My boyfriend has a hard time getting and staying hard. It's obviously a difficult situation to talk about, but he says he feels pressure when he's with me (versus previous random hookups he wasn't invested in), so he psyches himself out. When we do have sex, I'm almost always really satisfied and I care a lot about him, both things I express in and outside of the bedroom. But the situation seems to be only getting worse. We've stopped having sex during the week because our busy lives mean we don't have an hour or more to devote to sex (which is sometimes what it takes), or we can't have sex at all because of what he's experiencing. I'm afraid this is going to continue to get worse, not only sexually but emotionally in our relationship. How can I help him fix this, and reassure him in the meantime that I care about him and want to support him?
Because of the difficulty in defining the clinical entity of erectile dysfunction, there have been a variety of entry criteria for patients in therapeutic trials. Similarly, the ability to assess efficacy of therapeutic interventions is impaired by the lack of clear and quantifiable criteria of erectile dysfunction. General considerations for treatment follow:

Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.


All studies demonstrate a strong association with age, even when data are adjusted for the confounding effects of other risk factors. The independent association with aging suggests that vascular changes in the arteries and sinusoids of the corpora cavernosa, similar to those found elsewhere in the body, are contributing factors. Other risk factors associated with aging include depression, sleep apnea, and low HDL levels.

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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.
Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.
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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.
The circulatory system plays a central role in obtaining and sustaining erections. Augmentation of blood flow to the corporal bodies depends on the intravascular pressure in the penile artery. Vascular lesions—typically atherosclerotic, but occasionally fibrotic—and systemic hypotension will limit flow to the corpora. In certain patients, blood flow at rest may be sufficient to obtain an erection but not sufficient to maintain it during intercourse, when the pelvic musculature places greater demands on a compromised blood supply.
Psychological Causes of ED – Between 10% and 20% of ED cases have a psychological cause. Because arousal starts in the brain, psychological issues can be a significant contributing factor to erectile dysfunction. Mental health conditions like depression or anxiety can negatively impact your libido, making it more difficult for you to become aroused.
The role of the endothelium in ED has been noted for a number of years and the overlapping of ED and other conditions, especially coronary heart disease, CVD, affecting endothelial function/dysfunction, is clearly present. The endothelial cell is now known to affect vascular tone and impact the process of atherosclerosis, and impacting ED, CVD and peripheral vascular disease.16
By contrast, psychogenic impotence typically is abrupt in onset, often in relation to psychological trauma, and may wax and wane. Patients with psychogenic impotence may have total erectile failure with one partner but not another, or be impotent during sexual intercourse but not during self-stimulation. Normally occurring spontaneous erections in the morning suggest psychogenic rather than organic causes for impotence.
Another potential new treatment consists of penile low-intensity shock wave lithotripsy. This consists of 1500 shocks twice a week for 3–6 weeks. The purpose is to stimulate neovascularisation to the corporal bodies with improvement in penile blood flow and endothelial function. The use of low-intensity shock wave lithotripsy may convert PDE5 inhibitor non-responders to responders.47

Erythrocytosis has been noted in men on TRT, and should be monitored every 6–12 months depending upon the patients’ response to changes in haematocrit levels. For mild elevations, the dosage of testosterone can be decreased or the interval of using the medication can be increased. With the haematocrit greater than 50%, decisions to temporarily discontinue the medication or periodic phlebotomy may be indicated.38
Damage to the autonomic pathways innervating the penis may eliminate "psychogenic" erection initiated by the central nervous system. Lesions of the somatic nervous pathways may impair reflexogenic erections and may interrupt tactile sensation needed to maintain psychogenic erections. Spinal cord lesions may produce varying degrees of erectile failure depending on the location and completeness of the lesions. Not only do traumatic lesions affect erectile ability, but disorders leading to peripheral neuropathy may impair neuronal innervation of the penis or of the sensory afferents. The endocrine system itself, particularly the production of androgens, appears to play a role in regulating sexual interest, and may also play a role in erectile function.
In other cases, men who habitually use alcohol or other drugs may experience similar results. Alcohol is a depressant to the central nervous system. This means that a little bit might be able to lighten the mood, but too much can basically shut down all communication between the brain and the penis. When this happens, no amount of will or stimulation will result in an erection. Other drugs can also affect the body’s ability to achieve an erection, including heroin and MDMA, otherwise known as ecstasy.
In other cases, men who habitually use alcohol or other drugs may experience similar results. Alcohol is a depressant to the central nervous system. This means that a little bit might be able to lighten the mood, but too much can basically shut down all communication between the brain and the penis. When this happens, no amount of will or stimulation will result in an erection. Other drugs can also affect the body’s ability to achieve an erection, including heroin and MDMA, otherwise known as ecstasy.
How soon the drugs start working ranges from 15 to 60 minutes. Neither Viagra nor Levitra will work if you take them after a meal, which blocks their absorption. However, neither Cialis nor Stendra interact with food this way. The onset time determines how soon you can engage in intercourse. Stendra and daily-use Cialis are closest to being an "on demand" erectile drug; using the others requires more planning.
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 appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme. [24] The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.
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.

