If you bike a lot and have a very narrow saddle on your bicycle, consider switching to a "no-nose seat" which is wider at the back than a conventional saddle, allowing more of your weight to be distributed to the sitting bones. Make sure the seat is level or angled slightly downward and at a height that allows your knee to be just slightly bent at the bottom of the pedal cycle. Raising the handlebars on your bike so that you're sitting upright may also help.
Usually patients will try less invasive alternatives to treat impotence before opting for surgery. These alternatives may include supplements, herbs, lifestyle changes and even medications. In cases where other treatments do not work to resolve ED, surgery might be a last-resort option. Surgery involves implanting a penile prosthesis. This is a saline-filled silicone device or a malleable device. Although the likelihood of serious side effects is considered to be low, certain risks are associated with surgery to correct erectile dysfunction. These side effects may include: anesthetic risk, device infection, and device malfunction or mechanical failure. Some studies have found that five years following surgery around 10–20 percent of men experience device malfunction and failure. Infection rates are low. Around one percent of men who opt for this type of surgery get an infection.
Shape up. Because ED is often linked with restricted blood flow to the penis, keep your heart and arteries in good condition by maintaining a healthy weight, and following a diet high in fruits, vegetables and whole grains. Avoid saturated fats and trans fats. Regular aerobic exercise can improve blood flow to the genitals and reduce any stress that contributes to your ED.
The basis of ED herbal therapies is that they are anti-inflammatory, antioxidant and immunomodulatory, and can stimulate testosterone production. On the other hand, the synthetic drugs act via NO. The principal mediator of the relaxation of corporal smooth muscle of the penis has been shown to be NO, which is released mainly from parasympathetic nerves and endothelium . NO is believed to relax the corporal smooth muscle by activating soluble guanylate cyclase to increase cGMP content [14,15]. Penile rigidity depends on maximizing inflow of blood while minimizing outflow . The increased blood flow in the cavernous sinuses puts pressure on the walls of the surrounding veins, causing the lumen of the veins narrow, temporarily interfering with the flow of blood but causing tumescence. Normally, the parasympathetic nerve produces Ach. Ach acts on muscarinic receptors and nicotinic cholinergic receptors. When the parasympathetic nerve is stimulated, preganglionic neurons release Ach at the ganglion, which acts on nicotinic receptors on postganglionic receptors. Postganglionic neurons then release Ach to stimulate muscarinic receptors of the target organs. The muscarinic receptor M3, present in the endothelial cells and smooth muscle, is activated, and the M2 receptor in the heart may also be activated. This may result in the production of Ach, which can cause endothelial cells to produce NO. Ach released from postganglionic parasympathetic nerves acting through G-protein-mediated muscarinic receptors and nicotinic cholinergic receptors helps to release NO. Normally, M1, M2 and M3 receptors are found in secretory glands, heart, smooth muscle and endothelial cells, respectively. M1, M2 and M3 receptors cause activation of phospholipase C and generate inositol trisphosphate and diacylglycerol, which increase calcium. Activation of M4 may inhibit adenylate cyclase, decreasing the messenger cyclic AMP. This mechanism may be involved in the relaxation and contraction of cavernosal smooth muscle cells.
The neurovascular mechanism of erection is complex and involves multiple factors including hormones, neurotransmitters, elements of the autonomic nervous system (sympathetic and parasympathetic) and vasodilators such as NO. The common causes of ED include psychogenic disturbance with failure to relax cavernous smooth muscle, arterial insufficiency as a result of atheromatous disease, damage to the parasympathetic nervous system, spinal cord injury, diabetes or following pelvic surgery such as radical prostatectomy, radical cystectomy or bowel resection . It is important to note that cavernous nerves are unique in that although they belong to the autonomic nerves system they do not release either acetylcholine (Ach) or norepinephrine; however, they release NO in the penis. NO relaxes the smooth muscle of the corpora cavernosa via cyclic GMP (cGMP), allowing expansion of the cavernosal lacunar spaces, blood flow and erection. Thus, NO is not a direct dilator of the smooth muscle of cavernosal bodies, but it is an important mediator in this process. Erectile function may also be adversely affected by cigarette smoking, excess alcohol consumption, obesity and systemic diseases such as mononucleosis, hepatitis, HIV and cancer. Some men are prone to develop an erection that fails to subside after ejaculation (ie, priapism). The condition is associated with sickle-cell disease and leukemia, or may be a result of intracavernosal injection of drugs such as prostaglandin E1 . Peyronie’s disease causes a physical bend in the erect penis and also contributes to ED.
