Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.

Patients should continue testosterone therapy only if there is improvement in the symptoms of hypogonadism and should be monitored regularly. You will need periodic blood tests for testosterone levels and blood tests to monitor your blood count and PSA. Testosterone therapy has health risks, and thus doctors should closely monitor its use. Testosterone therapy can worsen sleep apnea and congestive heart failure.


*All medications have both common (generic) and brand names. The brand name is what a specific manufacturer calls the product (e.g., Tylenol®). The common name is the medical name for the medication (e.g., acetaminophen). A medication may have many brand names, but only one common name. This article lists medications by their common names. For information on a given medication, check our Drug Information database. For more information on brand names, speak with your doctor or pharmacist.
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]
The Prostate Cancer Prevention Trial was a landmark study by Thompson et al that prospectively assessed the time to developing CVD after the diagnosis of ED. There were 4247 men with no ED at study entry; 2420 developed incident ED (defined as the first report of ED of any grade) over 5 years. Those men that developed ED had a 1.45-fold higher probability of experiencing a CV event compared with men who did not develop ED.27

One report from a recent community survey concluded that erectile failure was the leading complaint of males attending sex therapy clinics. Other studies have shown that erectile disorders are the primary concern of sex therapy patients in treatment. This is consistent with the view that erectile dysfunction may be associated with depression, loss of self-esteem, poor self-image, increased anxiety or tension with one's sexual partner, and/or fear and anxiety associated with contracting sexually transmitted diseases, including AIDS.
Injection of vasodilator substances into the corpora of the penis has provided a new therapeutic technique for a variety of causes of erectile dysfunction. The most effective and well-studied agents are papaverine, phentolamine, and prostaglandin E[sub 1]. These have been used either singly or in combination. Use of these agents occasionally causes priapism (inappropriately persistent erections). This appears to have been seen most commonly with papaverine. Priapism is treated with adrenergic agents, which can cause life-threatening hypertension in patients receiving monoamine oxidase inhibitors. Use of the penile vasodilators also can be problematic in patients who cannot tolerate transient hypotension, those with severe psychiatric disease, those with poor manual dexterity, those with poor vision, and those receiving anticoagulant therapy. Liver function tests should be obtained in those being treated with papaverine alone. Prostaglandin E[sub 1] can be used together with papaverine and phentolamine to decrease the incidence of side effects such as pain, penile corporal fibrosis, fibrotic nodules, hypotension, and priapism. Further study of the efficacy of multitherapy versus monotherapy and of the relative complications and safety of each approach is indicated. Although these agents have not received FDA approval for this indication, they are in widespread clinical use. Patients treated with these agents should give full informed consent. There is a high rate of patient dropout, often early in the treatment. Whether this is related to side effects, lack of spontaneity in sexual relations, or general loss of interest is unclear. Patient education and followup support might improve compliance and lessen the dropout rate. However, the reasons for the high dropout rate need to be determined and quantified.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
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.
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.
Quitting smoking, exercising regularly, losing excess weight, curtailing excessive alcohol consumption, controlling hypertension, and optimizing blood glucose levels in patients with diabetes are not only important for maintaining good health but also may improve or even prevent progression of erectile dysfunction. It is unclear if such lifestyle changes can reverse erectile dysfunction. However, lifestyle improvements may prevent progression of the erectile dysfunction. Some studies suggest that men who have made lifestyle improvements experience increased rates of success with oral medications.
Physical examination should include the assessment of male secondary sex characteristics, femoral and lower extremity pulses, and a focused neurologic examination including perianal sensation, anal sphincter tone, and bulbocavernosus reflex. More extensive neurologic tests, including dorsal nerve conduction latencies, evoked potential measurements, and corpora cavernosal electromyography lack normative (control) data and appear at this time to be of limited clinical value. Examination of the genitalia includes evaluation of testis size and consistency, palpation of the shaft of the penis to determine the presence of Peyronie's plaques, and a digital rectal examination of the prostate with assessment of anal sphincter tone.
Hypogonadism may be suggested by the patient's general appearance. If testosterone deficiency antedates puberty, as in Klinefelter's syndrome, eunuchoid proportions—defined as an arm span 5 cm or more in excess of height, or a sole-to-pubis length exceeding crown-to-pubis length by more than 2 cm—may be present. In postpubertal males whose testosterone levels are markedly depressed, the secondary sexual characteristics may become atrophic. Testicles less than 4 cm in length or a prostate gland that is smaller than expected may be the only clues on physical examination to a pituitary tumor with secondary hypogonadism.
The recommended starting dose of tadalafil for use as needed for most patients is 10 mg taken orally approximately one hour before sexual activity. A doctor may adjust the dose higher to 20 mg or lower to 5 mg depending on efficacy and side effects. Doctors recommended that patients take tadalafil no more frequently than once per day. Some patients can take tadalafil less frequently since the improvement in erectile function may last 36 hours. Patients may take tadalafil with or without food. Tadalafil is currently the only PDE5 inhibitor that is FDA-approved for daily use for erectile dysfunction and is available in 2.5 mg or 5 mg dosages for daily use.
