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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.

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

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.

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.

Paraventricular Nucleus The hypothalamic paraventricular nucleus (PVN) contains premotor neurons that project from the parvocellular layer directly into the spinal cord.

These neurons have been shown to contain a variety of neurotransmitters: oxytocin, vasopressin, enkephalins, and dopamine. In rat models injection of a variety of neuromediators (oxytocin, glutamate, nitric oxide, dopamine agonists) into the PVN has been shown to elicit penile erection.

Additionally, in both rats and monkeys, stimulation of the PVN elicits erection. Lesion of the parvocellular layer of the PVN causes longer latencies and fewer noncontact erections in rats. Parvocellular PVN neurons have been shown to respond to stimulation of the dorsal nerve of the penis in rats, suggesting that the PVN may be a supraspinal reflex center for erections.viagra professional Canada

The PVN also receives input from the medial preoptic area (MPOA) suggesting that the PVN serves to integrate MPOA input before sending it downstream via autonomic pathways selectively activated within the PVN Medial Preoptic Area The MPOA of the hypothalamus is key to sexual behavior.

In rats and monkeys, MPOA stimulation elicits erection. In monkeys, increases in MPOA neuronal activity have been recorded during erection. Interestingly, MPOA lesions do not affect reflexive or noncontact erections.

All of this has led to debate as to the role of the MPOA in erectile function. The emerging theory is that the MPOA likely serves as an integration center of hormonal and sensory inputs for sexual behavior and redistributes these signals to the hypothalamic and brainstem structures thought to be more directly linked to erectile control, such as the PVN.

Other Supraspinal Centers Many other supraspinal areas have been shown in animal studies to be related to erectile function. In monkeys, isolated stimulation of the medial dorsal nucleus of the thalamus, ventral tegmental area, precallosal cingulate gyrus, and subcallosal and caudal gyrus led to erections.

Hippocampal stimulation in anesthetized rats increased intracavernous pressures as did desynchronization of the somatosensory cortex following cocaine administration. A center for descending the inhibition of spinal sexual reflexes has been localized to a group of neurons in the paragigantocellular reticular nucleus of the ventral medulla.

The exact role each supraspinal area plays in mediating erection is currently unclear. However, it is apparent that there are extensive interconnections between many supraspinal centers that contribute to descending pathways and exert powerful control, both inhibitory and excitatory, on the spinal responses driving erection.

Erectile dysfunction features among the most common and most troubling male sexual disorders. The inability to have and maintain an erection affects sexual life, confidence and ultimately – a relationship with a partner.

If you are suffering from erectile dysfunction, you have probably researched and tried a medley of pills and treatments. Some of them tend to be somehow effective, others miss the mark. You have probably heard about black ant pills and their ability to counter sexual problems but you are wondering whether these really work.

In order to find the answer to these questions, you will first have to understand erectile dysfunction. Figuring out the causes of the problem will help you choose the most efficient solution. You should also understand that male enhancement pills do work, as long as you choose real quality.

Definition and Causes

Erectile dysfunction is a serious sexual problem that appears to be affecting more men now than it used to in the past.

Nearly all men experience occasionally the inability to have or sustain an erection. If it happens a single time, there is no reason to worry. Stress, emotionality and other external factors could interfere with the ability of a man to have a satisfactory intercourse. Erectile dysfunction becomes a problem when it occurs on a regular basis and it interferes with the sexual activity of an individual.

The problem is exceptionally troublesome because many individuals consider it to be ‘shameful’ and refrain from seeking assistance.

Erectile dysfunction is caused by circulatory problems that prevent blood from reaching the penis, nerve diseases, psychological factors, as well as penis injury. Some medications can also result in the inability to have an erection. Psychological factors do get aggravated if an individual finds it impossible to handle the situation in a quick and efficient manner. This is when assistance has to be sought, preferably involving the selection of a proper treatment like the black ant sex pills.

