Furthermore, if feelings of sadness, bloating, or weight gain are prominent, it may be beneficial to measure a form of estrogen called estradiol. This form of estrogen can be elevated in men, particularly in those who are overweight, and may trigger these abnormal responses, increasing the risk of heart disease. Estradiol levels above 30 pg/mL are generally considered abnormal. Weight loss can help correct elevated estradiol, as can prescription “aromatase inhibitors,” such as Arimidex®. In addition, a nutritional supplement called chrysin has been shown in the laboratory to inhibit the aromatase enzyme that is responsible for converting testosterone to estradiol.24 You should consult your doctor to determine if this supplement may be helpful for you.
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

Even if you do not take blood pressure drugs, you should get your blood pressure checked as high BP also can be a sign of ED. In fact, men with ED are about 38% more likely to have high blood pressure than those without ED, according to a study that examined the medical records of more than 1.9 million men. That is not too surprising, since ED often occurs in men who smoke or are overweight—both of which are common risk factors for high blood pressure.
A limitation of the study is that the researchers did not assess the effects of untreated erectile dysfunction, or conversely, the effect of having an active sex life without taking erectile dysfunction drugs. The researchers also were unable to account for socioeconomic status; as a next step, they are planning a larger study that will include more health records and complete information on marital status, educational level and disposable income. They are also pursuing a separate analysis of outcomes from erectile dysfunction drugs in men with Type 1 and Type 2 diabetes.

There are a number of herbs and supplements for use in men with ED. However, the overall quality of the studies evaluating these treatments has been low. Therefore, evidence for the effectiveness and safety of these therapies is limited. Many of these therapies have known risks, and there’s a possibility that other risks are yet to be discovered. Always use CAM therapies with caution.
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.

Olsson et al. conducted a randomised, double-blind, placebo-controlled, parallel group, and flexible dose study in 224 men with ED and one CVD, including IHD (20 %) and hypertension (80 %). This study reported that the sildenafil-treated group showed 71 % improvement in ED compared with the placebo-controlled group (24 %).64 Furthermore, no treatment-related cardiovascular adverse events were reported.65 Conti et al. showed in an early study that sildenafil is an effective treatment for ED in patients with IHD; the majority of patients reported improvement in penile erection with it.66 Another double-blind, placebo-controlled study of patients with ED and stable CAD showed statistically significant improvement with sildenafil versus placebo in both the frequency of penetration and frequency of maintained erections after penetration.67


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.
Abstract | Full Text PDF | PubMed | Scopus (105) | Google ScholarSee all References Aspirin and β-blocker use have been suggested to decrease the risk of cardiovascular events with sexual activity, although their benefit has not been proved definitively.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
Crossref | PubMed | Scopus (35) | Google ScholarSee all References Also, if lower blood pressure level was the primary etiology of ED, all classes of antihypertensive agents should be expected to have relatively similar effects on erectile function because of their efficacy in lowering pressure, which has not been seen.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
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
PubMed | Google ScholarSee all References More recently, researchers have recognized that climbing stairs does not correlate closely with sexual activity in terms of autonomic, psychological, and emotional patterns of stress on the body.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
With early detection, doctors can suggest preventive measures like statins, blood pressure meds, revamping eating habits and getting more exercise. Try these two exercises that can cut your risk of heart disease in half. The study researchers told Science Daily, “Our study supports a more aggressive CVD risk assessment and management for persons with erectile dysfunction, including young men who may otherwise be categorized as low-risk due to their young ages.” Check out the sexual health conditions affecting millennial men.

