Erectile dysfunction becomes more common with age. However, the condition is even more common among men who have diabetes. Over time, diabetes can damage the blood vessels and nerves that control erections. In addition, some of the other conditions that often occur with diabetes, such as coronary artery disease, can also contribute to the development of erectile dysfunction.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Vardenafil has been shown to be significantly more effective than placebo in the treatment of ED secondary to diabetes mellitus and after radical retropubic prostatectomy.69x69Goldstein, I, Young, JM, Fischer, J, Bangerter, K, Segerson, T, Taylor, T, and Vardenafil Diabetes Study Group. Vardenafil, a new phosphodiesterase type 5 inhibitor, in the treatment of erectile dysfunction in men with diabetes: a multicenter double-blind placebo-controlled fixed-dose study. Diabetes Care. 2003; 26: 777–783
Abstract | Full Text | Full Text PDF | PubMed | Scopus (328) | Google ScholarSee all References Their mean resting systolic and diastolic blood pressure levels decreased by 6% and 11%, respectively, compared with baseline. These patients also experienced a mild decrease in mean resting right atrial pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. However, the hemodynamic response to exercise was preserved. Phase 2 and 3 trials showed no difference in the rate of adverse events between sildenafil and placebo in patients being treated with antihypertensive medications. The effects of sildenafil on blood pressure level were similar in patients who were taking antihypertensive medications compared with those who were not. In healthy volunteers, no consistent or significant doserelated electrocardiographic (ECG) changes were noted at 1 and 2 hours after doses of sildenafil ranging from 1.25 to 200 mg.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C
Another risk factor is that men with type 2 diabetes may produce less than normal amounts of testosterone, a condition called hypogonadism. A 2007 study found that one-third of men with type 2 diabetes had low testosterone levels. Those men were also more likely to have ED, though the link may have to do with weight, not diabetes per se. Being overweight or obese is a risk factor for hypogonadism.
Diabetic damage doesn’t stop with these small vessels, he said. “You really have two parallel situations: You need blood flow that feeds the muscle of the penis, and you need an artery dedicated to bringing blood rapidly when a man becomes aroused and wants to be sexually active,” he said. “That artery is also affected by diabetes. They’ll say ‘I can get a partial erection, but I can’t maintain it.’ ”
The links between hypertension and ED are increasingly recognized and the 2009 re-appraisal of European guidelines includes relevant statements.35,47 Erectile dysfunction is almost twice as frequent in hypertensive as in normotensive individuals and appears to be of higher severity. The relative risk of developing ED in hypertensive patients compared with normotensive individuals ranges from 1.3 to 6.9. Regarding pathophysiology, hypertension appears to cause ED per se, through a multitude of mechanisms that include prolonged exposure to elevated levels of systemic blood pressure, endothelial dysfunction, and circulation of vasoactive substance (with a pivotal role of angiotensin II) that lead to structural and functional alterations in the penile arteries. The largely unfounded (see earlier paragraph) notoriety of antihypertensive treatment for causing ED is one of the most predominant causes for non-adherence and discontinuation of antihypertensive therapy, and therefore, patients should be properly informed by physicians. Phosphodiesterase type 5 inhibitors are effective in hypertensive patients with ED and they can safely be co-administered with antihypertensive medication.39 Specifically for alpha-blockers, low starting doses of PDE5 inhibitors are preferred in patients already on alpha-blocker treatment, and likewise, low starting doses of alpha-blockers are encouraged in patients taking PDE5 inhibitors. Of clinical significance is that hypertensive men with ED are more likely to comply with their antihypertensive medication when under PDE5 inhibitors.
The wide range of prevalence rates noted among the studies can be attributed to a number of factors. First, prevalence rates are affected by the sensitivity and specificity of methods used to assess ED.1 In addition, a number of these studies used medical record review to identify patients with ED, as opposed to anonymous patient reports. It has been shown in other disease states that patients tend to underreport ED when questioned directly by their providers.3 Therefore, the use of validated questionnaires that are either self-administered in an anonymous, neutral setting or administered by an objective third-party interviewer are preferred.
Erne P, Schoenenberger AW, Zuber M, Burckhardt D, Kiowski W, Dubach P, Resink T, Pfisterer M. Effects of anti-ischaemic drug therapy in silent myocardial ischaemia type I: the Swiss Interventional Study on Silent Ischaemia type I (SWISSI I): a randomized, controlled pilot study, Eur Heart J , 2007, vol. 28 (pg. 2110-2117)https://doi.org/10.1093/eurheartj/ehm273
Crossref | Google ScholarSee all References Other investigators have suggested these medications may exert a hormonal effect. β-Blockers have been associated with decreased free and total testosterone levels in placebo-controlled trials.39x39Rosen, RC and Weiner, DN. Cardiovascular disease and sleep-related erections. J Psychosom Res. 1997; 42: 517–530
In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.
A cold slice of watermelon can do more than just satisfy thirst and hunger during the warm summer months; it can help with bedroom satisfaction. Citrulline, the amino acid found in high concentrations of watermelon, is found to improve blood flow to the penis. A 2011 study revealed men who suffered from mild to moderate ED and took L-citrulline supplementation showed an improvement with their erectile function and were very satisfied. Natural watermelon juice, or “nature’s Viagra,” can also be easier on the stomach, since taking pills like Viagra can cause nausea and diarrhea.
