Cardiovascular disease and ED represent 2 common disease processes that are often intimately associated with one another. These common pathophysiological links necessitate a solid scientific and clinical understanding of these 2 disorders and a team effort between the cardiologist and urologist to provide effective management strategies for these patients.
A substantial body of literature documents the prevalence of ED in men with diabetes. Unfortunately, the majority of these studies do not distinguish between type 1 and type 2 disease, and, therefore, it is difficult to determine if prevalence rates between the two forms of diabetes differ significantly. Acknowledging this limitation in the literature, prevalence estimates of ED in cross-sectional studies of diabetic populations range from 20 to 71% (Table 1). Most of these studies did not control for severity of disease, duration of disease, or control of hyperglycemia.
Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
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.

The most important way to protect your heart is to eat a Nutritarian diet and that means eating your G-BOMBS: greens, beans, onions, mushrooms, berries and seeds. Natural plant foods have numerous cardio-protective effects. For example, greens activate the Nrf2 system, which turns on natural detoxification mechanisms and protects blood vessels against inflammatory processes that lead to atherosclerotic plaque buildup.9
Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil is absorbed rapidly, and peak plasma levels of 127 to 560 ng/mL are seen in a fasting state approximately 1 hour (range, 0.5-2 hours) after ingestion.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C


The blood supply to your penis starts in your heart and flows through arteries in the belly to even smaller arteries that branch off to carry blood into the penis. With sexual stimulation, these blood vessels need to rapidly increase blood flow. If these blood vessels are blocked (atherosclerosis) by coronary artery disease, you may not be able to achieve or maintain an erection.11
If not properly controlled, both type 1 and type 2 diabetes can cause complications due to high blood sugar levels. Over time, these high levels can cause irreversible nerve damage and narrow your blood vessels. While nerve damage may affect the sensitivity of your penis, blood vessel damage can affect the blood flow to your penis and make it more difficult for you to get an erection.

Mancia G,  Laurent S,  Agabiti-Rosei E,  Ambrosioni E,  Burnier M,  Caulfield MJ,  Cifkova R,  Clément D,  Coca A,  Dominiczak A,  Erdine S,  Fagard R,  Farsang C,  Grassi G,  Haller H,  Heagerty A,  Kjeldsen SE,  Kiowski W,  Mallion JM,  Manolis A,  Narkiewicz K,  Nilsson P,  Olsen MH,  Rahn KH,  Redon J,  Rodicio J,  Ruilope L,  Schmieder RE,  Struijker-Boudier HA,  van Zwieten PA,  Viigimaa M,  Zanchetti A. European Society of HypertensionReappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document, J Hypertens , 2009, vol. 27 (pg. 2121-2158)https://doi.org/10.1097/HJH.0b013e328333146d
Having ED means that all, most, or some of the time, the penis fails to become or stay hard enough for sexual intercourse. If, on rare occasions, you cannot get an erection, you do not have ED. You also do not have ED if you have a decrease in sexual desire, have premature ejaculation, or if you fail to ejaculate or reach orgasm. ED means that you can’t get or keep an erection.
Abstract | Full Text PDF | PubMed | Scopus (3562) | Google ScholarSee all References The 9-year follow-up MMAS study also found that self-reported increased cholesterol and unsaturated fat intake correlated positively with the development of ED.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
Three longitudinal studies have estimated incidence rates of ED in men with diabetes. Unfortunately, none of these studies specifically examined men with type 2 disease. In a cohort of 278 diabetic men with type 1 or type 2 diabetes potent at study entry, the proportion of patients reporting ED at 5-year follow-up was 28%.7 A follow-up analysis of the Massachusetts Male Aging Study, a community-based cohort of men between 40 and 70 years of age, found that the incidence of ED in the diabetic men was 51/1,000 population-years.8 This figure was similar to the 68/1,000 person-years crude incidence rate of ED reported in a study of 1,010 men with diabetes.5 However, new studies need to be carried out in well-characterized populations of men with diabetes in order to better determine the incidence of ED and potential effects of interventions to reduce complications.
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.
• Medications: About 25 percent of ED cases are caused by drugs. Many medications, including common medicines prescribed for diabetes and its complications, can cause ED. The most common offenders are blood pressure drugs, antihistamines, antidepressants, tranquilizers, appetite suppressants, and cimetidine (an ulcer drug). In addition, over-the-counter medications, including certain eye drops and nose drops, have been associated with ED. That does not mean you should stop taking these medications! Rather, you should discuss them with your doctor to determine whether a different dosage, an alternate medicine, or additional treatments will resolve the ED.
Patients who use this therapy should be trained under the guidance of a urologist, and sterile technique must be used. The drugs must be injected into the shaft of the penis and into one of the penile erectile bodies (corpus cavernosum) 10–15 min before intercourse. Most patients do not complain of pain upon injection. Sexual stimulation is not required, and resulting erections may last for hours. Side effects include penile pain and priapism. The cost is about $12–20 per injection.
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
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 take a diuretic, you should stay on it until high blood pressure is under control. If erection problems persist, or blood pressure goes back up, then your doctor might switch to a drug that's less likely to cause erectile dysfunction. Or, a combination of medications might work better to control high blood pressure and lower the risk of erectile dysfunction.
Age is a critical risk factor for the development of ED and endothelial dysfunction.4,5 ED is the most common condition occurring in middle-aged and older men.5 Kinsey et al. reported that 25 % of 65-year-old men and 75 % of ≥80-year-old men have ED.39 Moreover, ageing also decreases endothelial function, which is responsible for IHD.5 The incidence and severity of ED increases with age (a man aged 70 years is three-times more likely to have ED than a man aged 40 years).40
Table 1 offers elements for distinction between organic and psychogenic disease.7 Of note is that in cases of organic origin, a psychogenic component may co-exist. The most common organic aetiology of ED is vasculogenic (see below ‘ED and CAD: common pathophysiology’).2,3 Co-existence of vascular disease, advancing age, and the presence of CVD risk factors and metabolic disorders increase the likelihood that ED is of vasculogenic aetiology.
bike seats erectile dysfunction boston medical group BP Cholesterol depression Diabetes diet discussion doctor ed ED Best Treatment BMG erectile dysfunction erectile dysfunction and prostate cancer fish oil men Heart Diseas Heart Disease High Blood Pressure Hypertension medications Men's Health Obesity prostate cancer scrotal temperature SDB sexual desire sexual dysfunction sexual foods sexual function sexual health Sleep apnea sleep disordered breathing Tips Treatment vegetables yoga
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.

