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Sex therapy can be a broad term. So let us use impotence therapy in this re­gards. The latter is also one form of counseling that you could take advantage and this would mean that you would have to do about ten to twenty minutes of a session on a regular basis. A psychologist can help you in the process. Nor­mally, a session might have to be held every day per week and during the ses­sion, you will be able to receive assignments as a patient in order to do at home and there- fore, you are instructed to read the books about sexuality, touching exercise that are used in order to take the pressure from the person and you will also need to improve the communication sexual skills that you have.

The therapy that you are following could be used to treat the impotence and thus, you will enjoy having normal sleep during the days and you will also manage to have your physical exams ready for all the other preparations. The sex therapy can also be useful when managing several sexual dysfunctions be­cause this will ensure that you are able to pass over the sexual communication skills that you lack, relationship conflicts, worries from work. In such cases, the sex therapy is always a good thing to decide on. There are other similar nat­ural cures for impotence that work very well. One thing to take care here is – that you need to actually evaluate what are the true causes of impotence or ED prevalent in yourself and choose a method accordingly.

Will the impotence therapy fit your needs?

The impotence therapy thing is extremely effective when the men are willing to take part actively in the treatment. For example, you should know that in instances where males are having stress related issues, opening this up to their partners about it has helped ease their issues with the problems and they have started to feel much better about things. If the husband is only going through counseling by himself, then the results might not be that effective. Moreover, the impotence therapy is likely to work in a lot of situations and so, you will be able to find the right answer for your problems. Sometimes, having partic­ipated in a lot of classes of impotence therapy with buy Sildenafil in Canada will help the husband regain confidence in his capabilities and he will be experiencing positive thoughts. When this is has happened, this will mean that the person can now feel more positive and more relaxed about it and thus, he will be able to perform better in bed and thus see his confidence being boost up.

Will the health insurance that you already have?

Some plans that are offered to the general public might offer impotence ther­apy. Once having selected the psychologist, you will be able to receive guid­ance and information from him or her in order to isolate the best medical problems that you might get for that insurance. Also, in such cases, psychol­ogist might have their fees adjusted and thus, you might have to get into your calculation the fees and taxes involved with the sex therapies involved.

Treatment of Premature Ejaculation
Serotonergic Antidepressants

Several scientific articles and reviews have addressed the use of serotonergic drugs in treating patients with premature ejaculation. Data earlier than 1995 on the use of clomipramine were reviewed by Althof and by Harvey and Balon. These data indicate that clomipramine at doses from 25 to 50 mg is effective in prolonging the intravaginal intercourse to at least two minutes in about 70% of men, compared to a 10% improvement in patients treated with placebo. Further, a study by Segraves et al. suggested that the intake of clomipramine could be limited to the day of intercourse. The minimum time between drug ingestion and maximum ejaculatory control, however, has not yet been fully established.

A prospective, doubleblind, placebo-controlled, cross-over design study examined the effect of 25 mg clomipramine, ingested as needed, 12 to 24 hours before anticipated sexual activity (coitus or masturbation) was evaluated in eight patients with primary premature ejaculation, six with combined premature ejaculation and ED, and eight controls. Significant increase in ejaculatory latency from two to eight minutes was reported by men with primary premature ejaculation but not by the other two groups of patients. Clomipramine inhibited nocturnal penile tumescence in all subjects. Moreover, the mechanism(s) by which clomipramine retards the ejaculatory latency is not totally clear. Clomipramine is a tricyclic antidepressant, which also acts centrally at the 5-HT-2 receptor to inhibit serotonin reuptake and thus promotes serotonin activities. Some studies have suggested, however, that clomipramine increases the sensory threshold for stimuli in the genital area, possibly through the inhibition of the adrenergic receptors in the peripheral sympathetic system. The effect of clomipramine on sexual function is not always consistent, and both spontaneous orgasms and ejaculation and anorgasmia have been reported to occur in some patients. Painful ejaculation is another possible side effect to the intake of clomipramine.

SSRIs, have also been used to treat premature ejaculation. Similar to clomipramine, these agents also have the potential for inducing variable effects on sexual function, including spontaneous orgasms and ejaculation, anorgasmia, or painful ejaculation. Further, the earlier reports on treatment of premature ejaculation with antidepressants have been criticized by Althof for the following reasons:

1. relying on the subject’s selfreport of ejaculatory latency;
2. inconsistent adherence to strict controls, dosages, washout periods, or investigator blindness;
3. lack of long-term follow-up;
4. lack of determination of drug effects on psychosocial or other sexual parameters;
5. lack of distinction between life-long and acquired conditions.

