (like smoking), and other concerns. Treatment is available and may involve prescriptions, habit changes, or other options.
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]
Do erectile dysfunction exercises help? Many people have erectile dysfunction (ED), but it is often possible to reverse this with exercises to strengthen muscles in the area. These include pelvic floor exercises. ED can often be due to lifestyle factors including obesity and low physical activity levels. Learn more about exercises for ED here. Read now
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[177] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[178][179]
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