ICI therapy often produces a reliable erection, which comes down after 20-30 minutes or with climax. Since the ICI erection is not regulated by your penile nerves, you should not be surprised if the erection lasts after orgasm. The most common side effect of ICI therapy is a prolonged erection. Prolonged erections (>1 hour) can be reversed by a second injection (antidote) in the office.
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.
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]
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.
Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.
Of particularly concern are antihypertensive medications for CVD (eg, digoxin, disopyramide [Norpace], gemfibrozil [Lopid]), anxiety, depression (eg, lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants), or psychosis (eg, chlorpromazine, haloperidol, pimozide [Orap], thioridazine, thiothixene). Antihypertensive drugs, such as diuretics (eg, spironolactone, thiazides) and beta blockers, may be associated with ED. Discontinuation or switching to alternative drugs, such as angiotensin-converting enzyme inhibitors or calcium channel blockers (eg, diltiazem, nifedipine, amlodipine), may reduce ED. The newer angiotensin II receptor antagonists may be less problematic with respect to ED, but long-term data is needed to evaluate this.
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:
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.

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).

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Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls. [39]  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.
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.
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.    
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.

Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.
It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.
The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken orally.[22]:20–21 Additionally, a cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for erectile dysfunction.[25] Penile injections, on the other hand, can involve one of the following medications: papaverine, phentolamine, and prostaglandin E1.[22]:25
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.
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

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]


If PDE5 drugs don't work or cannot be used because of potential side effects, your doctor can recommend other therapies. The drug alprostadil (Caverject, Edex, Muse) allows blood to flow more freely in the penis, leading to an erection. The drug can be injected with a tiny needle into your penis. Or, a small pellet (suppository) can be inserted into the opening of the penis. Suppositories and injections are effective in the majority of men.
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005).
Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits. [22] Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.

Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films.[43] Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion.[44] A link has also been found between relaxation following sexual arousal and testosterone levels.[45]


The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
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."
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