A 2009 study published in The Journal of Sexual Medicine found less volume of liquid in the body in conjunction with a depressed nervous system, led to a struggle with sexual performance. This is because alcohol can dehydrate the body, decreasing blood volume while increasing the hormone associated with erectile dysfunction — angiotensin. The body is able to work at optimal capacity by staying hydrated, since major biological activities and functions utilize water molecules.
Erectile dysfunction is a condition in which a man is unable to achieve an erection sufficient for sexual intercourse. In some cases the man is able to achieve an erection but unable to maintain it long enough to complete the sex act. Most men experience erectile difficulties at some point in their lives, but this is different from ED. According to the Mayo Clinic, those with ED will fail to achieve an erection at least 25 percent of the time. ED has several causes and alcohol consumption can be one of them.

ED may occur with or without other sexual dysfunction, including decreased libido (decreased interest in sexual activity), orgasmic dysfunction (troubles achieving an orgasm/climax), and ejaculatory dysfunction (problems with the fluid released during sex, including lack of ejaculation [anejaculation], small volume ejaculate, ejaculation that occurs too quickly [premature ejaculation], ejaculate that goes backward into the bladder [retrograde ejaculation] and pain with ejaculation).
No matter what the cause of erectile dysfunction, it is likely to cause feelings of stress and other emotional reactions. It’s also not uncommon for erection problems to cause tension in a relationship, particularly if one or both partners withdraws emotionally and the problem is not talked about. And it’s possible for a man’s renewed ability to have intercourse after a period of no sexual activity to stir up relationship issues.
And be aware that the vast majority of physical or psychological causes of erectile dysfunction are temporary. They may go away as quickly as they occurred. But if anything is bothering you or your partner, you should seek out confidential, professional advice. There is no point in worrying and not doing anything about it. It may just make the situation worse.
Depression and anxiety: Psychological factors may be responsible for erectile dysfunction. These factors include stress, anxiety, guilt, depression, widower syndrome, low self-esteem, posttraumatic stress disorder, and fear of sexual failure (performance anxiety). It is also worth noting that many medications used for treatment of depression and other psychiatric disorders may cause erectile dysfunction or ejaculatory problems.
Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from
ICI therapy often produces a reliable erection, which comes down after 20-30 minutes or with climax. Since the ICI erection is not regulated by your penile nerves, you should not be surprised if the erection lasts after orgasm. The most common side effect of ICI therapy is a prolonged erection. Prolonged erections (>1 hour) can be reversed by a second injection (antidote) in the office.
The association between psychiatric conditions and sexual dysfunctions, including ED, is well known. Data from population-based studies demonstrate a cross-sectional association between depressive symptoms and ED (65-68) and, among men seeking medical care for ED, depression is significantly associated with a greater severity of the impairment in erectile function (69,70). A meta-analysis of the available prospective studies has shown the role of depression as a significant risk factor for development of ED (71). However, the relationship seems to be bidirectional, as also ED has been associated with the occurrence of depression (72). In addition, treatment with PDE5i is related with an improvement in depressive symptoms (72). Most of this evidence comes from studies not specifically designed for the assessment of this relationship in younger men. However, few studies available in younger populations seem to confirm these results. In an internet-based survey, involving more than 800 North American medical students with a mean age of 25.7 years, ED was reported by 13% of them and it showed a significant association with depressive symptoms, whose frequency got higher as a function of ED severity (73). In a population of more than 2,500 very young Swiss men, aged 18–25 years, participating to a survey on sexual function while attending the medical screening for the evaluation of military capability, ED had a prevalence of 30%. Among the possible correlated conditions, mental health showed an independent association, besides the use of medications without medical prescription, a shorter sexual lifespan and impaired physical health (74). The results from this Swiss study were then prospectively extended on a sample of 3,700 men evaluated at baseline and 15.5 months later (75). Among a number of different possible predictors, including life-style, drug abuse, perceived physical fitness and BMI, only perceived impairment in mental health and depression, either newly occurred or continuously present, were associated with both persistence and development of ED (75). In a retrospective population-based study from Finland, involving almost 3,500 men aged 18–48 years, the role of depression as a significant predictor for ED was confirmed, but this study also showed that anxiety plays a significant role and that ED is significantly less frequent in men with a longer lasting sexual life, thus underlining the positive role of sexual experience and self-confidence (76). Anxiety is often involved in the pathogenesis of ED at the beginning of sexual life. In fact, anxiety can lead to an excessive focus on quality of erection, thus providing a cognitive distraction that negatively affects the arousal and consequently the erection itself (77-79). On the other hand, anxiety can result from one or more sexual failures, with loss of sexual confidence, increasing fears and avoidance for sexual experiences that, in the end, lead to an increased probability of new failures, thus creating a vicious circle (77). Cognitive distraction could be also provided by excessive worry for physical, and in particular genital, self-image. In fact, it has been proposed that when most mental energy is focused on monitoring body, psychological resources are distracted from sex, resulting in an impaired functioning (80,81). In line with this cognitive explanation, a recent study conducted on 367 military personnel younger than 40 years showed that a deteriorated genital self-image is associated with sexual anxiety which, in turn, is associated with a higher probability of sexual dysfunction (82).
