ED can be caused by many things. The most common causes in men with diabetes are problems related to blood vessel– and nerve-related complications. Sometimes, though rarely, ED can be caused by a hormonal imbalance. Depression can also cause ED, as can stress and excessive worrying about sexual performance. Certain medications can cause temporary ED.
In Western medicine approach, health and disease are clearly divided entities. The emphasis is on protection of the individual body from disease or how to replace the body’s lost functions. Antibiotic therapy is used to combat harmful bacteria during infections, exogenous synthetic hormones are used to replace hormone-deficient individuals and artificial prostheses are applied when an organ loses its functions. This is very different from the holistic Eastern approach where the treatment entity is taken as a whole, and the objective is to seek harmony between different bodily systems.
With great interest we have read the recently published review by Vlachopoulos et al, a very detailed and extensive overview of erectile dysfunction in the cardiovascular patients. Guidelines for the management of erectile dysfunction with heart failure were noted, as well as advice about dealing with erectile dysfunction (ED) in patients with cardiovascular disease (CVD). However, many others have written similar reviews and guideline concerning the care for ED as well as (female) sexual dysfunction in CAD in the past years (1-4), cardiologists should be familiar with this matter by now. The problem is the actual translation of this knowledge into actions in cardiologists' daily clinical practice. Our research group performed a survey among Dutch cardiologists, aiming to evaluate their inquiry about erectile function in day-to-day practice, to detect their attitude towards this discussion and their perceived barriers for addressing sexual activity. Results from this survey indicated that cardiologists (n=414) did not routinely discuss erectile dysfunction: 48.7% indicated to discuss sexual function 'sometimes' and only 16.9% said to discuss the subject regularly. Of respondents, 41.5% marked that care for patients' sexual quality of life is not their responsibility. Nevertheless, 42% indicated that they would benefit from training to obtain knowledge about treatment of erectile and sexual dysfunction in cardiologic patients. Barriers not to inquire about sexual activity included 'the patient does not ask about it' (53.7%), 'I do not have an angle or motive to start about it'(45.9%), as well as time constraints (42.9%) and lack of training in dealing with sexual dysfunction (35.2%). The more experienced the cardiologist was the less he/she stated the need for training or for a referral directory(5). Since all cardiologists should, meanwhile, know that ED is part of their responsibility, as it is a sentinel marker of CVD(6). It is now case to pay attention to the implementation of the care for erectile and other sexual dysfunction in the cardiology practice. Our study suggests that physicians' experience in the field plays an important role in discussing sexual activity and that sexual healthcare can be improved with more education about the subject. Furthermore a directory of the available healthcare professionals for the referral of patients with sexual dysfunction was indicated as mandatory. We suggest that attention of cardiologists should not only be focused on writing about ED and CVD, attention should be diverted to the actual implementation of care for patients with ED as well, in order to improve patient-centered healthcare in cardiology.
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
To date, there are no studies directly comparing the effectiveness of these three agents among diabetic men with ED, so it is impossible to state that one agent is superior to another in terms of effectiveness in diabetic patients. However, there are an number of studies that compare the individual agents to placebo in diabetic men with ED. For example, Boulton et al.41 completed a 12-week double-blind, placebo-controlled randomized clinical trial of the effectiveness of sildenafil in 219 men with ED and type 2 diabetes. They found that sildenafil resulted in a significant improvement in the ability to both achieve and maintain an erection adequate for sexual intercourse in men with type 2 diabetes. In a similar study, Rendell et al.42 randomized 268 diabetic men with ED to receive either sildenafil in a dose-escalation manner or placebo. At the conclusion of the 12-week study, 56% of the patients in the sildenafil arm reported improved erections, compared to 10% in the placebo arm (P < 0.001). Additionally, 61% of patients in the diabetic arm reported at least one successful attempt at sexual intercourse in the final month of the study, compared to 22% in the control arm (P < 0.001). Similar randomized studies have documented the effectiveness of both tadalafil43 and vardenafil44 in the treatment of diabetes-related ED.
The second way relates to the risk associated with the sexual activity in a patient with either overt or occult CVD. In this case, the diagnosis of ED should prompt an initial cardiovascular assessment based on the history and clinical examination in order to define the baseline risk according to (i) the likelihood of silent CAD18,31 (especially since ED patients have a high probability to have silent CAD) or to the stage of clinically evident CAD, (ii) other cardiovascular conditions either unrelated, or related to ED (e.g. heart failure, peripheral arterial disease).

"We think that if you have an active sex life it's probably an indicator of a healthy lifestyle, especially in the oldest quartile—those 70 to 80 years old," Andersson said. "From the perspective of a doctor, if a patient asks about erectile dysfunction drugs after a heart attack and has no contraindications for PDE5 inhibitors, based on these results you can feel safe about prescribing it."

The bad news: Men with diabetes are three times more likely to report having problems with sex than non-diabetic men. The most common sexual problem is Erectile Dysfunction, or ED, sometimes called impotence. Even worse, because ED is such a private issue, many men feel embarrassed to discuss the problem with their doctor, or even their partner, so the problem is never addressed.
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

In another study, 60 patients underwent stress exercise cardiovascular testing and Doppler ultrasonography for measurement of their cavernosal artery peak systolic velocity (PSV).17x17Kawanishi, Y, Lee, KS, Kimura, K et al. Screening of ischemic heart disease with cavernous artery blood flow in erectile dysfunctional patients. Int J Impot Res. 2001; 13: 100–103

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
Ginkgo is an herb that’s been used medicinally for thousands of years to treat a variety of ailments. This supplement may improve penile blood flow. Additionally, some reports suggest that ginkgo can increase bleeding risk. This makes it particularly dangerous for people using blood thinners. Other studies, including one from 2011, found no evidence of increased bleeding while using ginkgo.
Excess LDL cholesterol in your blood gets deposited in arteries, the blood vessels that feed the heart and brain. These deposits can join with other substances to form plaque, a thick, hard deposit in the blood vessel that leads to atherosclerosis. Plaque can narrow the passageway inside the artery and pinch off the flow of blood to the heart muscle, and to the penis.
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.)