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:
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, α-blockers are a well-known cause of retrograde ejaculation secondary to a reversible relaxation of bladder neck smooth muscle.50x50Meinhardt, W, Kropman, RF, Vermeij, P, Nijeholt, AA, and Zwartendijk, J. The influence of medication on erectile function. Int J Impot Res. 1997; 9: 17–26
Finding a potential early sign of heart disease is vital: Every minute in the United States someone dies from a heart disease-related event. Doctors know to watch for risks like obesity and high blood pressure; however, Men’s Health reports 50 percent of men who die from heart disease have never had one of these symptoms. For younger men, treating ED as an indicator of heart health could be a lifesaver.
Erectile dysfunction is common in the CVD patient. It is an important component of the quality of life and it also confers an independent risk for future CV events. The usual 3-year time frame between the onset of ED symptoms and a CV event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into CVD risk assessment for all men. Algorithms for the management of patient with ED have been proposed according to the risk for sexual activity and future CV events. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. Testosterone assessment may be useful for both diagnosis of ED, risk stratification and further management. There are issues to be addressed, such as whether PDE5 inhibition reduces CV risk. Management of ED requires a collaborative approach and the role of the cardiologist is pivotal.
You put your penis in the cylinder and start pumping. The suction creates a vacuum, so blood rushes in to fill the spaces in the spongy tissue of the penis, creating an erection. The erection lasts only as long as the blood stays in, so you slide the band down around the base of your penis, trapping the blood. It's safe to keep the band on for up to 30 minutes.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References The Framingham Heart Study found a baseline risk of myocardial infarction in a healthy 50-year-old nonsmoking man to be approximately 1% per year, or 1 chance per million per hour.87x87Anderson, KM, Odell, PM, Wilson, PW, and Kannel, WB. Cardiovascular disease risk profiles. Am Heart J. 1991; 121: 293–298
Despite its limitations in detecting CVD without significant stenosis, EST (with or without imaging) can further define the cardiovascular risk in patients with ED and no overt CAD and may be particularly helpful for identifying silent CAD in patients with diabetes. Chemical stress tests are appropriate for patients who cannot complete an EST or in whom ECG is non-interpretable. In patients with established CVD, an interpretable EST is mandatory in the indeterminate risk category and is at the discretion of the cardiologist in the low risk category (Table 3B), since it determines exercise ability and estimates cardiovascular risk associated with sexual activity.
With atherosclerosis, the blood vessels are not able to dilate properly, which is called endothelial dysfunction (see the Figure). Cholesterol builds up in the blood vessel walls and forms plaques, which make the vessels narrow and slow down blood flow. When a plaque becomes very advanced, it can completely stop blood from passing through, which is what happens in a heart attack. Atherosclerosis affects not only the blood vessels supplying the heart (coronary arteries), but also blood vessels throughout the entire body. Atherosclerosis causes angina (chest pain that is often exertional), heart attacks, strokes, claudication (pain in the legs with walking), and ED. Atherosclerosis affects different people in different places, but it often affects the penis first, then the heart and brain, and the legs last. Because the first stage of atherosclerosis, endothelial dysfunction, usually affects the penis first, ED can be a warning sign that a heart attack or a stroke may follow, often in the next 3 to 5 years. This warning sign can be a good thing if it alerts you and your doctor that you have atherosclerosis, because then you can take steps to treat the atherosclerosis and prevent a heart attack or stroke.
You may reduce your risk of ED by improving your heart health. Healthy lifestyle choices often encourage you to stop smoking, lose weight and increase physical activity. If ED persists, oral medications are a common first therapy for ED. If oral medications don’t work for you, the penile implant may be an option. The implant is concealed inside the body. It offers support for an erection whenever and wherever desired.
Erection is a neurovascular event that involves spinal and supra spinal pathways. The final common pathway involves the release of nitric oxide (NO) from both endothelial cells and neurons, which acts as a vasodilator causing penile engorgement and erection. NO is degraded by the enzyme phosphodiesterase (PDE) type 5 in the penis. Erectile dysfunction (ED), defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance, results when the neurovascular pathway is interrupted by medical conditions or drugs. A 15-item self-administered questionnaire, the International Index of Erectile Function (IIEF), is one of the most useful tools to evaluate erectile function (EF) in clinical trials, although of much less use in routine clinical practice. The MMAS (Massachusetts Male Aging Study) was the first major epidemiological investigation to study the prevalence of ED. The study found that ED was three times more common in patients with diabetes mellitus. The aetiopathogenesis of ED in diabetes is multifactorial, with vascular and neural factors being equally implicated. Hyperglycaemia is believed to give rise to biochemical perturbations that lead to these microvascular changes. In the MMAS, ED in diabetes was strongly correlated with glycaemic control, duration of disease and diabetic complications. The incidence increased with increasing age, duration of diabetes and deteriorating metabolic control, and was higher in individuals with type 2 diabetes than those with type 1.ED in men with diabetes often affects their quality of life and, as patients are often reluctant to come forward with their symptoms, a carefully taken history is one of the most useful approaches in identifying affected individuals. The PDE inhibitors have revolutionised the management of ED and oral drug therapy is currently first-line therapy for the condition. These agents act by potentiating the action of intracavernosal NO, thereby leading to a more sustained erection. Sildenafil was the first PDE5 inhibitor to undergo evaluation and has been studied extensively. More recently two other agents, vardenafil and tadalafil, have been introduced. All the drugs have been shown to be effective across a wide range of aetiologies of ED, including diabetes. The drugs have been shown to improve EF domain scores, penetration and maintenance of erection, resulting in more successful intercourse. Their effects are greater at higher doses. Sildenafil and vardenafil are shorter-acting agents, while tadalafil has a longer half-life allowing the user more flexibility in sexual activity. Common adverse effects include headache, nasal congestion and dyspepsia, all actions related to inhibition of PDE5. The drugs are generally well tolerated and withdrawal from the clinical studies as a result of drug-related adverse effects were rare. The use of PDE5 inhibitors in the presence of oral nitrates is absolutely contraindicated. The clinical studies to date have not evaluated the use of one drug in the case of treatment failure with another agent. Sublingual apomorphine, which stimulates central neurogenic pathways, is a new agent and may be a suitable alternative in those patients in whom PDE5 inhibitors are ineffective or contraindicated. In clinical trials, all IIEF domains except sexual desire were found to have improved after apomorphine. The median times to erection in these studies were 18.9 and 18.8 minutes for the 2 and 3mg doses, respectively. Intraurethral and intracavernosal alprostadil may be a useful alternative when oral drug therapy is ineffective or contraindicated. The management of ED in the diabetic patient may often involve a multidisciplinary approach where psychosexual counselling and specialist urologist advice is required in addition to the skills and expertise of the diabetologist. Finally, the introduction of the new oral agents have completely revolutionised the management of ED and allowed more individuals to come forward for treatment.
Treatments might be slightly different for different people, depending on their risk factors, but in general all treatment plans have similar elements: diet, exercise, and medications, if necessary (see the Table). Diet and exercise are the cornerstones of the treatment of atherosclerosis. Every diet should include low salt (especially for high blood pressure), low fat and cholesterol (especially for high cholesterol), and limited total calories (especially for patients who are overweight). People with diabetes mellitus should limit their intake of sugars and carbohydrates. Exercise helps to limit atherosclerosis. The more exercise, the better, but every little bit helps. The general recommendation is 30 minutes a day 5 days a week. Check with your doctor to be sure that an exercise program is safe for you. Cigarettes cause a variety of health problems, including atherosclerosis, so cigarette smoking should be stopped. If diet and exercise are not enough to control your atherosclerotic risk factors, then your doctor will prescribe medications. Heart attacks are prevented by controlling atherosclerotic risk factors, which means diet, exercise, and medications if necessary.

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
Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.
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