Sexuality and erection are controlled by multiple areas of the human brain including the hypothalamus, the limbic system, and the cerebral cortex. Stimulatory or inhibitory messages are relayed to the spinal erection centers to facilitate or inhibit erection (5). Two mechanisms have been proposed to explain the inhibition of erection in psychogenic dysfunction: direct inhibition of the spinal erection center by the brain as an exaggeration of the normal suprasacral inhibition and excessive sympathetic outflow or elevated peripheral catecholamine levels, which may increase penile smooth muscle tone and prevent the relaxation necessary for erection (8). Animal studies demonstrate that the stimulation of sympathetic nerves or systemic infusion of epinephrine causes detumescence of the erect penis (6,7). Clinically, higher levels of serum norepinephrine have been reported in patients with psychogenic ED than in normal controls or patients with vasculogenic ED (9).
ED usually has something physical behind it, particularly in older men. But psychological factors can be a factor in many cases of ED. Experts say stress, depression, poor self-esteem, and performance anxiety can short-circuit the process that leads to an erection. These factors can also make the problem worse in men whose ED stems from something physical.
Never ever use Viagra for ED or PE. It has got its own side effects. You can use this successfully for a couple of years to maximum up to 5 years after that our body stops responding to these allopathic salts and I have learnt this thing the hard way. Better way of handling this problem is by using herbal medicines which do not have side effects. Moreover there are herbal medicines which can also cure this problem and there is no need to continue the medicine after it is cured. Shivalik Gold is one such product, you can give it a try.

Can apple cider vinegar treat erectile dysfunction? Apple cider vinegar is thought to have many health benefits, but can it help treat erectile dysfunction (ED)? ED can result from cardiovascular problems, diabetes, and other factors. Apple cider vinegar may help improve symptoms of conditions related to ED. Find out how it may help, and how to use it safely. Read now
Quitting smoking, exercising regularly, losing excess weight, curtailing excessive alcohol consumption, controlling hypertension, and optimizing blood glucose levels in patients with diabetes are not only important for maintaining good health but also may improve or even prevent progression of erectile dysfunction. It is unclear if such lifestyle changes can reverse erectile dysfunction. However, lifestyle improvements may prevent progression of the erectile dysfunction. Some studies suggest that men who have made lifestyle improvements experience increased rates of success with oral medications.
When we say it’s a barometer of men’s health, it’s a signal. It’s an indicator that things may be right or not. And so when a man develops an erectile problem– and we’re talking about something that is occurring over time. It’s not something that just occurred overnight. When it occurs overnight, it’s more often than not a psychogenic, an anxiety reaction.
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. 