For the patient whose history suggests organic impotence, further history, physical and laboratory data will help identify the cause. The classification listed in Table 187.2 is based on the pathophysiologic scheme presented above, and includes mechanical problems that can interfere with erection. Vascular disease is the most common cause of impotence. In advanced cases, Lehriche's syndrome of aortoiliac occlusion will be suggested by bilateral thigh or calf claudication, loss of muscle mass in the buttocks and legs, and impotence. However, the majority of patients with vascular impotence have less severe vascular disease and many will have occlusive disease of the hypogastric-cavernous bed only. Even among patients without claudication, vascular disease is still a likely cause of impotence, especially if risk factors for atherosclerosis are present. Nonatherosclerotic disease is a consideration in the patient with a history of trauma or radiation to the pelvis, both of which cause fibrosis of vessels.
Because impotence can be due to health problems that can affect the whole body, and because it can interfere with one’s quality of life, it is important to talk with your doctor if you have trouble attaining or maintaining an erection. With increasing discussion of impotence in the media, coupled with advances in treatment, men are now much more comfortable talking with their doctors about impotence. It is currently estimated that between 15 and 30 million men in the United States are affected by impotence (Source: NIDDK).
It doesn't really matter what they are — sexual turnoffs vary wildly from person to person. But if the person you're getting it on with is doing stuff that's taking you out of the mood — even if it's stuff you feel like you're supposed to enjoy — it's time to swallow your pride and say something. Keeping it a secret might be saving you an awkward conversation in the short term, but in the long term, it could be seriously undermining your sex life. 
3. An intact, anatomically correct penis; 25% of impotence may be psychologic or 'partner-specific', 25% has an organic component and 50% of impotence is organic in nature; in organic impotence, nocturnal penile tumescence is absent Management-surgical Microvascular surgery to bypass occluded vessels–most effective in younger ♂, penile prosthesis Management-medical Combined therapy with phentolamine and papaverine–self-injected by the Pt, wielding an erection of 1 hr's duration is useful for arterial, neurologic, psychogenic impotence; other therapies–zinc, bromocriptine–Parlodel, isoxsuprine-Vasodilan, Voxsuprine, nitroglycerine, yohimbine–Yocon, Yohimex Etiology Smoking, CAD, HTN, DM, medications–hypoglycemic agents, vasodilators, cardiac drugs, antihypertensives, anger and depression; it is inversely correlated to dehydroepiandrosterone, HDL-C, and an index of dominant personality Primary impotence Complete absence of successful sexual coupling Secondary impotence Priapism, penile plaques, Peyronie's disease; drugs linked to impotence: antihypertensives–eg, methyldopa, guanethidine, reserpine, clonidine, due to ↓ BP, antidepressants–eg, phenelzine, isocarboxazide, amitriptyline–causing altered moods and decreased libido, tranquilizers–eg, chlordiazepoxide and lorazepam, and the muscle-relaxing diazepam, cimetidine, which ↑ prolactin, and is associated with impotence and loss of libido. Cf Infertility, Orgasmic dysfunction.
Damage to the autonomic pathways innervating the penis may eliminate "psychogenic" erection initiated by the central nervous system. Lesions of the somatic nervous pathways may impair reflexogenic erections and may interrupt tactile sensation needed to maintain psychogenic erections. Spinal cord lesions may produce varying degrees of erectile failure depending on the location and completeness of the lesions. Not only do traumatic lesions affect erectile ability, but disorders leading to peripheral neuropathy may impair neuronal innervation of the penis or of the sensory afferents. The endocrine system itself, particularly the production of androgens, appears to play a role in regulating sexual interest, and may also play a role in erectile function.
It is important that all erectile dysfunction is reported to your doctor, as sometimes it can be an indicator of something physically wrong with you that has to be treated. Also, your doctor is in the best position to find the reason for your erectile dysfunction. Routine questions and tests will provide a guide to the cause and allow your doctor to decide what kind of treatment you might need to deal with it. This may involve referral to a specialist. Detailed information can be found at the website of the Impotence Association – www.sda.uk.net
The inflatable type of device consists of cylinders that are implanted in the corpora cavernosa, a fluid reservoir implanted in the abdomen, and a pump placed in the scrotum. The man squeezes the pump to move fluid into the cylinders and cause them to become rigid. (He reverses the process by squeezing the pump again.) While these devices allow for intermittent erections, they have a slightly higher malfunction rate than the silicon rods.
Medications: Many common medicines produce erectile dysfunction as a side effect. Medicines that can cause erectile dysfunction include many used to treat high blood pressure, antihistamines, antidepressants, tranquilizers, and appetite suppressants. Examples of common medicines that can cause erectile dysfunction include propranolol (Inderal) or other beta-blockers, hydrochlorothiazide, digoxin (Lanoxin), amitriptyline (Elavil), famotidine (Pepcid), cimetidine (Tagamet), metoclopramide (Reglan), naproxen, indomethacin (Indocin), lithium (Eskalith, Lithobid), verapamil (Calan, Verelan, Isoptin), phenytoin (Dilantin), gemfibrozil (Lopid), amphetamine/dextroamphetamine (Adderall), and phentermine. Prostate cancer medications that lower testosterone levels such as leuprolide (Lupron) may affect erectile function. Some chemotherapies such as cyclophosphamide (Cytoxan) may affect erectile function.
The history can be useful in distinguishing organic from psychogenic impotence (Table 187.1). The patient with organic impotence describes problems with erection that progress over months to years. At first, the patient will have partial erections or seemingly firm erections that become flaccid during intercourse. With time, total erectile failure ensues. Organic impotence is constant and nonselective, meaning it is not better or worse with any specific partner or any type of stimulation.
Some may use alcohol as a way to get into the mood and overcome some of the nerves associated with having sex, but too much of a good thing can actually backfire. In fact, having a long history of alcohol abuse may lead to long-term erectile dysfunction. As many as 70 percent of men with chronic erectile dysfunction also have a history of alcohol abuse.
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED.  Studies indicate that men who exercise regularly have a lower risk of ED.
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