PubMed | Google ScholarSee all References However, other studies have noted that, when blood pressure levels are monitored after initiation of antihypertensive therapy, changes in blood pressure level are not correlated with sexual function.38x38Rosen, RC, Kostis, JB, Jekelis, A, and Taska, LS. Sexual sequelae of antihypertensive drugs: treatment effects on self-report and physiological measures in middle-aged male hypertensives. Arch Sex Behav. 1994; 23: 135–152
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.
Although ED is a common complication of diabetes, its effect on quality of life is not well understood. Recent work for the Exploratory Comprehensive Evaluation of Erectile Dysfunction (ExCEED) database demonstrates that in the general population of patients presenting to their urologist, ED negatively affects both general and disease-specific health-related quality of life (HRQOL).35 While this study provides insight into the detrimental affect of ED on quality of life, the cohort is somewhat selected, in that all of the patients were seen in sexual dysfunction clinics and therefore may have been more likely to be bothered by their condition and to report worse quality of life.
There are two kinds of surgery for ED: one involves implantation of a penile prosthesis; the other attempts vascular reconstruction. Expert opinion about surgical implants has changed during recent years; today, surgery is no longer so widely recommended. There are many less-invasive and less-expensive options, and surgery should be considered only as a last resort.
Third, men with Diabetes need to control their blood sugar levels. When your blood sugar is not under control, your body does not produce enough Nitric Oxide (NO) and vascular tissues don’t respond as effectively to NO. When enough blood flows into the penis, penile veins close off and block the blood from flowing out. This process results in an erection. If your body does not produce enough NO or if your penile tissues do not respond to NO, the pressure of the blood flowing into your penis is not sufficient to trap the blood, you penis will not get hard.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The significant sympathetic discharge associated with sexual intercourse may contribute to the development of arrythmias in susceptible patients.81x81Drory, Y, Fisman, EZ, Shapira, Y, and Pines, A. Ventricular arrhythmias during sexual activity in patients with coronary artery disease. Chest. 1996; 109: 922–924
Abstract | Full Text PDF | PubMed | Scopus (3562) | Google ScholarSee all References By 1996, fueled by the availability of the new oral agent sildenafil, the number of outpatient visits for ED as estimated by the National Ambulatory Medical Care Survey had increased to 1.3 million per year.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338
Penile prosthesis implant remains the most effective and permanent treatment for ED. Penile prosthesis implants can be broadly divided into malleable and inflatable prostheses (20). Malleable penile prosthesis, also known as semi-rigid prosthesis, does not allow for (physiological) flaccid state of the penis. The patient can bend the prosthesis upwards for sexual intercourse and downwards for concealment. Although the angle of prosthesis concealment has improved with recent devices, however due to the constant rigid state of the penis, they are still less comfortable compared to their inflatable counterparts, are more likely to cause social embarrassment and associated with higher risk of implant erosions (21). However, malleable prosthesis still has its place for the treatment of ED as these implants are easier to handle, easier to place and would benefit patients with impaired manual dexterity.
Low testosterone represents another link between erectile dysfunction and heart disease. A man’s testosterone levels gradually diminish beginning at age 30. By the time he reaches his 70s, testosterone levels may have dropped to a tenth of youthful levels. Diminishing testosterone levels contribute to loss of muscle, increased body fat, and reduced libido. Fatigue is common, as is depression. Low testosterone levels can also result in reduced concentration, irritability, passivity, loss of interest in activities, and even hypochondria.
Erectile dysfunction (ED) can be treated by urologists or other specialists or even by your general practitioner. Your doctor may recommend medication that works by relaxing penis muscles and increasing blood flow into the penis. Other treatments include therapy, implants, surgery and lifestyle changes, like exercising regularly, losing weight and eating right.
Before Viagra hit the market in 1998, there was no proven treatment for erectile dysfunction that men could take in pill form. Doctors were interested in yohimbe, an herb that increases heart rate and blood pressure. Some doctors prescribed it to their patients in combination with other treatments for erectile dysfunction. Even then it was not a recommended treatment and is still not today. Studies have not proven that it works.