In one study, men with a Vitamin D deficiency were nearly 33% more likely to have ED. But you don’t need that much sun exposure to get a healthy amount of Vitamin D. As little as 15–20 minutes a day is enough. Taking Vitamin D is a good idea, especially if you are over 65. Vitamin D can also help if you’re obese or dark-skinned (dark skin limits the amount of Vitamin D you naturally, produce)
Generally, erectile dysfunction (ED) is a neurovascular condition directly involving the endothelium of the corpora cavernosal arterial blood vessels in the penis, and is indirectly linked to cardiovascular diseases. The underlying mechanisms of ED are, however, complex and involve psychogenic, neurogenic, hormonal and vascular factors. ED occurs in aging men, with a prevalence of 52% in men 40 to 70 years of age [1-3]. Conditions that may cause ED include hypertension, diabetes, diseases of the prostate and heart, and obesity. ED may also be caused by the effects of certain medications as well as physical injury or anatomical deformity of the penis , or may result from endocrine disorders such as low testosterone, hypogonadism, adrenal insufficiency and hypothyroidism. Changes in blood flow to the male reproductive organs as a result of hardening of the arteries or atherosclerosis, hypertension and hypercholesterolemia may result in ED. It is generally accepted that there are vascular and neuropathic components to the pathophysiology of the disease, and ED has been recognized as a potential indicator of underlying cardiovascular disease. Chronic infections and/or inflammation of the prostate and irritation of the bladder may contribute to the pathogenesis of ED.
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Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Gutiérrez-González, Enrique; Castelló, Adela; Fernández-Navarro, Pablo; Castaño-Vinyals, Gemma; Llorca, Javier; Salas-Trejo, Dolores; Salcedo-Bellido, Inmaculada; Aragonés, Nuria; Fernández-Tardón, Guillermo; Alguacil, Juan; Gracia-Lavedan, Esther; García-Esquinas, Esther; Gómez-Acebo, Inés; Amiano, Pilar; Romaguera, Dora; Kogevinas, Manolis; Pollán, Marina; Pérez-Gómez, Beatriz. “Dietary Zinc and Risk of Prostate Cancer in Spain: MCC-Spain Study.” Nutrients. Jan 2019, 11(1).
Sildenafil citrate, tadalafil and vardenafil hydrochloride are contraindicated in patients with a known hypersensitivity to any organic nitrates (oral, sublingual, transdermal or by inhalation) due to the risk of developing potentially life-threatening hypotension. Concomitant use of PDE-5 inhibitors is contraindicated with HIV protease inhihibitors (indinavir, ritinovir, saquinavir) as well as ketoconazole, itraconazole, cimetidine and erythromycin, because these drugs are potent inhibitors of cytochrome P450 3A4 and can raise the plasma levels of PDE-5 inhibitors. Coadministration of PDE-5 inhibitors to patients taking alpha-adrenergic blockers such as alfluzocin or tamsulosin may lead to symptomatic postural hypotension, including dizziness and lighheadedness in some individuals.
Prescription drugs called “oral phosphodiesterase-5 (PDE5) inhibitors” are considered the “first-line non-invasive treatment” options for patients with ED. These include the drugs that go by brand names: Sildenafil, Vardenafil or Tadalafil. They work by helping the smooth muscle cells lining the blood vessels that supply the penis with blood to work properly. This allows a man to maintain an erection more easily.
Shindel, A. W., Xin, Z.-C., Lin, G., Fandel, T. M., Huang, Y.-C., Banie, L., … Lue, T. F. (2010, February 5). Erectogenic and neurotrophic effects of icariin, a purified extract of horny goat weed (Epimedium spp.) in vitro and in vivo. The Journal of Sexual Medicine, 7(4), 1518-1528. Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/j.1743-6109.2009.01699.x/full