Experimental hyperglycemia may also affect cavernosal smooth muscle cell contractile responses. In experimental diabetes, penile smooth muscle has augmented force responses to vaconstrictors, possibly mediated by changes in expression of protein kinase C and the RhoA-Rho kinase Ca2+-sensitization pathway.32 These changes may promote flaccidity and alter the relaxation responses to nitric oxide. End-stage penile dysfunction may occur as a result of diabetes, with progressive loss of normal cavernosal endothelium and smooth muscle cells from the corpus cavernosum.33 Replacement by fibrotic tissue may lead to complete erectile failure.34
The safety of PDE5 inhibitors in patients with IHD has been shown in multiple trials. Arruda-Olson et al. investigated the safety of sildenafil during exercise stress tests in patients with IHD to ascertain whether the drug induces or exacerbates myocardial ischaemia. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test.69 Another study that investigated 120 trials of sildenafil revealed that the rates of MI and cardiovascular death with sildenafil are as low as with placebo.70
Abstract | Full Text | Full Text PDF | PubMed | Scopus (164) | Google ScholarSee all References Several double-blind, placebo-controlled studies have shown vardenafil to be more effective than placebo in the treatment of ED secondary to a wide range of other etiologies as well.71x71Hellstrom, WJ, Gittelman, M, Karlin, G..., and Vardenafil Study Group. Sustained efficacy and tolerability of vardenafil, a highly potent selective phosphodiesterase type 5 inhibitor, in men with erectile dysfunction: results of a randomized, double-blind, 26-week placebo-controlled pivotal trial. Urology. 2003; 61: 8–14
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

