A number of drugs are known to cause ED in patients with DM (Table 1). For example, many EDDM patients are on antihypertensive medications. Replacement of thiazides or beta-blockers with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be sufficient to regain erectile ability.5 Furthermore, discontinuation of selective serotonin reuptake inhibitors, if these drugs are not essential for patient well-being, may be therapeutic. Careful monitoring following drug discontinuation will help to determine if ED is due to the medication or other underlying disorders. The benefits of continued drug therapy with these drugs should always be weighed against the likelihood of causing ED and impacting on the patient's QOL.
The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels.
Normal male sexual function requires a complex interaction of vascular, neurological, hormonal, and psychological systems. The initial obligatory event is acquisition and maintenance of an erect penis, which is a vascular phenomenon. Normal erections require blood flow into the corpora cavernosae and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.
On any matter relating to your health or well-being, please check with an appropriate health professional. No statement herein is to be construed as a diagnosis, treatment, preventative, or cure for any disease, disorder or abnormal physical state. The statements herein have not been evaluated by the Foods and Drugs Administration or Health Canada. Dr. Marchione and the doctors on the Bel Marra Health Editorial Team are compensated by Bel Marra Health for their work in creating content, consulting along with formulating and endorsing products.
This may seem like a lot to manage at a glance, however, just focus on one step at a time. If it is more exercise you want to start with, park your car further away from the front door at work so you have to walk a little more every day. Or go out on a walk to make your phone calls. If you need to eat better, try low-fat meat and chicken for lunch. Just keep it simple and don’t try to do it all at once.
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
Besides mammalian organs, insects and arthropods are also consumed as aphrodisiacs in Eastern medicine. These include scorpions, spiders, beetles, flies and other bugs (32). Penile erections can be observed following administration of neurotoxins as it causes repetitive firing of the somatic, sympathetic and parasympathetic neurons, resulting in autonomic and neuromuscular over-excitation. Scorpions are often used as an ingredient found in herbal wines. However, there is a general lack of literature regarding the consumption of scorpion neurotoxins for potency.
PubMed | Google ScholarSee all References However, other studies have noted that, when blood pressure levels are monitored after initiation of antihypertensive therapy, changes in blood pressure level are not correlated with sexual function.38x38Rosen, RC, Kostis, JB, Jekelis, A, and Taska, LS. Sexual sequelae of antihypertensive drugs: treatment effects on self-report and physiological measures in middle-aged male hypertensives. Arch Sex Behav. 1994; 23: 135–152
Does drinking water improve erectile dysfunction? Erectile dysfunction or ED is a common concern for men. Everyday factors, such as hydration levels, may affect a person's ability to get or maintain an erection. Drinking water may, therefore, help some men with ED. In this article, learn about the link between hydration and ED, and other factors that can cause ED. Read now
Branded Viagra can now be bought over the counter in pharmacies, but please check with your GP first if you have a medical condition. It's important to use a reputable pharmacy, as there is a large market in counterfeit drugs for erectile dysfunction, especially over the internet. These contain varying amounts of the active ingredient and sometimes completely different drugs.
Whereas management of sexual dysfunction in previously untreated hypertensive patients can be a challenging procedure, confronting the same clinical condition in individuals under antihypertensive regime can be even more demanding. In such cases there will always be a question hovering over physicians head. Is hypertension per se, antihypertensive medication or both, the causative factors provoking sexual dysfunction?
In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
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