More recent reports have been placebo controlled, and one study measured penile sensory threshold, sacralevoked response, and cortical somatosensory-evoked potential testing to gain insight into the mechanism of drug action. In this study, fluoxetine increased the penile sensory threshold, without changing the amplitude and latencies of sacral-evoked response and cortical somatosensory-evoked potential.

Also you can use Viagra with Priligy in Australia to treat premature ejaculation and make your sexual life brighless. Viagra (sildenafil) is indicated for the treatment of erectile dysfunction, defined as the inability to achieve and maintain penile erection required for successful intercourse.

α-Adrenergic Receptor Blockers

The use of α-adrenergic receptor blockers to delay premature ejaculation is based on the understanding that the sympathetic nervous system is responsible for the peristaltic movement of the seminal fluid through the male genital tract. Shilon et al. administered phenoxybenzamine to nine men with premature ejaculation, seven of whom reported an increase in their ejaculatory latencies. Cavallini reported the effects of treatment with two other α-1-blockers (alphuzosin and terazosine) on premature ejaculation in 91 men who were resistant to psychological therapy. The study was a double-blind, placebo-controlled, cross-over in which each drug and placebo were administered for two months. Approximately 50% of patients and their partners reported improved ejaculatory latencies for both α-blocking agents, as compared to approximately 13% for patients on placebo. Side effects, mainly hypotension and epigastric pain, were experienced by about 5% of patients on active drug. Another side effect of α-receptor blockade reported in the above referenced study with phenoxybenzamine is dry ejaculation (ejaculation without expulsion of the seminal fluid). These preliminary studies suggest that the effectiveness of α-blockers in treating premature ejaculation is close to that seen in treatment of benign prostatic hyperplasia. The final assessment of the role of α-receptor blocking agents in treating premature ejaculation, however, must await the results of large well-controlled trials to examine both efficacy and safety of long-term use.

Beyond hypertension, ED may also predict the presence of occult coronary disease. One study evaluated 50 men with ED and no clinical signs of cardiovascular disease. The men were age 40–60 years and underwent cardiac stress testing and coronary angiography.

Eighty percent of the men demonstrated significant cardiovascular risk factors. Stress testing showed myocardial ischemia in 56% of these men. Coronary angiography was performed in 20 of the men with ischemia. Angiography revealed left main stem or severe three-vessel disease in 6 of 20, with some degree of significant coronary artery disease (CAD) in 40% of the total. It is important to note that none of these 50 men showed any clinical signs of ischemic heart disease prior to this testing that was prompted only by the presence of ED.

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Thompson et al. reported a secondary finding in a randomized study of almost 10,000 men age 55 or older enrolled in the Prostate Cancer Prevention Trial.

The secondary finding was a direct association between ED and subsequent cardiovascular disease. Eighty-five percent of the men had no cardiovascular disease at the start of the study, with 47% of these men having ED at that time. Incident ED that occurred during the first 5 years of the study was associated with a 1.25 increased risk of subsequent cardiac event during follow-up. In reference to subsequent cardiovascular events, the risk was 0.015 per personyear among those without ED at study entry, and was 0.024 per person-year for those with preexisting ED at the time of study entry. These authors stated that this increased associated risk was similar to the risk associated with smoking or a family history of myocardial infarction, thus clearly echoing the concept that ED should prompt cardiac investigation in these patients.

A smaller investigation using 285 patients looked at the specific extent of CAD in relation to ED. They divided patients into age-matched groups based on acute single vessel disease, acute two or three vessel disease, or chronic coronary syndrome. A control group included those with normal angiography but with suspected CAD. They found that both multiple vessel disease and chronic coronary syndrome were independent predictors of ED. They also found that, in patients with established CAD, clinical presentation of ED comes before CAD in the majority of these patients by an average of 2–3 years.

Although ED has been found to affect about 75% of patients with chronic CAD, the topic is not generally an accepted part of cardiologists’ patient evaluation. Reportedly 25% of these patients experience severe ED. The same study also delved into specific cardiac disease states and their association with various degrees of ED. They found that ED had a prevalence of about 60% in men with a history of prior myocardial infarction or coronary artery bypass surgery.

These authors echoed the assumption that these outcomes were related to endothelial dysfunction and atherosclerosis. They also theorized that the endothelial damage that occurred as a result of smoking, hypertension, lipid disorders, and diabetes diffusely affected vasculature of the body, including the arterial blood supply to the corpora cavernosa of the penis. They warned that ED may be the warning sign for undiagnosed CAD.

