It’s crucial that any underlying medical condition, such as angina or diabetes, is detected. So if you’re experiencing problems with ED, book an appointment with your doctor. He or she will assess and examine you to try to establish the cause of the problem, and may refer you for tests. Don’t take any medicine for ED without first discussing it with your doctor.
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PubMed | Google ScholarSee all References Diabetes was found to play a major role in vasculogenic impotence in a study of 265 patients with ED who underwent color duplex ultrasonography of the cavernosal arteries after intracavernosal injection of prostaglandin E1.13x13Chung, WS, Shim, BS, and Park, YY. Hemodynamic insult by vascular risk factors and pharmacologic erection in men with erectile dysfunction: Doppler sonography study. World J Urol. 2000; 18: 427–430

According to the Cleveland Clinic, “because erectile dysfunction is caused by a complex set of psychosocial, neurologic, and vascular factors, a specific cause in a patient may remain ambiguous.” The root causes are often related to a blockage or dysfunction of blood vessels. For example, ED can be due to conditions like atherosclerosis or diabetes, hormonal imbalances or problems related to mental health. It’s been found that common causes typically include one or more of the following factors: (2)
Until recently, erectile dysfunction (ED) was one of the most neglected complications of diabetes. In the past, physicians and patients were led to believe that declining sexual function was an inevitable consequence of advancing age or was brought on by emotional problems. This misconception, combined with men’s natural reluctance to discuss their sexual problems and physicians’ inexperience and unease with sexual issues, resulted in failure to directly address this problem with the majority of patients experiencing it.
Beta-blockers: A popular blood pressure medication that affects part of the nervous system in an attempt to slow and regulate heartbeats, helping reduce blood pressure. Unfortunately, this same part of the nervous system is also responsible for causing erections, and when beta blockers are used, it indirectly reduces the amount of blood flow to the penis.
Hypertension can affect endothelial function in many ways. It can reduce endothelium-dependent vasodilatation by increasing the vasoconstrictor tone as a result of increased peripheral sympathetic activity.41–43 Another mechanism is hypertension-induced increase in cyclooxygenase activity that leads to an increase in reactive oxygen species; these in turn damage endothelial cells and disrupt their function.44–46 In some cases, endothelial NO synthase (eNOS) gene variations may relate to hypertension-associated endothelial dysfunction.6
In the past 6 years, the FDA has approved three oral agents for the treatment of ED: sildenafil, vardenafil, and tadalafil. All three are phosphodiesterase type 5 (PDE-5) inhibitors and work by potentiating the effect of nitric oxide in the penis. In particular, they block the hydrolysis of cyclic guanosine monophosphate to guanosine 5'-monophosphate, thus enhancing nitric oxide–mediated smooth muscle relaxation, increasing blood flow to the penis and facilitating erection.
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
Crossref | PubMed | Scopus (335) | Google ScholarSee all References Additionally, the presence of nephropathy has been correlated with onset of ED, as has the length of time the patient has had diabetes; most of these patients experience ED within 10 years of being diagnosed as having insulin-dependent or non–insulin-dependent diabetes mellitus.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
80. Montorsi F, Briganti A, Salonia A, Rigatti P, Margonato A, Macchi A, Galli S, Ravagnani PM, Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease. Eur Urol. 2003;44:360–364; discussion 364-365. [PubMed]
Abstract | PubMed | Scopus (136) | Google ScholarSee all References Another study evaluated 32 hypertensive men with ED and 78 normotensive men with ED with regard to age, body mass index, hormonal profile, penile arterial flow, risk factors for arterial disease, psychiatric disease, and neurologic disease measured by pudendal nerve conduction studies.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
Crossref | Google ScholarSee all References Different classes of β-blockers have been postulated to have differential effects on erectile function, with the nonselective β-blockers (eg, propranolol) having more deleterious effects than the more cardioselective medications (eg, atenolol, metoprolol).42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
For centuries, men have tried all sorts of natural remedies for erectile dysfunction (ED) -- the repeated inability to get or maintain an erection firm enough for sexual intercourse. But do they really work? It is simply not scientifically known at this point. Furthermore, you take these remedies at your own risk, because their safety profiles have not been established. What follows are commentaries by experts and reviews in the field of alternative treatments that are available over the counter for erectile dysfunction and impotence.
The number of men reporting improvement was at 88% during the study. The number of men involved in the study who reported impotence dropped from 75.3 % to 11.8%. The results of this study raise hope for men who have quit taking other blood pressure medications because they interfered with sexual function. Sexual dysfunction was defined for the study as decreased libido, impotence and poor sexual satisfaction.
