Erectile dysfunction (ED) affects 50% of men older than 40 years,  exerting substantial effects on quality of life.  This common problem is complex and involves multiple pathways. Penile erections are produced by an integration of physiologic processes involving the central nervous, peripheral nervous, hormonal, and vascular systems. Any abnormality in these systems, whether from medication or disease, has a significant impact on the ability to develop and sustain an erection, ejaculate, and experience orgasm.
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
This consensus development conference on male erectile dysfunction has provided an overview of current knowledge on the prevalence, etiology, pathophysiology, diagnosis, and management of this condition. The growing individual and societal awareness and open acknowledgment of the problem have led to increased interest and resultant explosion of knowledge in each of these areas. Research on this condition has produced many controversies, which also were expressed at this conference. Numerous questions were identified that may serve as foci for future research directions. These will depend on the development of precise agreement among investigators and clinicians in this field on the definition of what constitutes erectile dysfunction, and what factors in its multifaceted nature contribute to its expression. In addition, further investigation of these issues will require collaborative efforts of basic science investigators and clinicians from the spectrum of relevant disciplines and the rigorous application of appropriate research principles in designing studies to obtain further knowledge and to promote understanding of the various aspects of this condition.
Sildenafil is available as oral tablets at doses of 25 mg, 50 mg, and 100 mg. Patients should take sildenafil approximately one hour before sexual activity. In some men, the onset of action of the drug may be as early as 11-20 minutes. It's best for men to take sildenafil on an empty stomach for best results since absorption and effectiveness of sildenafil can be diminished if it is taken shortly after a meal, particularly a meal that is high in fat. Sildenafil and the other PDE5 inhibitors don't cause an immediate erection. Sexual stimulation is necessary for these medications to work.
The first step in treating the patient with ED is to take a thorough sexual, medical, and psychosocial history. Questionnaires are available to assist clinicians in obtaining important patient data. (See Presentation.) Successful treatment of sexual dysfunction has been demonstrated to improve sexual intimacy and satisfaction, improve sexual aspects of quality of life, improve overall quality of life, and relieve symptoms of depression. (See Treatment.)
In a prospective, multicenter, single-armed study of ED patients who exhibited a suboptimal response to PDE5 inhibitors, the investigators found that percutaneous implantation of zotarolimus-eluting stents in focal atherosclerotic lesions was both safe and feasible and was associated with clinically meaningful improvement on subjective and objective measures of erectile function. 
Chronic stress dumps adrenaline in your system multiple times a day. And that can lead to high blood pressure, heart disease, obesity, and diabetes. Chronic stress is like red-lining your car all day long. When you drive 100 mph all the time, something is going to break down. A high-stress environment can actually change the way your brain sends messages to your body. Dumping too much adrenaline into your bloodstream can affect blood flow and severely limit your ability to achieve and maintain an erection.
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
So what do you do? If the guilt is too much, you can tell your boyfriend. It might be the only way to clear your conscience — and hopefully, if you explain the reasons why you did such a boneheaded thing, he'll understand. It will be hard and it may create drama for months to come, but my guess is that you can recover, if he's not a horribly jealous guy.
Vardenafil and tadalafil belong to the same group of chemical compounds as sildenafil, namely phos-phodiesterase type 5 (PDE-5) inhibitors. Some men cannot benefit from sildenafil or the two newer PDE-5 inhibitors because they have low levels of nitric oxide. British investigators reported in late 2002 that three different types of compounds are being studied as possible medications for men with low levels of nitric oxide. They are Rho-kinase inhibitors, soluble guanylate cyclase activators, and nitric oxide-releasing PDE-5 inhibitors.
If PDE5 drugs don't work or cannot be used because of potential side effects, your doctor can recommend other therapies. The drug alprostadil (Caverject, Edex, Muse) allows blood to flow more freely in the penis, leading to an erection. The drug can be injected with a tiny needle into your penis. Or, a small pellet (suppository) can be inserted into the opening of the penis. Suppositories and injections are effective in the majority of men.
Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls.  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.
Diet can also affect a man’s ability to achieve or maintain an erection. As stated, men who indulge in alcohol may have trouble with erections, but men who have poor diets, suffer from diabetes, or who are overweight can also restrict blood flow to the penis or suffer from poor body image. All of these factors, especially when combined, can lead to erectile dysfunction.
Certain types of blood pressure medications, antiulcer drugs, antihistamines, tranquilizers (especially before intercourse), antifungals (hetoconazole), antipsychotics, antianxiety drugs, and antidepressants, known as selective serotonin reuptake inhibitors (SSRIs, including Prozac and Paxil), can interfere with erectile function. Smoking, excessive alcohol consumption, and illicit drug use may also contribute. In rare cases, low levels of the male hormone testosterone may contribute to erectile failure. Finally, psychological factors, such as stress, guilt, or anxiety, may also play a role, even when the impotence is primarily due to organic causes.
The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function.  About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. 
Everyone knows that regular exercise is good for the body and the mind, and in many cases, exercise can be good for relieving stress and helping men’s bodies produce more testosterone. In some cases, however, exercise can be detrimental. This is the case in cycling as long and regular rides can cause the nerves in the perineum to be compacted, leading to a loss of feeling in the penis and/or testicles. Over time, this nerve compaction and damage may lead to either erectile dysfunction or ejaculatory dysfunction.
Men with erectile dysfunction require diagnostic evaluations and treatments specific to their circumstances. Patient compliance as well as patient and partner desires and expectations are important considerations in the choice of a particular treatment approach. A multidisciplinary approach may be of great benefit in defining the problem and arriving at a solution.
A lot of the time, the issue is a combination of both. For instance, cortisol – which is an important steroid hormone in the body – is released in greater amounts when we're stressed. It's supposed to briefly shut down non-essential functions like reproduction and fighting off illnesses whilst you deal with the danger at hand. However, the chronic and ongoing stress of modern life increases our background cortisol levels, activating the sympathetic system and stopping an erection.
You’ve probably heard of Viagra, but it’s not the only pill for ED. This class of drugs also includes Cialis, Levitra, Staxyn, and Stendra. All work by improving blood flow to the penis during arousal. They're generally taken 30-60 minutes before sexual activity and should not be used more than once a day. Cialis can be taken up to 36 hours before sexual activity and also comes in a lower, daily dose. Staxyn dissolves in the mouth. All require an OK from your doctor first for safety.