Hypertension Erectile dysfunction has a high prevalence among patients with both treated and untreated hypertension. Large studies have confirmed that, not only was ED more prevalent in patients with elevated blood pressure than controls, but also that the degree of ED that experienced by patients with hypertension was also more severe in nature than in the general population.

One study highlighted the specific penile vascular effects of hypertension through the use of rat models.
The study found that hypertensive rats demonstrate impairment in endothelial-mediated relaxation of corporal cavernosal strips in response to acetylcholine. This finding suggested that a defect exists in endothelial-dependent reactivity as well as a reduction in nitric oxide in the presence of hypertension.

It is somewhat more difficult to evaluate the exact effect of hypertension on erectile function in humans. Patients are often being treated for their hypertension with medications that are themselves known to cause ED, such as beta blockers and thiazides. It is likely that the ED experienced in hypertensive men is caused by penile vascular arterial changes including atherosclerosis Obesity Obesity, which is an independent risk factor for cardiovascular disease, is also associated with ED. Esposito et al. showed that intervention with the modification of lifestyle behaviors that led to weight loss and decreased cardiac risk also led to the improvement in erectile function.

A decrease in body mass index may reduce the risk of both ED and endothelial dysfunction in obese men.
If obesity is positively associated with endothelial dysfunction and increased serum concentrations of vascular inflammatory makers, with what has been previously aforementioned, it would appear that a common pathway exists – patients suffer from both increased cardiovascular risk and ED per similar physiologic pathways.

In a more recent publication, Esposito et al. stated that obesity increases ED risk by 30–90% compared to controls. The authors again agreed that lifestyle changes aimed at reducing body mass index improves both erectile and endothelial function in men. In addition, they mentioned that Mediterranean-style diet may aid sexual function.

A separate literature review in 2006 was completely dedicated to the topic of the Mediterranean-style diet and its relation to sexual function. They found that sexual function can improve in as little as 2 years through exercise and adoption of the Mediterranean-style diet. Specifically, men consuming more fruits, vegetables, nuts, whole grain, and olive oil as compared with controls were found to have an improved endothelial function score and improved levels of inflammatory markers.

Atherosclerosis The most common recognized cause of ED is atherosclerosis. Atherosclerosis is known to be associated with such cardiovascular diagnoses as hypertension and dyslipidemia, which produce oxidative stress and damage to the endothelial cells.

The underlying pathophysiology seems to stem from endothelial cell dysfunction, which would be a common factor between general cardiovascular disease and ED. Failed vasodilation seen in ED is a direct effect of the inability of smooth muscle cells lining the arterioles to relax. Atherosclerosis has been found to be associated with up to 40% of cases of ED in men over age 50.

Cholesterol One group looked at cavernous biopsies of rabbits after three months of a cholesterol-rich diet versus controls. The control group showed normal muscle cells on biopsy while the high cholesterol group showed muscle cell degeneration. This tangible evidence of direct effect of high cholesterol diet on cavernous muscle cells suggests that abnormalities in lipid metabolism has a direct effect on cavernous smooth muscle cell degeneration, thus contributing to ED.

Hypercholesterolemia is a known direct risk factor for cardiovascular disease. Erectile dysfunction in association with hypercholesterolemia was documented in a group of healthy men with no known cardiac risk factors.

These otherwise healthy men with ED were found to have abnormal cholesterol levels at a rate of 60%. In addition, over 90% of these men with abnormal cholesterol levels were also noted to have penile arterial disease on Doppler ultrasound.

Saltzman et al. evaluated men with ED in which their only known risk factor was hypercholesterolemia. They were able to meet their treatment goals of total cholesterol less than 200 mg/dl and LDL less than 120 mg/dl. They found that ED improved in men with hypercholesterolemia when treated with a statin drug.

The resulting decreased cholesterol levels improved ED while also decreasing overall cardiovascular risk. Primary care physicians may theoretically have more success with patient compliance of statin drugs for current improved sexual function than for future cardiovascular risk. Of note, there is also contradicting evidence, based on literature review, that statins and fibrates may actually cause or worsen ED.

Should this be the case, it would be very difficult to determine the effect of cholesterol on ED, as in order to treat a known risk factor of ED, we may be in effect worsening ED with the use of medication.

Over the past decade, there has been an increased interest and focus of urologic research on the field of ED. Particular focus has been on ED and its correlation with cardiovascular disease. Many disease states already known to be associated with ED are also associated with cardiovascular disease. These disease states include hypertension, atherosclerosis, diabetes, peripheral vascular disease, obesity, sedentary lifestyle, and myocardial infarction.