But recently Brandon had some troubles keeping it up. At first, Kayla just thought it was her and that he needed some kind of a change to what they usually did, but later Brandon admitted that as of late, he just couldn’t seem to maintain an erection, and that it took way too much effort to go long. It wasn’t that he wasn’t aroused; his body just wasn’t keeping up.
Erectile dysfunction (ED) is common in cardiac patients and shares the same risk factors--smoking, hypertension, hyperlipidaemia and diabetes mellitus. Sexual activity is not unduly stressful to the heart and, providing patients are properly assessed using established guidelines, sexual intercourse can be enjoyed without increased risk. The treatment of ED in patients with cardiovascular disease has been transformed by the introduction of the oral phosphodiesterase type 5 inhibitors, the first of which was sildenafil. Success in restoring erectile function is possible in up to 80% of patients (depending on the aetiology) with minimal adverse effects. A synergistic hypotensive effect with nitrates, and almost certainly nicorandil, is the only major contraindication. ED in asymptomatic patients may be a marker of silent vascular disease or increased vascular risk factors and should alert the physician to the need for cardiac risk screening. ED is common in patients with cardiovascular disease and should be routinely enquired about. ED is a distressing condition for the man and his partner, and severely impairs quality of life. Patients with cardiovascular disease and patients with diabetes represent the largest group of patients with ED, the majority of whom benefit from the drug therapies currently available. Addressing ED in patients with cardiovascular disease can lead to a substantial improvement in quality of life and success is not difficult to achieve.
Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.56 Atherosclerosis is the major cause of myocardial ischaemia. Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis. Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.6 This process, coupled with paradoxical vasoconstriction, can result in major cardiovascular events such as MI.32
Mancia G,  Laurent S,  Agabiti-Rosei E,  Ambrosioni E,  Burnier M,  Caulfield MJ,  Cifkova R,  Clément D,  Coca A,  Dominiczak A,  Erdine S,  Fagard R,  Farsang C,  Grassi G,  Haller H,  Heagerty A,  Kjeldsen SE,  Kiowski W,  Mallion JM,  Manolis A,  Narkiewicz K,  Nilsson P,  Olsen MH,  Rahn KH,  Redon J,  Rodicio J,  Ruilope L,  Schmieder RE,  Struijker-Boudier HA,  van Zwieten PA,  Viigimaa M,  Zanchetti A. European Society of HypertensionReappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document, J Hypertens , 2009, vol. 27 (pg. 2121-2158)https://doi.org/10.1097/HJH.0b013e328333146d

The diagnosis of ED in a patient may affect its management in two ways.30 The first relates to the fact that the ED patient, irrespective of whether he has or has not established CVD, is ‘reclassified’ into a higher risk category for future CV events. Management in this case is altered in the sense that more aggressive treatment of risk factors, as well as a close follow-up, is warranted. Implementation of biomarkers in this setting is desirable.

When antihypertensive medication comes to the fore, certain issues need to be carefully addressed. This is due to the fact that medically induced erectile dysfunction is one of the major reasons for non-adherence and treatment discontinuation, a reality that could have deleterious consequences on patient’s cardiovascular profile and health quality in the long term[38,39].
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.
The pilot study by Vardi et al. (18) showed that LIESWT was effective in treating men with ED, suggesting a physiologic impact of LIESWT on cavernosal hemodynamics. The LIESWT is an effective penile rehabilitation tool that improves erectile function and potentially reverses underlying ED. Recent meta-analysis (19) of 14 studies showed that LiESWT could significantly improve the International Index of Erectile Function (IIEF) [mean difference: 2.00; 95% confidence interval (CI), 0.99–3.00; P<0.0001] and Erection Hardness Score (EHS) (risk difference: 0.16; 95% CI, 0.04–0.29; P=0.01). In addition, the therapeutic efficacy was noted to last for at least 3 months. LiESWT has been cited to a potential cure for ED, unlike other well established non-surgical methods of treatment (i.e., PDE5i, ICI and VED) being on demand treatments.
Viagra, Cialis, Levita, and Staxyn all work in a similar fashion and make it physically possible to get an erection when aroused. However, men whose blood pressure is poorly controlled and who take alpha-blockers for high blood pressure treatment should not take any of these treatments for erectile dysfunction as it may reduce blood pressure to critically low levels, causing fainting or sudden death. Also, you may be prohibited to use these drugs if you demonstrate any of the following:
While additional investigation is usually necessary, the medical and sexual history is essential and frequently the most revealing aspect of the ED assessment process. Questionnaires are an integral part of the history. The International Index of Erectile Function (IIEF), a 15-item, self-evaluation questionnaire is a validated instrument for assessing erectile function, orgasmic function, desire and satisfaction after sexual relations.8 An abridged version of the IIEF is a 5-item questionnaire the Sexual Health Inventory for Men (SHIM) or IIEF-5 (Table 2). Responses to the five questions range from 1 (worst) to 5 (best). Questions 2 to 4 may be graded 0 (if there is no sexual activity, or no sexual intercourse attempt) and the final score ranges from 1 to 25 points; a descending score indicates worsening of erectile function, with values ≤21 being diagnostic of ED.8 Importantly, validated questionnaires correlate with the extend of CAD9 and improve the predictive value of ED for total cardiovascular events compared with a single-question ED diagnosis.5 It cannot be overemphasized that the SHIM can be effectively used not only by andrologists and urologists but by a wide array of medical specialists, such as cardiologists, diabetologists, primary care physicians, etc.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil is absorbed rapidly, and peak plasma levels of 127 to 560 ng/mL are seen in a fasting state approximately 1 hour (range, 0.5-2 hours) after ingestion.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C

Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.