Three forms of penile prostheses are available for patients who fail with or refuse other forms of therapy: semirigid, malleable, and inflatable. The effectiveness, complications, and acceptability vary among the three types of prostheses, with the main problems being mechanical failure, infection, and erosions. Silicone particle shedding has been reported, including migration to regional lymph nodes; however, no clinically identifiable problems have been reported as a result of the silicone particles. There is a risk of the need for reoperation with all devices. Although the inflatable prostheses may yield a more physiologically natural appearance, they have had a higher rate of failure requiring reoperation. Men with diabetes mellitus, spinal cord injuries, or urinary tract infections have an increased risk of prosthesis-associated infection. This form of treatment may not be appropriate in patients with severe penile corporal fibrosis, or severe medical illness. Circumcision may be required for patients with phimosis and balanitis.
Endocrine evaluation consisting of a morning serum testosterone is generally indicated. Measurement of serum prolactin may be indicated. A low testosterone level merits repeat measurement together with assessment of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin levels. Other tests may be helpful in excluding unrecognized systemic disease and include a complete blood count, urinalysis, creatinine, lipid profile, fasting blood sugar, and thyroid function studies.
Penile implants: This treatment involves permanent implantation of flexible rods or similar devices into the penis. Simple versions have the disadvantage of giving the user a permanent erection. The latest (and most expensive) device consists of inflatable rods activated by a tiny pump and switch in the scrotum. Squeezing the scrotum stiffens the penis, whether the person is aroused or not. The penis itself remains flaccid, however, so the diameter and length are usually less than a natural erection, and hardness is lacking, although it's sufficient for intercourse.
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."
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.
Penile implants: This treatment involves permanent implantation of flexible rods or similar devices into the penis. Simple versions have the disadvantage of giving the user a permanent erection. The latest (and most expensive) device consists of inflatable rods activated by a tiny pump and switch in the scrotum. Squeezing the scrotum stiffens the penis, whether the person is aroused or not. The penis itself remains flaccid, however, so the diameter and length are usually less than a natural erection, and hardness is lacking, although it's sufficient for intercourse.
Patient can inject medications directly into the corpora cavernosa to help attain and maintain erections. Medications such as papaverine hydrochloride, phentolamine, and prostaglandin E1 (alprostadil) can be used alone or in combinations to attain erections. All of these medications are vasodilators and work by increasing blood flow into the penis. Prostaglandin E1 (Caverject, Edex) is easier to obtain; however, it is associated with penile pain in some individuals. The use of combinations of two or three of these medications can decrease the risk of having penile pain.
Aging, liver and kidney problems, and concurrent use of certain medications (such as erythromycin [an antibiotic] and protease inhibitors for HIV) slows the metabolism (breakdown) of sildenafil. Slowed breakdown allows sildenafil to accumulate in the body and potentially may increase the risk of side effects. Therefore, in men over 65 years of age, in men with significant kidney and liver disease, and in men who also are taking medications called protease inhibitors, the doctor will initiate sildenafil at a lower dose (25 mg) to avoid accumulation of sildenafil in the body. A protease inhibitor ritonavir (Norvir) is especially potent in increasing the accumulation of sildenafil, thus men who are taking Norvir should not take sildenafil doses higher than 25 mg and at a frequency of no greater than once in 48 hours. Other medications that may affect the level of sildenafil include erythromycin and ketoconazole.
ED means no erections from masturbation. According to the American Urological Association, ED is “the inability to achieve or maintain an erection sufficient for satisfactory sexual performance.” Huh? That’s absurdly vague. If you define “an erection” as what you see in porn, and “satisfactory sexual performance” as porn sex—instant, hard-as-rock erections that last forever with climaxes always on cue—then just about every guy has ED. What is ED, really? For practical purposes, it means that a man who’s sober (no alcohol or other erection-impairing drugs) cannot raise even a semi-firm erection after extended masturbation.
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.
Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.
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