The latest research has been aimed at verifying a direct correlation between ED and cardiovascular disease. There has even been suggestion that ED is often the first clinical manifestation of underlying cardiovascular disease in up to 30% of men presenting with erectile dysfunction. If so, it would be increasingly important for men to disclose symptoms of ED to their primary care providers, as ED might represent an opportunity to evaluate these men for cardiovascular disease. Unfortunately, a reported 90% of men with ED do not discuss this information with their primary provider.

It can be speculated that the reason for underreporting ED is due to patients’ embarrassment in addressing sexual issues with a healthcare provider. Other possibilities are that patients believe the issue resolves without intervention, or that ED is just a normal symptom of aging. Doctors caring for these patients may then be missing the opportunity to prevent cardiovascular morbidity and mortality.

The MMAS of the early 1990s opened the door to increased awareness of the correlation between ED and cardiovascular disease.

This study was the first large scale, population-based study investigating ED, revealing that increased prevalence of ED correlated directly with increasing age. The study evaluated 1,290 randomly selected men and found a clinically significant correlation between ED and other medical comorbidities independent of age. These comorbidities included hypertension, hypercholesterolemia, diabetes, and cardiovascular disease. Patients treated for hypertension had a 15% likelihood of also having complete ED and those with cardiac disease had a 39% likelihood of ED.

Schouten recently conducted a longitudinal, population-based study focused specifically on erectile rigidity as an independent indicator for upcoming cardiovascular events. They found that severely reduced erectile rigidity had a hazardratio of 3.8 for the presentation of cardiovascular disease within 6 years. They agreed that a single question focused on the presence of ED should be incorporated into cardiovascular risk assessment in men. They also stated that men presenting only with the complaint of ED should be evaluated for cardiovascular risk

Risk factors for ED have been delineated in large prospective studies, such as Massachusetts Male Aging Study (MMAS), Boston Area Community Health Survey (BACHS), and Health Professionals Follow-up Study (HPFS). The MMAS study reported on males between ages 40 and 70 years and found that erectile function declined precipitously with age. Overall, the study found that 52% of men within this age range suffered from some degree of ED. Diabetes, heart disease, and hypertension increased the risk of ED significantly in this study.

Erectile dysfunction was studied in men aged 45–70 years with a 14-year follow-up in the HPFS. Excluding men who developed prostate cancer, the relative risk (RR) of development of ED as per self-assessment was 1.5 for current smokers and 1.9 for obese men. In contrast, moderate exercise decreased the risk of ED. Interestingly, these risk factors produced greater effect in men 55 years or younger.

The BACHS was created specifically to assess urologic symptoms in a diverse cohort.

• This study found a dose-response effect of tobacco cigarettes on ED, although there was not a significant increase in the odds of developing ED until over 20 pack-years of the habit.
• They also found that low socioeconomic status, independent of other risk factors, including race, was a risk factor for ED.

Erectile Physiology A successful male penile erection requires two processes. Cavernosal artery smooth muscle relaxation and increased venous outflow resistance. In order to sustain an erection one must achieve and maintain a high arterial inflow and a low venous outflow. Cavernosal arterial smooth muscle relaxation is an active process and the initial event of an erection. viagra tablets online

1. Smooth muscle relaxation leads to arterial dilation which results in increased penile blood flow that in turn causes radial and longitudinal cavernosal expansion. This process is mediated by nitric oxide released through stimulation of nonadrenergic, noncholinergic nerves (NANC).

2. Nitric oxide binds to smooth muscle cells stimulating the production of cyclic GMP, which then decreases intracellular calcium and causes relaxation. Cyclic AMP, a second minor messenger, acts in a similar manner to decrease intracellular calcium and causes muscle relaxation.

Venous outflow resistance, in contrast to arterial smooth muscle relaxation, is a passive process. As the cavernosal tissues engorge and expand, they compress the subtunical venous sinuses and cause the outflow resistance necessary to maintain an erection.

Understanding the psychological aspects of ED requires understanding the connection between the brain and the penis. There are two basic inputs leading to sexual arousal and, therefore, erections. One is physiological and results from direct stimulation of the penis. This reflexogenic input is centered in the sacral regions of the spinal cord and is primarily under parasympathetic nervous system control.

The other is psychological and results from mental experiences in the brain which are transmitted to the penis. This psychogenic input is mediated in the cerebral cortex. The brain is the source of both excitatory and inhibitory influences on erections. The inhibitory pathway is under serotonergic control, while the excitatory pathway is under the influence of the neurotransmitter oxytocin. The medial parietooccipital region of the limbic system has a primarily inhibitory role, such as in the fight-or-flight response. The sexual centers of the brain, particularly the midbrain, hypothalamus, and amygdala respond to gonadal hormones and, thus, are part of the hormonal feedback system that shapes sexual behavior. The reticular activating system has an important triage role through its connections between higher and lower brain structures as they process sexual stimuli.

