Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
The causes of ED are numerous but generally fall into two categories: organic or psychogenic. The organic causes can be subdivied into five categories: vascular, traumatic/postsurgical, neurological, endocrine-induced, and drug-induced. Examples of the psychogenic causes are depression, performance anxiety, and relationship problems. In people with diabetes, the main risk factors are neuropathy, vascular insufficiency, poor glycemic control, hypertension, low testosterone levels, and possibly a history of smoking.
In most men, ED is recognised as sharing vascular aetiology with IHD.17 ED and IHD share common risk factors, such as hypertension, hyperlipidaemia, diabetes, obesity, lack of physical exercise, cigarette smoking, poor diet, excess alcohol consumption and psychological stress, including depression.30 Endothelial dysfunction has been implicated as a common mechanism between CAD and ED and it has an important role in the development of atherosclerosis.31
Evaluation of functional capacity is the mainstay for the management of patients with ED.30 However, it should be kept in mind that in men with heart failure sexual activity may affect the heart differently from physical activity of similar METS due to differences in psychological anticipation and sympathetic activation.30,49 Cardiac echocardiography may offer valuable information for left ventricular performance and valvular function. For risk categories of heart failure patients and their management, please refer to Table 3 and Figure 5.

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:


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.

In TCM, the meridian system is thought to represent a path through which the life energy qi flows and as discussed in earlier section, the “Jing” (kidney) qi plays an important role in penile erection. Acupuncture helps to correct the imbalances to relieve physical symptoms by stimulating various meridian points. The Shensu (BL23), Zusanli (ST36) and Neiguan (PC6) points represents important acupoints for penis stimulation and thus has a positive homeostatic effect on the autonomic nervous system, and potentially modulate NO release (55,56). While some studies have showed up to a third of patients reported improvement in penile erection and sexual activity, systematic review showed insufficient data to conclude that acupuncture is an effective intervention for treating ED (56,57). Therefore, further scientific research is required to investigate whether there are specific benefits of acupuncture for men with ED before acupuncture can be accepted as evidence-based practice.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Erectile dysfunction is a common physiological disorder. According to estimates from the National Institutes of Health, ED affects 10 million to 20 million men in the United States; another 10 million men are affected by partial ED, defined as present but diminished erectile function.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Since then, several other oral PDE-5 inhibitors have been developed, including vardenafil and tadalafil, which generated considerable interest in both the scientific and lay communities. There was also much concern about their safety, especially in men with cardiovascular disease. Compared with the 2 newer PDE-5 inhibitors vardenafil and tadalafil, sildenafil has been available for a much longer time; therefore, the vast majority of published cardiovascular safety studies have been performed on this medication. Recommended starting and maximum doses of oral PDE-5 inhibitors are shown in Table 1.
Crossref | PubMed | Google ScholarSee all References Regular exercise can significantly decrease the patient's risk of having a myocardial infarction during sexual intercourse by increasing the patient's functional reserve, decreasing the heart rate, and increasing the stroke volume.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409

If your doctor says it's OK, you may be able to stop taking blood pressure medications temporarily to see if your sex life improves. To make sure your blood pressure remains within a safe range, you may need frequent blood pressure readings while you're not taking the blood pressure lowering medication that may be causing your sexual difficulties. This can be done with a home blood pressure monitoring device for convenience.

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.


PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
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.
Counselling or sex therapy (58% of people find this works for them) –mind-related causes of erectile dysfunction can affect anyone. They are more likely if you experience erectile dysfunction at a younger age. Talking to a counsellor or therapist can help some people overcome erectile dysfunction related to these problems, possibly for good. They can also help you if your erectile dysfunction is causing you stress, as this can make matters worse.
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
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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
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.
Undoubtedly, heart disease is and will continue to be one of the major health problems of modern society. Approximately one death every forty seconds occurs due to cardiovascular (CV) disease in the United States alone and arterial hypertension is one of the greatest culprits for it[1]. Considering the fact that around 25% of the global population suffer from arterial hypertension, predicted to reach 1.5 billion people in the foreseeable future, it is easily deducted that a respectful part of the general population is under major and constant CV risk[2,3].
Phosphodiesterase Inhibitors. The cornerstone of first-line therapy is the PDE-5 inhibitor. No other class of oral agents approaches the efficacy of PDE-5 inhibitors. Yohimbine, trazodone, phentolamine, L-arginine, and OTC herbal remedies have been used with very limited success. The superiority of yohimbine over placebo in the treatment of organic ED is a matter of dispute.9 A recent trazodone study failed to detect any difference between trazodone and placebo on sexual function.10 Oral phentolamine, although available in Mexico, has not been approved by the US FDA for the treatment of ED. Apomorphine, a central dopaminergic receptor drug, has recently been voluntarily withdrawn from FDA consideration for the treatment of ED. The efficacy of ginkgo biloba and Korean red ginseng has yet to be demonstrated by randomized, placebo-controlled trials.
There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.

