This may be the oldest excuse in the book as a reason not to have safe sex, but research has confirmed that condoms may interfere with some men’s ability to have and hold an erection. For example, a 2006 study found that, over a three-month period, about 37 percent of men lost at least one erection when putting on a condom, or during sex with a condom, SexualHealth.com reported.
In some cases, nocturnal penile tumescence testing is performed to find out whether the man has erections while asleep. Healthy men usually have about four or five erections throughout the night. The man applies a device to the penis called a Rigiscan before going to bed at night, and the device can determine whether he has had erections. (If a man is able to have normal erections at night, this suggests a psychological cause for his impotence.)
An analysis of 14 studies involving more than 90,000 patients with ED confirmed the relation between ED and an increased risk of cardiovascular events and mortality.  Compared with patients without ED, those with ED had a 44% increased risk of cardiovascular events, a 25% increased risk of all-cause mortality, a 62% increased risk of MI, and a 39% increased risk of cerebrovascular events. Treatment of ED, either through lifestyle interventions or by pharmacologic means, may improve prognosis and reduce risk.
The neurologic pathways required for erection originate in the cerebral cortex where visual, auditory, and psychic stimuli are processed, and in the pudenal nerve, an afferent nerve that transmits tactile sensations from the genitals to the sacral segments of the spinal cord and cortex. Efferent signals from the spinal cord pass along the pelvic parasympathetic nerves and dilate the corporal vessels. The specific neurotransmitters have not been fully defined; acetylcholine, and perhaps vasoactive intestinal peptide, appears to be important. There are many causes of neurogenic impotence. Anything that disrupts neural pathways or blocks neurochemical transmission will have an adverse effect on erection. Psychologic factors probably interfere with erection by inhibiting corticosacral efferent pathways.
As with most other organ system in the human body, changes and loss of function is normal consequence of the ageing process. This is also true of the endocrine system, specifically the levels of testosterone production from the Leydig cells of the testicle. Accompanying the decrease in testosterone is a decrease in erections which also has a component in decrease in the blood supply to the penis making erection not as frequent and not as rigid compared with a young man’s erectile function. Although these changes are in itself not life threatening, they can impact a man’s relationship with his partner, and also ED may be a harbinger of other undiagnosed conditions such as coronary artery disease (CAD), hypercholesterolaemia or diabetes mellitus.6
"Data shows the longer you ride, the higher your chance of developing ED in terms of distance per week," Gittens says. If you cycle for exercise or socialization, you don't have to necessarily give it up, just make some modifications. Gittens suggests riding for shorter distances, giving yourself a rest every once in a while, finding a comfortable seat, and getting a bike that’s sized appropriately.
After the history, physical examination, and laboratory testing, a clinical impression can be obtained of a primarily psychogenic, organic, or mixed etiology for erectile dysfunction. Patients with primary or associated psychogenic factors may be offered further psychologic evaluation, and patients with endocrine abnormalities may be referred to an endocrinologist to evaluate the possibility of a pituitary lesion or hypogonadism. Unless previously diagnosed, suspicion of neurologic deficit may be further assessed by complete neurologic evaluation. No further diagnostic tests appear necessary for those patients who favor noninvasive treatment (e.g., vacuum constrictive devices, or pharmacologic injection therapy). Patients who do not respond satisfactorily to these noninvasive treatments may be candidates for penile implant surgery or further diagnostic testing for possible additional invasive therapies.
Stiffy Solution: Frustratingly enough, the only solution to exhaustion-based impotence is to get some rest, which is obviously difficult (or your dude wouldn't be having this problem in the first place). But if your guy has been resistant to getting help for his insomnia or asking for different hours at work, the inability to get his nine iron out on the putting green might be the thing that finally motivates him to make a life change. So, at least there's that.
The history can be useful in distinguishing organic from psychogenic impotence (Table 187.1). The patient with organic impotence describes problems with erection that progress over months to years. At first, the patient will have partial erections or seemingly firm erections that become flaccid during intercourse. With time, total erectile failure ensues. Organic impotence is constant and nonselective, meaning it is not better or worse with any specific partner or any type of stimulation.
My boyfriend, 25, can't get hard anymore!! He WANTS to have sex, but he just won't get hard, when just about a month ago he would get hard just by looking at me. We have been together for six months, and I'm starting to think he might be bored of me or that I'm the problem. He says it's not me at all. Our relationship is great, but I don't know what to do. Please help!!
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date.  Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.
An approach to the diagnosis and management of the impotent patient is presented in Figure 187.1. Apparent and likely causes of impotence should be considered first and, if possible, eliminated before the work-up continues. For instance, observing the patient for a few weeks off offending medication may be all that is necessary to establish the cause of impotence. When no obvious or remediable cause is present, the next step is based on the clinical impression of the likelihood of organic versus psychologic impotence. If the latter is considered more likely, it is perfectly reasonable to refer the patient directly for sexual therapy, with the option of reconsidering the diagnosis if, after appropriate therapy, there is no improvement. While an occasional patient with organic impotence will be misrouted, many more with psychogenic impotence will be spared an unnecessary and costly evaluation for organic causes. When organic impotence is likely, a serum testosterone level is the initial screening test for hypogonadism and should be obtained prior to urologic referral. Patients with low testosterone levels require further endocrine evaluations as depicted in Figure 187.1.