These connect to one of two coordinating nerve centers along the spinal cord. More simply stated, erections are the result of friction and fantasy. An implication of these two inputs to erectile response is that mental experiences, i.e., thoughts, feelings, memories, and fantasies, have a central role in normal sexual response and are crucial factors in the development of sexual dysfunctions.

Bancroft and Janssen have proposed a dual control model of erectile function that includes both excitatory and inhibitory influences on sexual response, which is similar to the model of CNS control over erections described above. This model emphasizes that higher brain functions (e.g., thoughts and feelings) can impact erectile response positively or negatively. For example, a common manifestation of ED is the man who, while experiencing sexual arousal, becomes anxious about his performance and loses his erection.

The inhibitory influence of sympathetic nervous system arousal on erectile response is the biological basis to many of the psychological origins of ED.

Everhard and colleagues have posited a complex feedback process for sexual arousal that incorporates physiological response, the immediate situation or context, emotional arousal, and cognitive appraisal. This understanding of the neurological control involved in sexual response highlights the interdependence of psychological and physiological aspects of ED.

Because the brain is intimately involved in the control of erections, a wide variety of psychological factors impact erectile response and may lead to erectile dysfunction (ED).

This chapter reviews the assessment of psychological factors in ED, the immediate and underlying psychological conditions involved, and the development of ED over time. Outcome research on psychological treatments for ED is also reviewed. The goal of the chapter is to help health care providers to conduct a comprehensive evaluation of ED that is sensitive to psychological factors.

A comprehensive understanding of erectile dysfunction (ED) must incorporate both the physical and the psychological aspects of erectile response. An erection is best characterized as a psychophysiological phenomenon that depends on a complex interplay of biological and psychological factors. Impairment in any of these aspects may lead to erectile dysfunction. The focus of this chapter is on the assessment of psychological factors that contribute to erection difficulties. The evidence regarding the outcome of psychological treatments and the integration of medical and psychological treatments are also reviewed.

The definition of psychological factors to be used here encompasses a variety of mental aspects of sexuality.

1. First are the behavioral aspects, which primarily involve who does what to whom in the sexual encounter.
2. Second are the emotional aspects of the sexual response, that is, feelings during sex, as well as the emotional needs associated with sex.
3. Third are the cognitive aspects of sexual response, which include knowledge, beliefs, and attitudes about sexuality.
4. Fourth are the interpersonal aspects, i.e., the couple’s interaction and the quality of the relationship, both sexual and emotional.
5. Fifth are the cultural aspects of sexuality, which entail the expectations and norms that shape sexual behavior.

It is also important to note that, while most of these aspects of sexuality are either observable or may be described by the patient, much of what is referred to as psychological is either unconscious or inaccessible to the individual himself.

Nitric Oxide NO is emerging as an essential neurotransmitter within the CNS for erectile response. NO appears to act in several regions of the brain, including the MPOA and PVN.

Injection of NO-synthase (NOS) inhibitors into the PVN prevents penile erection induced by dopamine agonists and oxytocin.

NO production increased in the PVN of rats during noncontact erections, confirming the role of NO production during erection.

ACTH and a-MSH Adrenocorticotropic hormone (ACTH) and its related peptide a(alpha)-melanocyte stimulating hormone (a-MSH) have been shown to elicit erectile responses in addition to increased grooming, stretching, and yawning behaviors when given intracerebroventricularly to lab animals.

This proerectile effect appears to be due to the stimulation of melanocortin-3 (MC3) receptors which are prevalent in the hypothalamus and limbic system. The role of these peptides in erectile response is not entirely known, but they appear to induce erection by acting at sites distinct from those in the PVN stimulated by dopamine and oxytocin.  Additionally, Melanotan II, an a-MSH synthetic analog, has had proerectile effects in humans with psychogenic impotence.

Other Neurotransmitters Excitatory amino acids, such as l-glutamate, N-methyl-d-aspartate (NMDA), amino-3-hydroxy- 5-methyl-isoxazole-4-propionic acid (AMPA), and trans-1-amino-1,3-cyclo-pentadicarboxylic acid (ACPD) have been shown to have proerectile effects when injected into the MPOA or PVN of lab animals. Gamma-amino butyric acid (GABA) appears to function as an inhibitor in the reflex pathways for penile erection. Stimulation of opiod m receptors appears to centrally prevent penile erection and impair copulation likely through the prevention of the increased NO production in the PVN during sexual activity.