At the same time, people with diabetes are susceptible to a type of blood vessel damage known as endothelial dysfunction. A recent study found that men with ED are at a greater risk of heart disease, which is also associated with endothelial dysfunction. If blood vessels aren't in good working order, the penis may not get enough blood for an erection.


What comes after an ED diagnosis in diabetic patients? Often, Dr. Eid will instantly refer these men to a cardiologist. “If a patient has diabetes and is newly diagnosed, a significant portion of these men are going to develop coronary artery disease in the next 2-3 years,” he said. “One of the things we do is recommend is that they see a cardiologist and perhaps have a stress test or some sort of evaluation.”
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

Evaluation of functional capacity is the mainstay for the management of patients with ED.30 However, it should be kept in mind that in men with heart failure sexual activity may affect the heart differently from physical activity of similar METS due to differences in psychological anticipation and sympathetic activation.30,49 Cardiac echocardiography may offer valuable information for left ventricular performance and valvular function. For risk categories of heart failure patients and their management, please refer to Table 3 and Figure 5.
A recent systematic review and meta-analysis of relevant studies in this field confirmed that erectile dysfunction is associated with increased risk of CV events and all-cause mortality[89]. The pooled relative risks were 1.44 (95%CI: 1.27-1.63) for total CV events, 1.19 (95%CI: 0.97-1.46) for CV mortality, 1.62 (95%CI: 1.34-1.96) for myocardial infarction, 1.39 (95%CI: 1.23-1.57) for cerebrovascular events, and 1.25 (95%CI: 1.12-1.39) for all-cause mortality, for men with vs without erectile dysfunction. Of note, the relative risk was higher in intermediate-compared with high- or low-CV-risk populations and with younger age, with obvious clinical implications. Interestingly, the relative risks were higher when erectile dysfunction was diagnosed with the use of a questionnaire compared with a single question (RR = 1.61; 95%CI: 1.38-1.86 vs RR = 1.27; 95%CI: 1.18-1.37, respectively; P = 0.006).
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.

Crossref | PubMed | Scopus (23) | Google ScholarSee all References, 73x73Rajagopalan, P, Mazzu, A, Xia, C, Dawkins, R, and Sundaresan, P. Effect of high-fat breakfast and moderate-fat evening meal on the pharmacokinetics of vardenafil, an oral phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction. J Clin Pharmacol. 2003; 43: 260–267


The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.
Artery size also explains the onset of ED before occurrence of CAD. Coronary arteries are 3–4 mm in diameter, while the penile artery is 1–2 mm in diameter.17 Endothelial dysfunction and plaque burden in the small arteries may cause symptoms of ED before they affect blood flow in large arteries. Also, an asymptomatic lipid-rich plaque in the coronary arteries carries the risk of rupture that leads to acute coronary syndrome or death, so ED may be predictive of these serious events without warning cardiac symptoms.17
Cardiovascular disease and erectile dysfunction (ED) are closely interrelated disease processes. Erectile dysfunction reportedly affects 10 million to 20 million men in the United States and more than 100 million men worldwide. Each year, about 500,000 persons in the United States survive a myocardial infarction, and an estimated 11 million have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many patients. We explore the relationship between ED and the presence of cardiovascular disease in the general population. We also review the prevalence and pathophysiological associations of ED and cardiovascular disease. The risks of sexual activity for patients with cardiovascular disease are discussed, as are prevention and treatment strategies for ED in this patient population.
Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).
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.
Some doctors prefer to start a man on the lowest dose of an oral medicine and increase the dose until an effective one is found. Others prefer to start with the highest dose and go to a lower dose only if a man complains of side effects. In either case, it’s important for a man to communicate with his doctor to let him know how the dose he’s using is working.
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