Some Erectile Dysfunction Statistics

Statistics show that one out of 10 men suffers from erectile dysfunction. The number of people that are experiencing erection problems in the US solely totals 30 million. The figure is quite impressive, ranking erectile dysfunction among the most common sexual problems.

Some diseases increase the chance of erectile occurring. Nearly 50 percent of the men suffering from diabetes experience erection problems. Another factor that increases the risk of erectile dysfunction is age – the chance of it occurring increases dramatically after the age of 65.

Smokers are another group of men that tend to experience erectile dysfunction more commonly than others. According to statistics, the smokers of one pack of cigarettes per day are 50 percent more likely to experience erection problems than men of the same age group who are non-smokers.

Black Ant Male Enhancement Pills and Erectile Dysfunction: Myths and Facts

Herbal pills have been around for some time but as male sexual problems are becoming more prominent, this treatment is gaining popularity.

Black ant male enhancement pills feature among the most demanded erectile dysfunction treatments. This is an all-natural supplement that contains a mix of herbs popular among Tibetan healers. Some of the main ingredients are saffron, a blend of Chinese herbs, caterpillar fungus, Tibetan yak testis and deer penis.

The regular taking of Black Ant pills results in bigger erections, higher sexual stamina, intense orgasm and powerful ejaculations. These male enhancement pills are also suitable for the treatment of premature ejaculation.

It all sounds great but do the black ant pills really work? The pill has to be taken approximately 30 minutes before the expected intercourse. The ingredients produce results for several hours, which will be sufficient for satisfactory sexual performance. Chinese medicine is known for its reliance on herbs and all natural products. Most of these traditional remedies are highly effective and the same applies to black ant products.

The bottom line is that there is no risk involved because black ant pills are all-natural. Apart from successfully treating erectile dysfunction, these herbal pills can also affect a number of health conditions, including problems of the cardiovascular system. Taking a single pill every day for a specific period of time will produce consistent and sustainable results; significantly improving your sexual life and helping you combat one of the most common and most devastating sexual problems for men.

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So it is very important to make the right choice by getting the best tablet for you and lead a very happy and satisfying sexual life. It is also very important that you come in contact with your family doctor before you wish to take this tablet. He or she would be the best person to guide you. Do remember to read the different reviews that people provide after taking the tablet. In this case you can remain quite confident that you have chosen the right place to get it ordered online. Show your inner power and make your partner satisfied on bed.

Most guys with erectile dysfunction have it backwards. They see or are told about increased effects of having lost control of their erection & sexual energy – the impulses & sensations within their body – and mistakenly believe these same effects are causing their weakened erection.

The effects of aren’t linear – they can definitely add to and even speed up what the cause of erectile dysfunction is doing. But mistaking them for the cause is what stops an effective erectile dysfunction treatment from making any difference.

Let’s look at a handful of common examples.

Erectile Dysfunction ‘Cause’ #1: Medical Conditions (like diabetes and hypertension)

Anywhere between 35-50% of guys with diabetes suffer erectile dysfunction. It’s attributed to high blood-sugar levels where something called arteriosclerosis, the thickening and hardening of the walls of the arteries, can come about. Around 15% of men with high-blood pressure from hypertension suffer erectile dysfunction.

Now, there are diets that help diabetes, for example, as demonstrated in the documentary “Raw for 30 Days” (even though it’s not recognized by mainstream medicine). However, if someone applied that particular diet and their blood-sugar levels dramatically reduced, they would still most probably respond to the sexual impulses in their body in the same way that led to them to indulge in high-sugar foods.

The more common effect of this mistaking tension for ‘strength’ and weak erections follows.

Erectile Dysfunction ‘Cause’ #2: Drugs

Indulgence in drugs that are an effect of ED include pharmaceutical and recreational, and also combining the two. Read that again.

I was pointing out that guys are compelled to take drugs of any kind because they have lost or are in the process of losing control over the sexual impulses in their body, which will make a flailing erection worse. Like, for example, taking Viagra and Ecstasy together.