Remember what I said before about how it's not you? Okay, sometimes it is you. But it's not that you're not sexy — it's that for men, as well as women, relationship problems (like fighting all the time, or having clashing expectations about where things are going) can severely mess up your sex drive and ability to become aroused. Which makes sense — if you're spending 90 percent of your time together fighting about whether you're going to move in, switching gears to make 10 percent of your time together into a sexy sex party is pretty damned difficult.
Let’s admit that not “talking about anything that could possibly be uncomfortable” is a sure-fire recipe for total disaster. Maybe you’re exaggerating, but if he can’t deal with anything even slightly difficult, then that is a bigger problem than pillow talk. Think about how exactly it would affect everything else in your relationship. He can’t choose not to deal. When good things are happening, it’s a shame he can’t say "I love you0". But when hard things happen, he can’t just say: "Um, pass."
Diabetes is one of the most common causes of ED. Chronically high blood sugar levels can result in nerve damage that affects your body’s ability to translate pleasurable sexual stimulation into an erection. Diabetes can also lead to issues with circulation, which reduces blood flow to the penis and makes it more difficult to keep an erection that is hard enough for intercourse.
The inflatable type of device consists of cylinders that are implanted in the corpora cavernosa, a fluid reservoir implanted in the abdomen, and a pump placed in the scrotum. The man squeezes the pump to move fluid into the cylinders and cause them to become rigid. (He reverses the process by squeezing the pump again.) While these devices allow for intermittent erections, they have a slightly higher malfunction rate than the silicon rods.
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
There was never any claim for Normal Sexual Decline as being applicable to all men all of the time. The point is that males and females should be made aware of what to reasonably expect and to be aware as well as to the incomplete writings / hidden agendas of the reports in this area. Research has clearly show what to reasonably expect. Meta Analysis can illucidate what is very likely normal for most males / what is hidden, etc.
PDE5 inhibitors, the primary second-line therapy, have been the mainstay of ED treatment since the release of sildenafil (Viagra) in 1998, with the subsequent development of many others, and still more in the development stage. These medications do improve erectile quality for the majority of men, and they work by enhancing blood flow in the corpora cavernosa. These medications are generally used on demand and need to be taken about an hour before sexual intimacy. Tadalafil (Cialis) is longer acting and does come in a daily preparation potentially eliminating the ‘on-demand’ need. The daily dosing of tadalafil, 2.5–5 mg\day, has also been approved by the FDA for treatment of symptoms of BPH.41 PDE5 inhibitors are contraindicated in men taking nitrates, but otherwise PDE5 inhibitors are very safe and effective. When PDE5 inhibitors are coadministered with nitrates, pronounced systemic vasodilation and severe hypotension are possible. Many patients with ED are elderly and have the same risk factors as patients with CAD, so these drug combinations are commonly considered or encountered in clinical practice.42
When sexually stimulated there is a release of a chemical, nitric oxide (NO) in the blood vessels of the corpus cavernosum. The NO stimulates the production of a compound called cGMP, which causes relaxation of the smooth muscle in the blood vessels supplying the corpus cavernosum. PDE 5 is an enzyme that breaks down cGMP. By inhibiting the breakdown of cGMP by PDE5, these medications allow cGMP to build up in the penis. cGMP causes muscles in the corpora cavernosa of the penis to relax. When the muscle is relaxed, more blood can flow into the penis and fill the spaces in the penis. As the penis fills with blood, the veins in the penis are compressed, and this results a hard erection. When the effect on PDE5 decreases, the cGMP levels go down and the muscle in the penis contracts, causing less blood to flow into the penis and allowing the veins to open up and drain blood out of the penis.
Her remark was entirely destructive of poetry, since it was to the effect that poetry had nothing whatever to do with her; all her friends spent their lives in making up phrases, she said; all his feeling was an illusion, and next moment, as if to taunt him with his impotence, she had sunk into one of those dreamy states which took no account whatever of his existence.
Psychological factors — Psychological issues such as depression, anxiety, guilt or fear can sometimes cause sexual problems. At one time, these factors were thought to be the major cause of impotence. Doctors now know that physical factors cause impotence in most men with the problem. However, embarrassment or "performance anxiety" can make a physical problem worse.
In this study, ED proceeded CVD in almost 70% of cases. Similarly, many men with ED have been found to have pre-existing CVD. A study by Vlachopoulos et al evaluated the incidence of asymptomatic CVD in 50 men with ED.22 These authors found that 19% of men with ED had asymptomatic CVD. Similarly, Mulhall and colleagues found that 20% of men presenting with ED and vascular insufficiency on penile duplex had asymptomatic CVD.23
Hypogonadism may be suggested by the patient's general appearance. If testosterone deficiency antedates puberty, as in Klinefelter's syndrome, eunuchoid proportions—defined as an arm span 5 cm or more in excess of height, or a sole-to-pubis length exceeding crown-to-pubis length by more than 2 cm—may be present. In postpubertal males whose testosterone levels are markedly depressed, the secondary sexual characteristics may become atrophic. Testicles less than 4 cm in length or a prostate gland that is smaller than expected may be the only clues on physical examination to a pituitary tumor with secondary hypogonadism.
The link between chronic disease and ED is most striking for diabetes. Men who have diabetes are two to three times more likely to have erectile dysfunction than men who do not have diabetes. Among men with erectile dysfunction, those with diabetes may experience the problem as much as 10 to 15 years earlier than men without diabetes. Yet evidence shows that good blood sugar control can minimize this risk. Other conditions that may cause ED include cardiovascular disease, atherosclerosis (hardening of the arteries), kidney disease, and multiple sclerosis. These illnesses can impair blood flow or nerve impulses throughout the body.