A study published in May 2014 in The Journal of Sexual Medicine found that some men can reverse erectile dysfunction with healthy lifestyle changes, such as exercise, weight loss, a varied diet, and good sleep. The Australian researchers also showed that even if erectile dysfunction medication is required, it's likely to be more effective if you implement these healthy lifestyle changes.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Yes, and there’s the rub. High blood pressure, especially if untreated, can lead to erectile dysfunction (ED). So can medications your doctor prescribes to bring down your high blood pressure. Fortunately, not all meds cause ED. Thiazides, diuretics or “water pills,” are common ED culprits. So are beta blockers. These effective heart meds slow your system down, and also affect blood flow where you need it -- in your penis -- at the right time. Alpha blockers, another class of medications that lower high blood pressure, are less likely to cause ED. So talk with your good doc about medication choices and side effects, so you can choose the right med for you.
The pathophysiological basis for the predictive ability of ED has been discussed above. It should be emphasized, however, that ED should not only be viewed as a manifestation of obstructive CAD that could be identified by ischaemia revealing tests. Owing to the inflammatory and pro-thrombotic activation of the disease,13 it should also be regarded as an early warning sign of an imminent acute event (mainly acute myocardial infarction)22 due to the rupture of a subclinical plaque, and thus identification of the risk should ideally include plaque vulnerability tests. Finally, an issue that has important clinical implications is by how long the clinical manifestation of ED precedes the clinical manifestation of CAD. According to studies, men with ED and no cardiac symptoms have an increased incidence of experiencing a cardiac event, both acute and chronic, in the ensuing 2–5 years, thus providing a ‘window of opportunity’ for risk reduction management in these patients.2
The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
The authors observe that multiple factors may be involved. In addition to decreased exercise capacity, patients with chronic heart failure have blood vessel and circulation abnormalities that can reduce blood flow into the penis and interfere with the ability to maintain an erection. And erectile dysfunction can be caused or worsened by many of the medications that are commonly prescribed to treat chronic heart failure.
PubMed | Google ScholarSee all References As with sildenafil, use of nitrate or NO-donor medications is contraindicated while taking tadalafil because of the potential for marked hypotensive interactions.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
De Berardis et al.6 assessed general HRQOL in 1,460 men with type 2 diabetes in Italy. Within the cohort, 615 men reported that they never experienced ED, 346 stated that they occasionally had ED, and 449 stated that they frequently had ED. They then compared general HRQOL among these three groups. In the univariate analysis, they found that degree of ED negatively correlated with general HRQOL scores in all eight domains of the Short Form 36 (SF-36) health survey questionnaire. In the multivariate analysis, ED was not independently associated with physical function, bodily pain, or role limitations due to physical problem scores but was independently associated with general HRQOL outcomes in the domains of general health (P = 0.004), role limitations due to emotional problems (P = 0.001), vitality (P = 0.001), social functioning (P = 0.01), and overall mental health (P = 0.002). Another study examining the effect of ED on quality of life in hemodialysis patients, more than half of whom had diabetes, also noted an independent, negative effect of ED on the emotional domains of general HRQOL.39
When it comes to combating heart disease, most information sources promote drugs and surgery as the only viable options, with lip service to dietary advice that simply does not work. As a result, the demand for high-tech, expensive, but largely ineffective medical care is soaring, causing medical costs and insurance rates to skyrocket. This chase for "cures" is both financially devastating and futile. Morbidity and premature mortality from heart disease continue to rise, with no sign of abating.
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55
Core tip: The prevalence of erectile dysfunction is approximately 2-fold higher in hypertensive patients compared to normotensive individuals. However, erectile dysfunction remains under-reported, under-recognized, and under-treated in hypertensive patients. Lifestyle modification should be the mainstay of treating erectile dysfunction in patients with untreated hypertension. Switching antihypertensive therapy should be considered in treated hypertensive patients, unless administered drugs are absolutely indicated for the individual patient. Otherwise, phosphodiesterase-5 inhibitors should be used, since they are both effective and safe in hypertensive patients. Finally, erectile dysfunction offers the opportunity to recognize asymptomatic cardiovascular disease with obvious benefits for cardiovascular event prevention.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Overall, sexual intercourse does not lead to an extremely exaggerated heart rate or blood pressure level when performed in a familiar setting with one's usual partner.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999
Although DM patients often correctly assume that their ED is of organic origin, a psychogenic component should be considered, especially in the younger patient. If this is the case, the patient may benefit from psychosocial therapy that includes anxiety reduction and desensitization, cognitivebehavioral intervention, sexual stimulation techniques, and interpersonal assertiveness with couples communication training.6 Not all healthcare providers offer these options. Freudian-based psychotherapy for EDDM has not been proved to be efficacious.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Erections result from relaxation of the corpora cavernosa, which is mediated either by increasing intracellular cyclic guanosine monophosphate (cGMP) or cyclic adenosine monophosphate or by inhibition of their degradation. Increased parasympathetic tone results in a decrease in norepinephrine release and an increase in the release of acetylcholine; subsequently, NO synthase activity increases, which releases NO from both endothelial cells and nonadrenergic, noncholinergic neurons.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
There are no studies specifically assessing the effectiveness of intraurethral suppositories of prostaglandin E1 (PGE-1) in diabetic men. A single randomized clinical trial of the effectiveness of this agent in the general population of men with ED documented that 60% of those who tried this agent were able to achieve successful sexual intercourse.53 Unfortunately, in clinical practice, this agent appears to be considerably less effective.54
Another study showed a forty percent increase of blood flow to the heart within one year of starting a dietary program designed similar to the one described in my book, The End of Heart Disease. Of pertinent note is that, in the same study, the patients following a high-protein Atkins’ diet decreased blood flow to the heart by forty percent in one year.8 These dangerous high-protein diets are a certain path to erectile impotence and a premature cardiac death.
If you’re taking medication to treat blood pressure, depression, pain, allergies, inflammation, seizures, or heart conditions, you’re one of the tens of millions of people at risk for medically induced erectile dysfunction. It’s just the nature of drug side effects. Yet erectile dysfunction is one of the least talked about side effects of prescription medication.
The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.