In prescribing sildenafil, a doctor considers the age, general health status, and other medication(s) the patient is taking. The usual starting dose for most men is 50 mg, however, the doctor may increase or decrease the dose depending on side effects and effectiveness. The maximum recommended dose is 100 mg every 24 hours. However, many men will need 100 mg of sildenafil for optimal effectiveness, and some doctors are recommending 100 mg as the starting dose.
Most bouts of ED can be explained away by stress, anxiety, or nervousness. If erectile dysfunction becomes frequent, don’t panic, but cover your bases by seeing a doctor to rule out scarier causes like diabetes or prostate cancer. Medications like antidepressants can also cause boner loss. Unless you can’t get it up after a date because you spent the day snorting coke and fucking your ex (in which case figure some shit out before you see other people) this line places the blame on the stress of work and away from your partner. While a woman will usually be understanding, she may fear you can’t get hard because you’re not attracted to her. Ease these anxieties with this line. Even if work was great and you’re having trouble getting it up because of other stress, like a text from an ex or family shit you’re not ready to disclose, I’ll allow a little white lie in this instance.
Penile blood flow is measured using a Doppler probe and a 2.5 cm blood pressure cuff. Systolic pressures in the right and left corpora cavernosa are measured and the penile–brachial index is calculated taking a ratio of penile systolic pressure to brachial systolic pressure. These measures should be repeated before and after 3 minutes of exercising the pelvic and leg muscles. In normal men, the PBI should be 0.9 or greater. Ratios between 0.7 and 0.9 suggest vascular impotence; a ratio below 0.6 is diagnostic. Pelvic arteriography can be done if revascularization is considered.
However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy.  A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
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.
The availability of phosphodiesterase-5 (PDE5) inhibitors—sildenafil, vardenafil, tadalafil, and avanafil—has fundamentally altered the medical management of ED. In addition, direct-to-consumer marketing of these agents over the last 15 years has increased the general public’s awareness of ED as a medical condition with underlying causes and effective treatments.
Organic Impotence. Diabetes mellitus, thyroid disease, and dysfunction of the pituitary gland or testes can cause impotence, as can certain medications. Other organic causes include arterial ischemia associated with atherosclerosis of the aorta and common iliac arteries, extensive pelvic surgery such as radical prostatectomy, spinal cord injury and other neurologic disorders, and a history of cigarette smoking. Because certain medications can cause impotence, it is recommended that in cases of recent impotence it be determined whether the patient has started on a new drug. The most common offenders are diuretics, antihypertensives, and vasodilators. Alcohol, which sometimes is ignored as a drug, is often a contributor to the problem of impotence.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.
Estimates of the prevalence of impotence depend on the definition employed for this condition. For the purposes of this consensus development conference statement, impotence is defined as male erectile dysfunction, that is, the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Erectile performance has been characterized by the degree of dysfunction, and estimates of prevalence (the number of men with the condition) vary depending on the definition of erectile dysfunction used.
As blood flows into the penis, the corpora cavernosa swell, and this swelling compresses the veins (blood vessels that drain the blood out of the penis) against the tunica albuginea. Compression of the veins prevents blood from leaving the penis. This creates a hard erection. When the amount of cGMP decreases by the action of a chemical called phosphodiesterase type 5 (PDE5), the muscles in the penis tighten, and the blood flow into the penis decreases. With less blood coming into the penis, the veins are not compressed, allowing blood to drain out of the penis, and the erection goes down.
It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.
While erectile dysfunction can occur at any age, the risk of developing erectile dysfunction increases with age. According to the Massachusetts Male Aging Study, the prevalence of erectile dysfunction was 52% in men 40-70 years of age. The prevalence of complete erectile dysfunction increases from 5% at 40 years of age to 15% among men 70 years of age and older.
Medical conditions, such as hypertension, diabetes mellitus, and cardiovascular disease (CVD), and psychological conditions, such as depression and anxiety, also contribute to sexual dysfunction in middle-aged or elderly men. CVD and hypertension cause a narrowing and hardening of the arteries, leading to reduced blood flow to the corporal bodies, which is essential for achieving an erection. Diabetes is a common aetiology of sexual dysfunction, because it can affect both the blood vessels and the nerves that supply the penis. Men with diabetes are four times more likely to experience ED, and on average, experience ED 15 years earlier than men without diabetes.7 Obesity is also correlated to the development of several types of dysfunction, including a decrease in sex drive and an increase in episodes of ED.8
Erectile dysfunction may be an unpleasant condition that no one really wants to talk about, failing to acknowledge it won’t make the problem go away. Your best defense against health problems like this is to learn everything you can about it so you can tackle the problem at the root. If you’re ready to stop living in embarrassment about your sexual function, become an advocate for yourself and your own health and talk to your doctor.
I'm a college guy who has only had sex a handful of times, and I've noticed a bit of a reccurring issue. During any foreplay and all that good stuff, I have a nice big erection, but as soon as I'm about to stick it in, the erection disappears like a frightened turtle. Then once the 30 seconds of embarrassing made-up explanations concludes, the erection is back.