Unconventional CV risk factors, such as impaired erections during masturbation and reduced flaccid acceleration, are interesting parameters to implement in Sexual Medicine context, because they can help fill the gap of information on CV risk, left by the conventional risk factors (the so-called residual risk) (38). However, it should be recognized that not all the healthcare professionals who deal with the complaint of ED (i.e., general practitioners, diabetologists, cardiologists, sport physicians, nurses, etc.) have the facilities or competence for the specific assessment of these parameters. In contexts different than Sexual Medicine and Andrology, the assessment of conventional risk factors is certainly more convenient. Metabolic syndrome (MetS) represents a cluster of metabolic derangements easily and commonly evaluated in several different medical contexts. In a population of more than 600 subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for ED, the presence of MetS was associated with an increased incidence of MACE during 4.3 years of follow-up in younger (first tertile of age: 18–52 years) (Figure 3, Panel A and B) but not in middle aged and older men (second and third tertiles of age: 53–60 and 61–88 years, respectively) (Figure 3, Panel B). Similar to MetS, the algorithms for estimating the risk of developing MACE are easily computed and they take into account factors largely available in a clinical setting. In Europe, the most commonly used algorithm is the SCORE, which takes into account age, smoking habits, systolic blood pressure and total cholesterol (26). These parameters are introduced in a calculation tool that returns the 10-year risk of developing the first MACE. The same estimated risk rate can obviously be derived from different combinations and extent of the single risk factors and, as aforementioned, age has a heavy weight in the amount of risk, even when the other parameters are normal. For overcoming this overestimation, the concept of vascular age, based on the predicted CV risk, has been introduced. Vascular age of a subjects with a specific CV risk profile corresponds to the chronological age of a subjects who has the same estimated risk but only due to chronological age, because of the absence of the other modifiable risk factors (i.e., a non-smoker, normotensive and normocholesterolemic subject) (39,40). Vascular age carries the advantage of easily and directly communicating the concept of high relative risk to patients, in particular to younger ones, who are by definition at low absolute risk (“Your CV risk is the same of a man that is 15 years older than you”). Based on this interesting and useful concept of vascular age, we recently studied the clinical consequences of having a high discrepancy between the estimated vascular and the actual chronological age in our population of men consulting for ED. In our sample, a greater difference between vascular and chronological age was associated with higher glucose and triglyceride levels as well as with impaired penile colour Doppler ultrasound parameters, suggesting a CV impairment (41). When evaluating the subset of men for whom information on incident MACE during a mean follow-up of 4.3 years was available, a greater difference between vascular and chronological age was associated with the incidence of MACE in younger, but not in older men (42).
In patients with low testosterone, testosterone treatment can improve libido and erectile dysfunction, but many men still may need additional oral medications such as sildenafil, vardenafil, or tadalafil. Some studies suggest that men with ED and low testosterone may respond better to PDE5 inhibitors when given testosterone therapy; however, this is controversial.
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.
Can red ginseng help treat erectile dysfunction? Red ginseng is a Korean herb that has been touted as a possible remedy for erectile dysfunction. But how effective is it? In this MNT Knowledge Center article, learn about red ginseng, what it is, what research there is on it treating erectile dysfunction, and other health benefits of this herb. Read now
As shown in Figure 2, in younger patients consulting for ED, the organic component plays the predominant role. These data provide evidence for the need to adequately investigate possible organic causes of ED in younger and apparently fit men. The organic causes of ED can be classified into three categories: metabolic and CV, endocrine and neurologic conditions.
If the inability to get or maintain an erection happens to you once or twice, you may not need to see a doctor. Many lifestyle factors, such as stress or drinking too much alcohol, can affect your sexual ability. If you notice the problem is happening on a routine basis and it’s impacting your ability to have a satisfying sex life, then it’s time to consider seeing a doctor.

Sexual dysfunction is common in patients with diabetes mellitus. Vascular, neurological and hormonal alterations are involved in this complication. Many studies showed altered endothelium-dependent and neurogenic relaxations in corpus cavernosum from diabetic patients with erectile dysfunction (ED). This finding has been associated with a lack of nitric oxyde (NO) production and a significant increase in NO synthase (NOS) binding sites in penile tissues, induced by diabetes. Advanced glycation endproducts (AGEs) concur to diabetic vascular complications by quenching NO activity and by increasing the expression of mediators of vascular damage such as vascular endothelial growth factor (VEGF), possessing permeabilizing and neoangiogenic effects, and endothelin-1 (ET-1), with vaso-constricting and mitogenic action. Moreover, the differential gene expression for various growth factors in penile tissues may be involved in the pathophysiology of ED associated with diabetes. Neuropathy is also likely to be an important cause of diabetic ED: morphological alterations of autonomic nerve fibers in cavernosal tissue of patients with diabetic ED have been demonstrated. Finally, androgens enhance nNOS gene expression in the penile corpus cavernosum of rats, suggesting that they play a role in maintaining NOS activity. However, sexual dysfunctions in women with diabetes has received less attention in clinical research. Several studies suggest an increased prevalence of deficient vaginal lubrication, making sexual intercourse unpleasant. Sexual dysfunction is associated with lower overall quality of marital relation and more depressive symptoms in diabetic women.

Like all diabetic complications, ED can occur even when you have followed your doctor’s advice and carefully managed your diabetes. Also like all diabetes complications, ED is less likely to occur with good blood sugar control. Poorly controlled diabetes and high cholesterol increase the chances of vascular complications, which may lead to ED or other circulatory problems. In addition, regular smoking and alcohol use can contribute to ED.
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