"Smoking is a short- and long-term cause of erectile dysfunction," warns Feloney. "In the short-term nicotine constricts the blood vessels that you need to get an erection, and in the long-term nicotine contributes to hardening of the arteries that can cause erectile dysfunction." Some approaches for quitting include making a clean break, avoiding the triggers of smoking, trying a nicotine patch or gum, and joining a smoke cessation program.

Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
Alcohol is a depressant, not an aphrodisiac or a libido enhancer. Excessive consumption can interfere with the ability to achieve an erection at any age, and even occasional drinking can make erectile dysfunction worse in older men. Feloney advises using alcohol in moderation: "In small amounts, alcohol can relieve anxiety and may help with erectile dysfunction, but if you drink too much, it can cause erectile dysfunction or make the problem worse."
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.
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).

Ageing is one of the most important unmodifiable risk factors for the development of metabolic disorders and CV diseases. Accordingly, the common algorithms for the estimation of risk of forthcoming diabetes or CV events include age as a factor of the equations (24-29). The weight attributed to age for estimating the risk in these equations is often so significant that younger men are automatically considered at low risk, irrespective of the other possible risk factors. However, even in younger subjects, overlooking the contribution of cardio-metabolic factors to pathogenesis of ED is a mistake that can lead to the loss of the opportunity of early recognition of patients who deserve a change in life-style or a pharmacological correction of risk factors. ED, besides being considered one of the clinical manifestations of metabolic and cardiovascular diseases (CVD), is regarded as an early marker of CV events (17). In fact, according to Montorsi’s hypothesis (30), impairment of penile artery blood flow occurs before that of coronary or carotid arteries, whose diameter is greater and needs longer time to acquire a clinically relevant damage. The clinical consequence of this pathological event is that ED often manifests earlier than myocardial infarction or stroke. In particular, it has been demonstrated that ED occurs on average three years before the first major adverse CV event (MACE) (31). Quite surprisingly, although CV risk increases with ageing, the role of ED as a harbinger of forthcoming MACE becomes progressively less evident. Data derived from almost 2,500 community-dwelling men aged 40–79 years, involved in the Olmsted County study show that ED is associated with an almost 50-fold higher risk of incident heart diseases in men aged 40–49 years, whereas the difference in risk between ED and non-ED men progressively declines in older men (32). The different CV risk associated with ED in different age bands has been confirmed by the meta-analysis of the available longitudinal studies (33). These observations suggest that, in younger men, the role of ED as a marker of CV risk is even more dramatic than in older ones and as a consequence, investigating the presence of metabolic or CV conditions in younger ED patients is pivotal for identifying men in whom an early life-style modification may avoid serious CV consequences. Even more than erection during sexual intercourse, erection during masturbation is considered a physiologic function that mirrors metabolic and CV health. In fact, erections during masturbation are far less affected by relational and psychological components than sex-related ones (34). In a population of subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, more than 2,500 men reported autoeroticism in the previous 3 months. Among these men, the impairment of erection during masturbation was associated with family and personal history of CVD (35), as well as with impaired response to the test with the intracavernous injection (ICI) of prostaglandin E1, which suggests an arteriogenic damage of penile arteries and predicts forthcoming MACE (36). For a subset of these men (n=862), information on the occurrence of MACE during a mean follow-up of 4.3 years was available and those who reported impaired erections during masturbation had a significantly higher incidence of MACE (35). However, when considering separately younger and older men, this association was confirmed only in younger ones, and it was still significant after excluding men reporting severe ED during masturbation (35). This suggests that the impairment of erection during masturbation is a symptom not completely overlapping with sex-related ED and that it can provide different and supplementary information, in particular when assessed in younger and apparently healthy men. Similarly to what is observed for erection during masturbation, acceleration of blood in penile arteries, as measured by the colour Doppler ultrasound in flaccid conditions, is associated with an adverse CV profile in men consulting for ED. A reduction in flaccid acceleration, which can be used by clinicians to objectively verify the arteriogenic origin of ED and to characterize the extent of a self-reported symptom, has been also associated with a future risk of CV events, with the association being significant in younger but not in older men (37).
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.
A man needs to try the medicine at least four times before he concludes that it doesn’t work for him. It is unlikely that a man with diabetes who has other medical problems such as high blood pressure, is taking multiple medicines, and has not had sexual intercourse for several years will be able to have an erection adequate for intercourse the first time he takes a pill. Most men need to try the medicine several times before they have the desired results.

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• Medications: About 25 percent of ED cases are caused by drugs. Many medications, including common medicines prescribed for diabetes and its complications, can cause ED. The most common offenders are blood pressure drugs, antihistamines, antidepressants, tranquilizers, appetite suppressants, and cimetidine (an ulcer drug). In addition, over-the-counter medications, including certain eye drops and nose drops, have been associated with ED. That does not mean you should stop taking these medications! Rather, you should discuss them with your doctor to determine whether a different dosage, an alternate medicine, or additional treatments will resolve the ED.
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