Is your erectile dysfunction due to psychological (stress, relationship problems, etc.) or physical factors? Your doctor may ask if you note erections at night or in the early morning. Men have involuntary erections in the early morning and during REM sleep (a stage in the sleep cycle with rapid eye movements). Men with psychogenic erectile dysfunction (erectile dysfunction due to psychological factors such as stress and anxiety rather than physical factors) usually maintain these involuntary erections. Men with physical causes of erectile dysfunction (for example, atherosclerosis, smoking, and diabetes) usually do not have these involuntary erections. Men with psychogenic erectile dysfunction may relate the onset of problems to a "stressor," such as failed relationship. Your doctor may suggest a test to determine if you have erections during sleep, which may suggest that there may be a psychological cause of the erectile dysfunction.
Since endothelial dysfunction, CVD and ED are closely associated in epidemiological studies, the question for clinicians is whether to recommend the man presenting with ED undergo a cardiovascular (CV) evaluation. Clearly, based on numerous studies, ED can be considered at least a ‘marker’ for possible further vascular disease or CVD.15 In their report, Vlachopoulos and coworkers make the point that the man presenting with ED, the clinician, is offered an opportunity to attempt to improve the health of the man by addressing lifestyle modification, and consider further vascular evaluation owing to the clear relationship between endothelial dysfunction, ED and CVD.19
Cardiovascular diseases: The most common cause of cardiovascular diseases in the United States is atherosclerosis, the narrowing and hardening of arteries that reduces blood flow. Atherosclerosis (a type of vascular disease) typically affects arteries throughout the body; hypertension, high blood cholesterol levels, cigarette smoking, and diabetes mellitus aggravate atherosclerosis. Hardening of the arteries to the penis and pelvic organs, atherosclerosis, causes insufficient blood flow into the penis. There is a close correlation between the severity of atherosclerosis in the coronary arteries and erectile dysfunction. For example, men with more severe coronary artery atherosclerosis (hardening of the arteries in the heart) also tend to have more erectile dysfunction than men with mild or no coronary artery atherosclerosis. Some doctors suggest that men with new onset erectile dysfunction undergo evaluation for silent coronary artery diseases (advanced coronary artery atherosclerosis that has not yet caused angina or heart attacks).
Research is mixed on the effectiveness of acupuncture as an erectile dysfunction cure, but one study published in November 2013 in the Journal of Alternative and Complementary Medicine found that acupuncture can be beneficial for men experiencing erectile dysfunction as a side effect of antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and serotonin noradrenaline reuptake inhibitors (SNRIs).
Men are very susceptible to visual stimulation, particularly as children and teenagers. Seeing anything appealing (say, a person or image) activates pathways in the brain that tell nerves in your lower spinal cord to trigger a release of nitric oxide, which relaxes blood vessel walls and floods your penis with blood, making it hard. Nitric oxide is the key chemical here, as you need a mix released from your nerves AND from your blood vessels to get an erection. If the blood vessels, nerves, or both are damaged, it's difficult to get a hard erection. That's why your doctor may well be interested if you're struggling with erections, as it could be a sign of early heart disease or diabetes.
Prostaglandins (alprostadil): Alprostadil can be injected into the penis or inserted as a pellet through the urethra. It causes an erection without sexual stimulation that usually lasts about 60 minutes. The danger with this method is that too high a dose can cause priapism, an erection that won't go away. This condition requires immediate medical attention as it can cause serious bruising, bleeding, pain and permanent penile damage. Once the doctor is sure of the right dose, the man can self-inject at home.
Most older men suffer not ED but erection dissatisfaction. Starting around age 50 (often earlier among smokers and/or diabetics), erections change. In some men, the process is gradual, in others, it happens more quickly. Either way, older men lose the ability to raise erections solely from sexual fantasies. Direct fondling of the penis becomes necessary. When erections appear, they rise more slowly and do not become as firm as they were during men’s thirties and forties. And minor distractions may cause wilting—the doorbell or an ambulance siren. These changes alarm many men, who jump to the conclusion that they must have ED. If you can still raise erection durings masturbation, you don’t. What you have is erection dissatisfaction.
Picture the scene. You get home from the bar with your date. You both decided to leave a little early, after only two drinks, because the chemistry was really there and both of you wanted to cut to the chase and get intimate. To discover each other's bodies. To eat of the fruits of passion. In short, to have sex. You stick the key in the lock, swing the door open, and invite her into your beautiful place. OK, well it might not be exactly beautiful. It might be a bit of a mess, frankly. But you don't let that ruin the moment. You turn around and passionately kiss her. How the two of you make it to your bedroom with some clothing still on is anybody's guess. You jump on the bed and hurriedly strip. God — can't this go any faster, you wonder?
This penile tumescence monitor is placed at the base and near the corona of the penis. It is connected to a monitor that records a continuous graph depicting the force and duration of erections that occur during sleep. The monitor is strapped to the leg. The nocturnal penile tumescence test is conducted on several nights to obtain an accurate indication of erections that normally occur during the alpha phase of sleep.
Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits.  Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.