However, population-based studies of ED in prostate cancer survivors also document that ED has a negative effect on general health. Penson, et al.36 studied HRQOL in 2,306 prostate cancer survivors 2 years after their diagnosis. They noted that men with ED (defined as erections that were insufficient for sexual intercourse) had significantly worse general HRQOL when compared to prostate cancer survivors who were potent. Importantly, this association remained in a multivariate analysis that controlled for 31 other potential confounding variables. Finally, this association was noted in both the physical and mental domains of general quality of life, indicating that ED has a much broader effect on quality of life than one might expect.
Luckily, awareness of ED as a significant and common complication of diabetes has increased in recent years, mainly because of increasing knowledge of male sexual function and the rapidly expanding armamentarium of novel treatments being developed for impotence. Studies of ED suggest that its prevalence in men with diabetes ranges from 35–75% versus 26% in general population. The onset of ED also occurs 10–15 years earlier in men with diabetes than it does in sex-matched counterparts without diabetes.
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, vol. 44 (pg. 360-364)https://doi.org/10.1016/S0302-2838(03)00305-1
Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included.
Erectile dysfunction is frequent in patients with established CAD with prevalence rates ranging between 47 and 75% in studies.2,4,14 The AssoCiatiOn Between eRectile dysfunction and coronary Artery disease (COBRA) trial tested the hypothesis that the ED rate differs in CAD patients according to the clinical presentation (acute vs. chronic coronary syndromes) and the extent of vessel involvement (one vs. two to three vessel disease)15 (Figure 3). The overall ED prevalence in CAD patients was 47%, whereas in the normal coronary angiography group the ED rate was 24%. When separately considered, the ED rate was 22% in patients with acute coronary syndromes (ACS) and one-vessel disease and 55 and 65% in patients with ACS and multi-vessel disease and with chronic coronary syndrome, respectively. The study also showed that both severity (IIEF <10) and duration (>24 months) of ED were predictive of severe coronary involvement at angiography. This study offers pathophysiological and mechanistic explanations related to the clinical setting. In patients with multi-vessel disease, regardless of the clinical presentation, the advanced coronary and systemic atherosclerosis is the reason for the high rate of ED. However, in the setting of acute myocardial infarction with one-vessel disease, ED is far less frequent because the atherosclerotic burden is modest (i.e. abrupt occlusion of a single non-obstructing plaque in the absence of extensive atherosclerosis) in both the coronary and penile circulations.15,16
In another scientific article published in 2015 in the American Journal of Lifestyle Medicine, respondents who were not taking cholesterol-lowering medication experienced an average 42 mg/dl decrease in LDL cholesterol and an average decrease in triglycerides of 79.5 mg/dl about one year after switching to a Nutritarian diet. Furthermore, case histories presented in that publication documented atherosclerosis reversal.7
Diabetes is known to sabotage two body parts that provide essential components of an erection: nerves and blood vessels. Studies suggest that diabetic nerve damage (neuropathy) is the most important risk factor for ED in people with diabetes. If pelvic nerves that trigger penis muscles to relax are impaired, there may be a break in the chain between brain and penis, disrupting erection. Some researchers suspect that an inadequate supply of oxygen to the nerves causes this damage.
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.
Erectile dysfunction (ED) is defined as the persistent inability to attain and maintain an erection that is sufficient to permit satisfactory sexual performance (1). The current pharmaco-therapeutic research in ED focuses on underlying endothelial dysfunction as the root cause for ED and introduction of phosphodiesterase type 5 inhibitors to potentiate nitric oxide (NO) action and cavernosal smooth muscle vasodilation, has revolutionized modern ED treatment over the past two decades (2). In contrast to Western Medicine, the traditional and complementary medicine (TCM) aims at restoration and better overall bodily regulation with medicine to invigorate qi (energy) in vital organs such as kidney, spleen and liver; to enhance physical fitness, increase sexual drive, stabilize the mind and improve the overall situation resulting in natural and harmonious sexual life (3).
While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.
Surgery for erectile dysfunction is usually considered only after all other options have failed. The two surgical options include the insertion of a semi-rigid rod or the implantation of a three-piece inflatable prosthesis. Penile prosthesis implantation has low infection, complication, and malfunction rates. However, since placement of an implant requires permanent injury to the erectile tissue of the penis, implant treatment is considered irreversible.
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.
Many products contain undocumented “fillers” that can cause allergic reactions. In recent years, the FDA has found over 300 herbal products that contain hidden, deceptively labeled, or dangerous ingredients4. And since 2015, the FDA has released public warnings on more than 160 ED supplements and “male enhancement” products found to contain dangerous ingredients and contaminants5 . An independent study of FDA data, conducted in 2018, found almost 800 herbal supplements that contained unlisted ingredients6.
When dealing with certain medical conditions, it is important to focus treatment toward the root of the problem. If you were to properly manage your high blood pressure without the use of any confounding medications and instead employ a lifestyle change, both ailments would likely disappear. While this would be the ideal case, it isn’t the reality for most patients. Medications are great for controlling high blood pressure, but it’s important to speak with your doctor about any concerns before taking them.
Erections are extremely complicated and surprisingly fragile. Erections involve chemical signals, nerve impulses, complicated blood pressure changes, and overall fitness in systems ranging from your heart and hormones to your mood. When medication changes how one of these factors works—like blood pressure drops or depression medication—ED is a common side effect. The problem with these completely predictable medically induced side effects is how people react.
