In the short term, alcohol relaxes muscles in the penis, letting blood to flow in (which is a good thing). However, alcohol also prevents other blood vessels from closing and trapping all the extra blood. Erections depend on trapping increased blood flow in the erectile tissue of the penis. If you don’t trap that extra blood, you don’t get an erection. In the long run, excessive alcohol consumption can cause liver scarring, high blood pressure, and can damage your blood vessels resulting in erectile dysfunction.
Patients with both ED and cardiovascular disease who receive treatment with an oral PDE5 inhibitor require education regarding what to do if anginal episodes develop while the drug is in their system. Such education includes stressing the importance of alerting emergency care providers to the presence of the drug so that nitrate treatment is avoided.
Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.
Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.
Psychotherapy and/or behavioral therapy may be useful for some patients with erectile dysfunction without obvious organic cause, and for their partners. These may also be used as an adjunct to other therapies directed at the treatment of organic erectile dysfunction. Outcome data from such therapy, however, have not been well-documented or quantified, and additional studies along these lines are indicated.
For the past few months I’ve been dating a lovely man but our relationship is at risk because he can’t get it up. He says he fancies me and always seems turned on. Sometimes he gets hard - but when we try for sex he loses his erection. On the few occasions he has got hard, he doesn’t orgasm. I’ve always been a very sexual person and would like a lot of sex. We’re hardly having any. I find it difficult to orgasm even if he tries other things because I keep thinking. Why can’t he have proper sex with me?
Stop trying to force the erection - it’s not possible to give yourself an erection just by trying hard enough, if it were then you wouldn’t be reading this. An erection is known as an ‘unconscious response’, meaning you can’t control it by thinking about it. In fact focusing on your erection too much is more likely to block it, so try instead to focus something else, such as:
He can follow the common general physical advice: Sleep well, eat well, exercise, and moderate or abstain from drinking and drugs. He can also visit the doctor to see if there’s any medical reason for his condition (anything from heart disease to diabetes and obesity). Sometimes, impotence is a side effect of prescription drugs. If his anxiety is extreme, it never hurts to see a professional therapist. Whenever there’s even a chance of a medical problem, my advice is always: Why not check with a professional?
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.  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.
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Parasympathetic input allows erection by relaxation of trabecular smooth muscle and dilation of the helicine arteries of the penis. This leads to expansion of the lacunar spaces and entrapment of blood by compressing venules against the tunica albuginea, a process referred to as the corporal veno-occlusive mechanism. The tunica albuginea must have sufficient stiffness to compress the venules penetrating it so that venous outflow is blocked and sufficient tumescence and rigidity can occur.
The general medical history is important in identifying specific risk factors that may account for or contribute to the patient's erectile dysfunction. These include vascular risk factors such as hypertension, diabetes, smoking, coronary artery disease, peripheral vascular disorders, pelvic trauma or surgery, and blood lipid abnormalities. Decreased sexual desire or history suggesting a hypogonadal state could indicate a primary endocrine disorder. Neurologic causes may include a history of diabetes mellitus or alcoholism with associated peripheral neuropathy. Neurologic disorders such as multiple sclerosis, spinal injury, or cerebrovascular accidents are often obvious or well defined prior to presentation. It is essential to obtain a detailed medication and illicit drug history since an estimated 25 percent of cases of erectile dysfunction may be attributable to medications for other conditions. Past medical history can reveal important causes of erectile dysfunction, including radical pelvic surgery, radiation therapy, Peyronie's disease, penile or pelvic trauma, prostatitis, priapism, or voiding dysfunction. Information regarding prior evaluation or treatment for "impotence" should be obtained. A detailed sexual history, including current sexual techniques, is important in the general history obtained. It is also important to determine if there have been previous psychiatric illnesses such as depression or neuroses.
The penis contains three cylinders, the two corpora cavernosa, which are on the top of the penis (see figure 1 below). These two cylinders are involved in erections. The third cylinder contains the urethra, the tube that the urine and ejaculate passes through, runs along the underside of the penis. The corpus spongiosum surrounds the urethra. Spongy tissue that has muscles, fibrous tissues, veins, and arteries within it makes up the corpora cavernosa. The inside of the corpora cavernosa is like a sponge, with potential spaces that can fill with blood and distend (known as sinusoids). A layer of tissue that is like Saran Wrap, called the tunica albuginea, surrounds the corpora. Veins located just under the tunica albuginea drain blood out of the penis.
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.
In diabetics, impotence that develops acutely in the setting of hyperglycemia and poor metabolic control is usually reversible. This is not true of the slowly progressive impotence of long-standing diabetes that is a manifestation of autonomic neuropathy. Intracavernosal self-injection of vasoactive drugs such as papaverine, which relaxes arteriolar smooth muscle is a promising new approach to treatment that is particularly suited for diabetic patients whose erectile dysfunction is on a neuropathic basis. It also has been used with success in spinal cord patients.