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Diabetes mellitus (DM) is strongly associated with an increased risk of erectile dysfunction (ED), the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance, but this condition can be successfully treated in the majority of diabetes patients. ED is present in 32% of type 1 and 46% of type 2 DM patients. Several population- based studies of ED prevalence calculated the odds ratios for the association between ED and various chronic diseases. An odds ratio must be sufficiently greater than 1.0 to identify an increased risk. Diabetes has an odds ratio, ED risk multiplier of 4.1, compared with 1.7 for hyperlipidemia and 1.6 for hypertension. Erectile dysfunction in diabetes mellitus (EDDM) patients has been considered to have an organic etiology. Healthcare providers have long realized that ED can be the first symptom of DM.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References Patients with prior cardiac events should be encouraged to enroll in cardiac rehabilitation programs before restarting sexual activity.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
Based on this testing, EDDM patients were treated with behavioral therapy, intracavernosal (papaverine, PGE-1, or Trimix) or intraurethral PGE-1, a vacuum constriction device (VCD), or implantation of a penile prosthesis. Novel surgical procedures, ligation of incompetent cavernosal veins or penile revascularization, were seldom efficacious with EDDM and were soon abandoned. Although these nonsurgical therapies were efficacious, they were not widely requested because of their invasive or mechanical nature.
88. Böhm M, Baumhäkel M, Teo K, Sleight P, Probstfield J, Gao P, Mann JF, Diaz R, Dagenais GR, Jennings GL, et al. Erectile dysfunction predicts cardiovascular events in high-risk patients receiving telmisartan, ramipril, or both: The ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (ONTARGET/TRANSCEND) Trials. Circulation. 2010;121:1439–1446. [PubMed]

Organic nitrates are drugs that widen arteries by increasing their supply of nitric oxide; that's how they open the partially blocked coronary arteries in patients with angina. But because nitrates and ED pills both act on nitric oxide, the drugs don't mix; healthy volunteers given Viagra followed an hour later by nitroglycerin see their blood pressures drop by 25–51 mm Hg, a potentially dangerous amount. All experts agree that men who are taking nitrates cannot use ED pills; this includes all preparations of nitroglycerin (short-acting, under-the-tongue tablets or sprays), long-acting nitrates (isosorbide dinitrate or Isordil, Sorbitrate, and others, and isosorbide mononitrate, Imdur, ISMO, and others), nitroglycerin patches and pastes, and amyl nitrite or amyl nitrate (so-called poppers, which some men use for sexual stimulation).


In the vessels that supply the heart, healthy arteries enlarge in diameter up to 50% during exercise when sufficient nitric oxide is present. Because of its brief half-life, a continual supply of nitric oxide is required for optimal effect. If the supply of nitric oxide is inadequate, endothelial dysfunction—a core factor in heart disease—is made worse. Endothelial dysfunction can trigger the growth of coronary plaque.8
Medicines known as PDE5 inhibitors can help two-thirds of men with ED. These include Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil). You may need to take several doses over time before they work properly, and you may need to adjust the dose. National guidelines say you can be prescribed these drugs from six months after a heart attack, providing your condition is stable.
Despite all the options and alternatives, sometimes there’s no suitable alternative to a prescription that contributes to ED. You might have an adverse reaction to an particular medication or an alternative is unavailable in your state, health insurance plan, or your budget. There are good reasons you were prescribed your original medication in the first place.
Abstract | Full Text PDF | PubMed | Scopus (49) | Google ScholarSee all References Also, cigar smoking and passive exposure to cigarette smoke have been shown to significantly predict onset of ED.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
SOURCES: American Urological Association, "AUA Guideline on the Management of Erectile Dysfunction: Diagnosis and Treatment Recommendations." Barksdale, J. Pharmacotherapy, May 1999; vol 19: pp 573-581. Ferrario, C. Journal of Clinical Hypertension, November/December 2002; vol 4: pp 424-432. Fogari, R. American Journal of Hypertension, January 2001; vol. 14: pp 27-31. Grimm, R. Hypertension, January 1997; vol 29: pp 8-14. Llisteri, J. American Journal of the Medical Sciences, May 2001; vol. 321: pp 336-341. WebMD Medical Reference provided in collaboration with The Cleveland Clinic: "Hypertension: Treatment With ACE Inhibitors."
Crossref | PubMed | Scopus (24) | Google ScholarSee all References Almost every class of antihyper-tensive medication has been implicated in causing ED; however, most of these studies, published as case reports or patient surveys, have been relatively subjective and uncontrolled.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
To reduce the risk of side effects from these medications, including sexual problems, take medications exactly as prescribed. If you still have side effects, talk to your doctor about other possible medications that may have fewer side effects. On the other hand, you should not take any medication that promotes and erection while on medication to lower blood pressure.
ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.
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