Currently, there are four orally active drugs are available to treat ED. These include: sildenafil citrate (Viagra [Pfizer, USA]), vardenafil hydrochloride (Levitra [Bayer, Germany]), tadalafil (Cialis [Eli Lilly, USA]) and avanafil (Stendra, Spedra [Vivus Inc, USA]). These drugs inhibit the enzyme phosphodiesterase type 5 (PDE-5), which is responsible for the hydrolysis of cGMP. PDE-5 inhibitors and cGMP act as effectors of dilation of smooth muscle of cavernosal bodies. PDE-5 inhibitors are contraindicated in patients taking any kind of nitrate therapy for angina, and may not be appropriate for men with certain health conditions, such as severe heart disease, heart failure, history of stroke or heart attack, uncontrolled high blood pressure or diabetes, and patients with pigmental retinopathy. PDE-5 inhibitors are less effective in men with diabetes and men who have been treated for prostate cancer. PDE-5 inhibitors are also not effective in men with retinitis pigmentosa, a genetic disease involving PDE-5 deficiency. The common side effects of PDE-5 inhibitors include gastrointestinal upset, headache, nasal congestion, back pain and dizziness. The PDE-5 inhibitors may interact with other medications including antihypertension drugs. Nonetheless, the PDE-5 inhibitors are generally safe and effective for most men. The primary mechanism of action of these drugs is through the mediation of NO. NO is one of the key molecules involved in ED. It is a short-lived, highly permeable, pleiotropic, gaseous molecule, secreted from the postganglionic cavernosal parasympathetic nerves, endothelium of the cavernosal blood vessels, platelets in the cavernosal sinuses and phagocytic cells (monocytes, macrophages and neutrophils). NO acts on platelets to inhibit platelets adhesion and aggregation. NO causes relaxation of the smooth muscle of the cavernosal blood vessels of the penis, leading to vasodilation, tumescence and stimulation. Release of NO in the corpus cavernosum of the penis during stimulation activates the enzyme guanylate cyclase, which results in increased levels of cGMP, producing smooth muscle relaxation in the corpus cavernosum and resulting in increased blood flow (5). NO is mainly produced from cavernosal nerves, which are nonadrenergic, noncholinergic nerves within the penis, and acting via its second messenger cGMP. It has been suggested that maintaining normal body weight and mild exercise, as well as dietary supplementation of folic acid, zinc, calcium, vitamin C, vitamin E and L-arginine, a precursor of NO, can support the biochemical pathway leading to NO release . NO is an effector molecule that is involved in a number of intracellular functions such as vasorelaxation, endothelial regeneration, inhibition of leukocyte chemotaxis and platelet adhesion . A small proportion of autonomic nerves do not release either Ach or norepinephrine . For example, the cavernous nerves predominantly release NO in the penis. The exact mechanism is not known, but it is believed to be through increased intracellular calcium. Another gaseous molecule produced in the corpora cavernosa is hydrogen sulphide (H2S), which is also known to be involved in erectile function . H2S activates ATP-sensitive potassium channels in smooth muscle cells. Some reports indicate that NO acts in large vessels and H2S in small vessels. A high level of tumour necrosis factor-alpha has been shown in ED patients . Although current ED therapies using PDE-5 inhibitors are safe and effective, approximately 40% of ED patients do not respond to currently available treatment [11,12]. For these patients, herbal therapy may be useful.
Reiter, W. J., Pycha, A., Schatzl, G., Pokorny, A., Gruber, D. M., Huber, J. C., & Marberger, M. (1999, March). Dehydroepiandrostone in the treatment of erectile dysfunction: A prospective, double-blind, randomized, placebo-controlled study [Abstract]. Urology, 53(3), 590-594. Retrieved from http://www.sciencedirect.com/science/article/pii/S0090429598005718
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The estimated range of men worldwide suffering from ED is from 15 million to 30 million23. According to the National Ambulatory Medical Care Survey (NAMCS), for every 1,000 men in the United States, 7.7 physician office visits were made for ED in 1985. By 1999, that rate had nearly tripled to 22.3. This is in USA, where statistics are clearly compiled, the level of awareness and education is high as compared to sub Saharan countries like Uganda. This is a clear indication that there are many silent men, particularly couples affected by ED.
Long considered an aphrodisiac by the Chinese, ginseng may do more than just rev your engine. A 2013 South Korean study found that taking the herb for just a few weeks improved guys’ performance in the bedroom, including helping them last longer before finishing. Meanwhile, a study in Spermatogenesis found that ginseng can also help make for harder, longer-lasting erections and improve testosterone levels, which in turn boosts libido. “Ginseng is a promising herbal therapy for ED because it helps promote relaxation of smooth muscle in the penis, increase dopamine levels in the brain, and increase pressure in the cavernosal nerves of the penis which helps nitric oxide synthesis,” Walker explains.
Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Ashwagandha’s reputation as a sexual enhancement herb is supported by research. One animal study showed that extracts of ashwagandha increased production of sex hormones and sperm, presumably by exerting a testosterone-like effect. In another clinical trial, the herb (taken at a dose of 3 gm per day for 1 year) was given to healthy male adults 50–59 years of age. Among benefits noted: serum cholesterol levels decreased, gray hair was reduced, and a vast majority (over 70%) reported improvement in sexual performance.
Yohimbine. This chemical is found in the bark of an African tree called yohimbe. It has been used as a male aphrodisiac in Africa, and under medical supervision it has been used as a prescription drug to treat ED. Supplements made from yohimbe bark are also available without a prescription, but they can be life-threatening if used at high doses, according to the Natural Medicines Comprehensive Database. The supplement can interact in a harmful way with certain drugs, such as blood pressure medications, and should be avoided by anyone with liver, kidney, heart, or diabetes problems or problems with anxiety or depression. Like DHEA, yohimbine should not be taken without a doctor's supervision.
If you can't take one of these oral medications, your physician may have you try Caverject (alprostadil for injection), a hormone that you inject into your penis using a fine needle, or Muse (alprostadil urogenital), a tiny suppository that you insert into the tip of the penis. Both of these will bring on an erection within five to 15 minutes without sexual stimulation.