Surgical intervention for a number of conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply. Erectile dysfunction is a common complication of treatments for prostate cancer, including prostatectomy and destruction of the prostate by external beam radiation, although the prostate gland itself is not necessary to achieve an erection. As far as inguinal hernia surgery is concerned, in most cases, and in the absence of postoperative complications, the operative repair can lead to a recovery of the sexual life of patients with preoperative sexual dysfunction, while, in most cases, it does not affect patients with a preoperative normal sexual life.
A lot of guys don’t want to admit it, but not being able to get or keep an erection happens more often than you’d think. Guys usually have trouble getting or keeping an erection when they’re nervous, scared or worried about something. They might be worried about how they’ll “perform,” or they could be feeling guilty about having sex. They might be afraid of getting a sexually transmitted disease (STD), or, if they are with a girl, getting their partner pregnant. Drugs (including some anti-depressants) and alcohol can also prevent you from getting and/or maintaining an erection.
For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact.
Don’t give up or blame yourself - you shouldn’t assume that your situation is impossible to improve or that your partner is disappointed in you. Studies show as long as you don’t stop trying to engage your partner sexually, they will still respond positively. If you communicate and stay positive you can work with your partner to get the result you’re looking for.
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Geographic, Racial, Ethnic, Socioeconomic, and Cultural Variation in Erectile Dysfunction. Very little is known about variations in prevalence of erectile dysfunction across geographic, racial, ethnic, socioeconomic, and cultural groups. Anecdotal evidence points to the existence of racial, ethnic, and other cultural diversity in the perceptions and expectation levels for satisfactory sexual functioning. These differences would be expected to be reflected in these groups' reaction to erectile dysfunction, although few data on this issue appear to exist.
In patients who either fail to respond to first or second-line therapy, or are not interested in the conservative therapies, penile prosthesis implantation is available. Malleable and rigid implants were available for many years, but in 1973 the world of penile prosthetics took a giant leap forward with the advent of the inflatable penile implant. Most implants done nowadays are of the inflatable variety. Adverse events including malfunction and infection are rare, and patient satisfaction is very high.45
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.
It is essential to discuss erectile dysfunction with your doctor, so any serious underlying causes can be excluded and treatment options can be discussed. Many men are embarrassed discussing this issue with their doctor, or even their partner. Open communication with your doctor, and in your relationship, is important for effectively managing this common problem.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
This inflatable penile prosthesis has 3 major components. The 2 cylinders are placed within the corpora cavernosa, a reservoir is placed beneath the rectus muscle, and the pump is placed in the scrotum. When the pump is squeezed, fluid from the reservoir is transferred into the 2 cylinders, producing a firm erection. The deflation mechanism is also located on the pump and differs by manufacturer.
Conditions associated with reduced nerve and endothelium function (eg, aging, hypertension, smoking, hypercholesterolemia, and diabetes) alter the balance between contraction and relaxation factors (see Pathophysiology). These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.
Currently, placement of a penile prosthesis is the most common surgical procedure performed for erectile dysfunction. Penile prosthesis placement is typically reserved for men who have tried and failed (either from efficacy or tolerability) or have contraindications to other forms of therapy including PDE5 inhibitors, intraurethral alprostadil, and injection therapy.
However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. 
The term "impotence," as applied to the title of this conference, has traditionally been used to signify the inability of the male to attain and maintain erection of the penis sufficient to permit satisfactory sexual intercourse. However, this use has often led to confusing and uninterpretable results in both clinical and basic science investigations. This, together with its pejorative implications, suggests that the more precise term "erectile dysfunction" be used instead to signify an inability of the male to achieve an erect penis as part of the overall multifaceted process of male sexual function.
Psychosocial problems are important and may cause erectile dysfunction by themselves or together with other causes of erectile dysfunction, such as diabetes and heart disease. Relationships are complicated and many factors cause tensions, which can affect sexual relations. For some men, these problems can become ongoing and it can help to talk through the issue with a skilled counsellor. It is important to know that the longer erectile dysfunction is left untreated, the greater the effect on relationships. This is another reason why early treatment of erectile dysfunction is important.
The pathogenesis of organic ED is related to dysfunction of the endothelium. Endothelial cells can become injured through a variety of mechanisms, most of which cause oxidative stress on the tissues. Many of these causes of oxidative stress are related to lifestyle issues which lead to hypertension, diabetes and dyslipidaemia (figure 1). Endothelial cell dysfunction results in reduction of endothelium-dependent vasorelaxation as well as increased adhesion of leukocytes to the endothelium. Endothelial cell injury then leads to a variety of sequelae, including ED, other types of vasoconstriction, atherosclerosis and thrombus formation.18
The Prostate Cancer Prevention Trial was a landmark study by Thompson et al that prospectively assessed the time to developing CVD after the diagnosis of ED. There were 4247 men with no ED at study entry; 2420 developed incident ED (defined as the first report of ED of any grade) over 5 years. Those men that developed ED had a 1.45-fold higher probability of experiencing a CV event compared with men who did not develop ED.27
In some cases, ED can be a warning sign of more serious disease. One study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease. The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. This does not mean every man with ED will develop heart disease, or that every man with heart disease has ED, but patients should be aware of the link.