Smoking is an independent risk factor for ED. Tobacco smoking causes direct toxicity to endothelial cells, including decreased eNOS activity, increased adhesion expression and impaired regulation of thrombotic factors.6 A meta-analysis of 19 studies by Tengs and Osgood suggested that 40 % of the impotent men studied were current smokers compared with 28 % who had never smoked.49
Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
Relation between erectile dysfunction prevalence and type of coronary syndrome (A). Time interval (months) between erectile dysfunction and coronary artery disease symptom onset in chronic coronary syndrome according to the number of vessels involved (B). ACS, acute coronary syndrome; CCS, chronic coronary syndrome, G1: ACS and 1-VD; G2: ACS and 2-,3-VD; G3: CCS. VD, vessel disease; C: the control group with normal coronary angiography. With permission from Montorsi et al.15
The third Princeton Consensus (Expert Panel) Conference recommends assessing cardiovascular risk in all patients with ED and CVD. This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class.57 The consensus also recommended that all patients with ED and CVD should undergo lifestyle changes, such as exercise, smoking cessation, healthy diet and weight reduction. These measures are likely to reduce cardiovascular risk and improve erectile function.58
After getting a diagnosis of ED, most patients can begin treatment right away, but treatment may be delayed for some patients until the health of the heart is more fully assessed or improved. The most common treatment for ED is a pill (phosphodiesterase-5 inhibitor; PDE5-I): Viagra (sildenafil), Cialis (tadalafil), or Levitra (vardenafil). Each of these pills improves erections when taken before sexual activity; alternatively, a low dose of Cialis can be taken once a day. These medicines work by allowing the blood vessels that supply blood to the penis to dilate better during sexual stimulation. The PDE5-Is decrease blood pressure a little bit, but they are safe with most other medications and with other blood pressure pills. The PDE5-Is are not safe with nitrate medications like nitroglycerin, Nitrostat, Nitro Paste, Imdur, isosorbide mononitrate, and Isordil. Mixing a PDE5-I with a nitrate medication could result in severely low blood pressure and even death. Inform all medical professionals (including the ambulance or emergency department) about your most recent ED pill ingestion so that nitrates can be avoided. If you have high blood pressure or benign prostatic hypertrophy (enlarged prostate) and take medicines called α-blockers, your doctor may need to start you on the lowest dose of the PDE5-I.
People sometimes refer to ED as "impotence," although the two aren't really the same condition. ED is the physical inability to develop or maintain an erection that is rigid enough for sex. Impotence is a broader term. While one cause of it is ED, impotence may also involve a lack of sexual desire, an inability to ejaculate, or problems with orgasm.
Some blood pressure medicines can also cause erectile dysfunction. Thiazide diuretics and beta-blockers are most likely to cause problems, but this is not a common effect of these medicines and will not happen to everyone. If you are taking either of these medicines and are worried about erectile dysfunction, your GP may be able to change your medicines.
DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.
High blood pressure and erectile dysfunction (ED) often go hand in hand. While having high blood pressure (hypertension) itself may not initially cause any symptoms, it will damage your arteries over time, leading them to become less flexible and progressively more narrow. This not only increases the risk of heart attacks and stroke, but has the potential to compromise blood flow to many organs in the body, including the penis, if left untreated.
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.
Abstract | PubMed | Scopus (136) | Google ScholarSee all References In a prospective review of 3250 men aged 26 to 83 years without ED at their first examination, total cholesterol and high-density lipoprotein (HDL) cholesterol levels were found to be strongly predictive of onset of ED after controlling for age, diabetes mellitus, stress level, cardiovascular disease, and prostate disease.25x25Wei, M, Macera, CA, Davis, DR, Hornung, CA, Nankin, HR, and Blair, SN. Total cholesterol and high density lipoprotein cholesterol as important predictors of erectile dysfunction. Am J Epidemiol. 1994; 140: 930–937
Having your current medication checked – if you are taking medication already, it could be that your erection problems are a side effect. Have a doctor check whether this is the cause of your problems and if it is, you might be able to switch medications and then find that your erectile dysfunction goes away completely – or at least improves. Medications that can cause erection problems include:
After analyzing 28 previous studies on the link between ED and heart disease, the researchers found a connection between erectile dysfunction and poor endothelial function. “Blood vessels are unable to fully dilate and allow blood to flow through,” explains Medicalnewstoday.com. “Endothelial dysfunction is an early sign of atherosclerosis, a condition in which plaque builds up in the arteries, raising the risk of heart attack and stroke.” The researchers also determined that there was a thickening of one of the inner two layers of the carotid artery—another heart-disease indicator.
Although the results provide evidence that PDE5 inhibitors may benefit heart health, the retrospective study design makes it impossible to ascertain direct cause and effect, Andersson noted. It is possible that using erectile dysfunction drugs simply indicates a more active sex life, which could itself contribute to, or be a marker of, a heart-healthy lifestyle overall.
Crossref | PubMed | Scopus (53) | Google ScholarSee all References A study of 24 patients with ED and untreated essential hypertension showed decreased levels of free and total serum testosterone compared with normal controls.31x31Hughes, GS, Mathur, RS, and Margolius, HS. Sex steroid hormones are altered in essential hypertension. J Hypertens. 1989; 7: 181–187
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
Cigarette smoking is an established risk factor in the development of atherosclerotic vascular changes and thus would be expected to play a role in the development of vasculogenic ED. The MMAS 9-year follow-up study found that the risk of developing moderate or complete ED in smokers was nearly doubled (odds ratio, 1.97) compared with that in matched nonsmokers.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
Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18
Men with diabetes tend to develop erectile dysfunction 10 to 15 years earlier than men without diabetes. As men with diabetes age, erectile dysfunction becomes even more common. Above the age of 50, the likelihood of having difficulty with an erection occurs in approximately 50% to 60% of men with diabetes. Above age 70, there is about a 95% likelihood of having some difficulty with erectile dysfunction.