What about other drugs that apparently relax the body? Marijuana, while it’s natural and relaxes the body, and in the moment it might make you feel more horny where you’re willing to indulge in your senses more than normal, will make your penis limp in the long-term.

It’s just like heroine, cocaine, amphetamines, opiates, barbiturates and many others that can feel good in the moment and seem like they increase libido – eventually they will take their toll and train your body to rely on external forces rather than the natural systems within your body.

Erectile Dysfunction ‘Cause’ #3: Smoking & Alcohol

Of course, these are just another form of drug. But they are the most prevalent because they are legal (even though, statistically, they kill more than all other drugs combined!).

Cigarettes harm and hamper circulation and blood supply and contribute to hardening of the arteries, including those in the penis. Aside from the obvious lung cancer, they also increase disorders of the blood vessels.

And like other recreational drugs, alcohol can temporary relax you which may seem to help your erections but, long-term, it depresses your central nervous system and impairs your sexual function – ‘drinkers’ droop’ is a real long-term effect.

It seems that because sometimes there is a seemingly immediate positive effect after consumption, the tendency to try to recreate and increase the resulting feeling causes guys to over-do it and they stuff up their natural libido.

Erectile Dysfunction ‘Cause’ #4: Hormonal Imbalances

While testosterone doesn’t directly dictate libido levels (think of young boys who get erections yet have close to zero testosterone) it does affect dopamine levels which can tend to artificially trigger the erection chain-of-command.

By age 40-50, testosterone levels begin to decline until 70 years old where it’s about 30% of what it was. This seems to correlate with increased instances of erectile dysfunction in older men. Yet, only about 5% of men who seek medical treatment for erectile dysfunction are testosterone deficient.

Again, there is a gap in perception about an ED cause and a consequential effect.

Erectile Dysfunction ‘Cause’ #5: Psychological Factors

Stress, anxiety, guilt, depression, low self-esteem, fear of sexual failure, all represent 10-20% of cases of men with erectile dysfunction. But nobody points out or even asks about the root cause of why these negative mental states come about in the first place and apparently sustain themselves.

They are treated as self-standing.

It’s true that with performance anxiety your brain releases chemicals that constrict the smooth muscle of the penis and its arteries. This decreases blood-flow into the penis and, also, increases blood-flow out of the penis, which equals a reduced erection.

But as stated above, the effects aren’t linear – that is, they can definitely add to and even speed up what the cause of erectile dysfunction started. They are still just effects though.

The question is: Effects of what?

What Is This Cause Of Erectile Dysfunction?

Well, often if there is an existing physical problem then mental tension, in whatever form, will make it worse (and vice versa), which brings up the crux of the conflicting information on erectile dysfunction.

You don’t have lack of control over your penis and sexual libido because of some other problem… you have some other problem (or two) because you’ve gradually lost control of your penis and libido. After all, sexual energy is the most powerful and potent force available to man.

The effect of having lost control over your sexual energy spreads and materializes to other areas of your life, like the 5 points listed above (although we could name many more). But the root problem or cause of erectile dysfunction is how you physically and mentally relate to impulses within your body, or more specifically, the lack of impulses.

The extreme case of this is a public figure who holds a powerful position, who is more than wealthy enough, and who has a lovely wife & kids. Then one day a ‘scandal’ breaks out that he was fooling around with his personal-aid. And he loses everything he had.

He was compelled to react to his impulses despite the obvious risks of being ‘caught’ because, like guys who suffer erectile dysfunction, the public figure had lost control over his sexual energy. Now, he might patch things up with his family. He might recover politically and bounce back financially.

However, unless he becomes conscious of the connection he has with the sexual impulses & sensations in his body, he’s in exactly the same boat as a man with erectile dysfunction – he is dealing with effects and his negative sexual history will only get worse.

In Conclusion

I’m not saying one should ignore the effects of things like smoking cigarettes, over-consumption of alcohol, diabetes, others listed above and more because the nature of a weakened erection is cyclical – effects help to feed into the cause, just like mental and physical factors, which is where confusion comes in.