Gene therapy has the potential to become a future management option for patients with CAD and ED. Animal studies have been conducted to evaluate the effects of gene therapy. A rat model was studied by Bivalacqua et al. to evaluate the effect of the combination of eNOS gene therapy and sildenafil. This research suggested that erectile response was greater in male rats with diabetes treated with combination eNOS gene therapy and sildenafil, compared with male rats with diabetes treated with eNOS gene therapy or sildenafil alone.76–78
Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References Most adverse effects are mild and are related primarily to vasodilation (headache, flushing, nasal congestion), gastrointestinal disturbances (dyspepsia), or retinal effects such as vision changes.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
"If you have an active sex life after a heart attack, it is probably safe to use PDE5 inhibitors," said Daniel Peter Andersson, MD, PhD, a postdoctoral researcher at Karolinska Institutet in Stockholm and the study's lead author. "This type of erectile dysfunction treatment is beneficial in terms of prognosis, and having an active sex life seems to be a marker for a decreased risk of death."

Get your diabetes under control. According to Dr. Nehra, the most important number you need to stay on top of is your A1C, which is a blood test that lets you know how well your blood sugar has been controlled for the past few months. Lifestyle changes can help and so can medications. Diabetes medications do not add to your risk for erectile dysfunction, says Nehra.
Most studies into the effect of beta-blockers on ED point to negative effects of first- and second-generation beta-blockers, while beta-blockers with vasodilating effects can improve erectile function. Alpha-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors seem to have a neutral effect on erectile function. Multiple previous studies have demonstrated a beneficial effect of angiotensin receptor blockers on erectile function and they should probably be the favoured antihypertensive agents in patients with ED.29

Crossref | PubMed | Scopus (171) | Google ScholarSee all References Incidence increased notably with age in this patient cohort: only 1.1% of diabetic men aged 21 to 30 years had ED compared with 47.1% of all diabetic patients older than 43 years. Diabetic patients often have other cardiovascular risk factors that may play a role in the development of ED. However, in an analysis of the PBI in 441 patients with ED and various cardiovascular risk factors (diabetes mellitus, hypertension, hyperlipidemia, tobacco use), diabetes was the only risk factor that was significantly and independently associated with a decrease in the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Abstract | Full Text PDF | PubMed | Scopus (3562) | Google ScholarSee all References By 1996, fueled by the availability of the new oral agent sildenafil, the number of outpatient visits for ED as estimated by the National Ambulatory Medical Care Survey had increased to 1.3 million per year.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338
Crossref | PubMed | Google ScholarSee all References Patients with vascular risk factors (diabetes mellitus, hypertension, heart disease, and hyperlipidemia) had significantly decreased peak systolic velocities and increased end-diastolic velocities. Patients with diabetes mellitus had increased end-diastolic velocities and decreased resistive indices, indicating a disorder of venous trapping during erections. Another study examined corpora cavernosal tissue removed at penile prosthesis placement in 21 diabetic men and 42 nondiabetic controls.23x23Saenz de Tejada, I, Goldstein, I, Azadzoi, K, Krane, RJ, and Cohen, RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med. 1989; 320: 1025–1030
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
A nutrient-dense, plant-rich (Nutritarian) diet is a huge defense. When men eat for optimal health, they protect their heart, prostate, brain, and, in effect, the entire body. A nutrient-dense, plant-rich (Nutritarian) diet floods the body with protective nutrients, and supports a healthy weight. It not only normalizes risk factors for heart disease and diabetes, but also offers a substantial level of protection against common cancers.
There are a number of reasons a man may not achieve the desired result from an oral erectile dysfunction drug. In some cases, a man may experience drug side effects severe enough to outweigh any potential benefit of taking the drug. Possible side effects of these drugs include headache, facial flushing, nasal congestion, and transient abnormal vision. (In October 2007, the FDA added a warning about sudden hearing loss to the package labels of oral erectile dysfunction drugs. While it’s not absolutely clear that the drugs can cause sudden hearing loss, a number of cases have been reported in men within hours or days of taking one of the drugs.)
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