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
On any matter relating to your health or well-being, please check with an appropriate health professional. No statement herein is to be construed as a diagnosis, treatment, preventative, or cure for any disease, disorder or abnormal physical state. The statements herein have not been evaluated by the Foods and Drugs Administration or Health Canada. Dr. Marchione and the doctors on the Bel Marra Health Editorial Team are compensated by Bel Marra Health for their work in creating content, consulting along with formulating and endorsing products.

Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
Due to their vasorelaxing effect, administration of PDE-5 inhibitors in hypertensive individuals was initially confronted with great suspicion. A wealth of clinical data however has proven that PDE-5 inhibitors are associated with few side effects and provoke a small and insignificant reduction in blood pressure with minimal heart rate alterations in both normotensive and hypertensive patients as well. As a matter of fact, they can be safely and effectively administered to hypertensive individuals even when they are already taking multiple antihypertensive agents[51-56]. The sole exception to the rule is co-administration with organic nitrates, which is an absolute contraindication due to profound and possibly hazardous hypotension effect[57,58]. Moreover, precaution should be taken when PDE-5 inhibitors are combined with a-blockers where, due to possible orthostatic hypotension effect, lower starting doses should be implemented in the therapeutic regime[59-62].
Higher consumption of fiber-rich vegetables, fruits and beans helps to keep blood pressure in the favorable range.10 Beans, nuts and seeds have unique cholesterol-lowering capabilities.11-13 Berries and the flavonoids they contain have a blood pressure-lowering effect, plus berries and pomegranate have potent antioxidant and anti-inflammatory effects that protect against the development of heart disease.14-18
Erectile dysfunction (ED) is common, affecting almost 40% of men over 40 years of age (with varying degrees of severity) and increases in frequency with age.1 Erectile dysfunction and cardiovascular disease (CVD) share common risk factors including age, hypercholesterolaemia, hypertension, insulin resistance and diabetes, smoking, obesity, metabolic syndrome, sedentary lifestyle, and depression.2 Cardiovascular disease and ED also share a common pathophysiological basis of aetiology and progression.3 Numerous studies have established that ED (i) is frequent in men with established CVD, (ii) co-exists with occult coronary artery disease (CAD) and (iii) is an independent risk factor for future cardiovascular (CV) events both in men with established CVD and in men with no known CVD.2,4,5 In the latter group, ED precedes CAD, stroke, and peripheral arterial disease by a significant period that usually ranges from 2 to 5 years (average 3 years).2 Although the ED patient can be managed by various medical specialties, and preferably a collaborative approach is most effective, this review is oriented to the cardiologist. While this review deals exclusively with sexual health of men, female sexual health and its potential relation with CVD is also an interesting, yet underexplored, field. As in men, moderating common risk factors seems to improve female sexual health and may serve as an opportunity to decrease CVD risk, with the identification of sexual dysfunction being the starting point.6
The art of acupuncture has become the new treatment for everything from back pain, depression, and even ED. Impotence could be more of a state of mind, and acupuncture may help. Through this alternative therapy, fine needles are placed in various parts of the body to relieve pain or stress. Although there are many mixed studies for acupuncture and ED, many tend to confirm positive results. A 1999 study found acupuncture improved the quality of erection and even restored sexual activity in 39 percent of participants.
Erectile dysfunction (ED) is common, affecting almost 40% of men over 40 years of age (with varying degrees of severity) and increases in frequency with age.1 Erectile dysfunction and cardiovascular disease (CVD) share common risk factors including age, hypercholesterolaemia, hypertension, insulin resistance and diabetes, smoking, obesity, metabolic syndrome, sedentary lifestyle, and depression.2 Cardiovascular disease and ED also share a common pathophysiological basis of aetiology and progression.3 Numerous studies have established that ED (i) is frequent in men with established CVD, (ii) co-exists with occult coronary artery disease (CAD) and (iii) is an independent risk factor for future cardiovascular (CV) events both in men with established CVD and in men with no known CVD.2,4,5 In the latter group, ED precedes CAD, stroke, and peripheral arterial disease by a significant period that usually ranges from 2 to 5 years (average 3 years).2 Although the ED patient can be managed by various medical specialties, and preferably a collaborative approach is most effective, this review is oriented to the cardiologist. While this review deals exclusively with sexual health of men, female sexual health and its potential relation with CVD is also an interesting, yet underexplored, field. As in men, moderating common risk factors seems to improve female sexual health and may serve as an opportunity to decrease CVD risk, with the identification of sexual dysfunction being the starting point.6
No matter what the cause of erectile dysfunction, it is likely to cause feelings of stress and other emotional reactions. It’s also not uncommon for erection problems to cause tension in a relationship, particularly if one or both partners withdraws emotionally and the problem is not talked about. And it’s possible for a man’s renewed ability to have intercourse after a period of no sexual activity to stir up relationship issues.
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