3. Testosterone replacement. Before oral medications like Viagra, testosterone was routinely used to treat erectile dysfunction as it is central in the male sexual response, including the desire for sex and the process of getting an erection. Testosterone can be administered in a number of ways, for example orally, by means of an injection, skin patch, or subcutaneous (under the skin) pellet.
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."
Classically the neuro-physiology of ejaculation traces the 3 Phases in which ejaculation is a complex event involving the (I) the propulsion of sperm and seminal plasma into the prostatic urethra which is accompanied by (II) bladder neck closure and (III) coordinated contractions of the bulbocavernosus and ischiocavernosus muscles, striated muscles of the pelvic floor, lower limbs and trunk. In the Asian Society of the Aging Male Study  63% have reduced erection, 68% reduced or absent ejaculation and 19% pain or discomfort at ejaculation. Disorders of ejaculation can be due to: (I) disorders of production of sperm or seminal plasma/prostatic secretions (II) disorders of propulsion. In the case of anejaculation (absence of ejaculatory) which is the ultimate disorder of ejaculation, the causes can be best classified as (I) primary or secondary. After covering psychogenic causes of ejaculation failure, the organic causes due to non-dynamic and obstructive etiologies in the prepubertal and post pubertal male will be highlighted. More details will be given on retarded ejaculation, premature ejaculation, aspermia, painful and weak (poor propulsive force) ejaculation. The evaluation of the patient must include a detailed history taken from the patient and often his partner. Aside from haematologic tests, various forms of radiological and ultrasonic imaging, neurophysiologic studies may be required. For the general practitioner the commonest scenario will be in the ED Clinic with abundant men with performance anxiety presenting with premature ejaculation. In the male aging clinic lack of arousal is the commonest cause of retarded orgasm and ejaculation but this group is plagued by decreased touch sensitivity, the need for more direct stimulation, reduced drive to orgasm, a less intense orgasm, ejaculation being weaker and of reduced quantity and disturbing complaints of a longer recovery period and less number of attainable orgasms per day or week. Thus it is not mere rumor that “by the time a man reaches 55, the refractory period to ‘do it again for a man’ increases to 12 hours or even up to a week”. In the STD clinic, painful or bloody ejaculation is frequently seen. The Condom may cause condom retarded orgasm/ejaculation.
Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.
Thirty-three medicinal plants both cultivated (Table 1) and wild harvested (Table 2) were documented and identified in the area of study. In the description below these results of these two table are combined as presented below. All the identified medicinal plants in both tables belong to 25 families and 30 genera. The family Rubiaceae (4) is the most represented followed by Alliaceae, Euphorbiaceae, Mimosaceae, Papilionaceae and Caesalpinaceae families which have two species each and the rest with one species. The composition is that 42.4% are shrubs, 39.4% herbs and herb climbers and 18.2% trees. Leaves (57.6%) are the commonest plant parts followed by roots (42.1%), barks (27.3%) and the rest of the plant parts harvested have less than 10% of the parts harvested. From Allium cepa, Allium sativum, Rhus vulgaris, Warburgia ugandensis, Cleome gynandra and Tarenna graveolens, three different plant parts, are harvested for use in sexual impotence and erectile dysfunction. In the case of Impetiens species and Urtica massaica, the whole plants are harvested while the rest of the species one or two different plant parts are used. The conservation status of these documented plants is that 27.3% are cultivated while 72.7% are collected from wild places. The common methods of plant medicine preparation included boiling, chewing, pounding, cooking, roasting and smoking. The commonest method of herbal administration was by oral means as food, herbal teas or by mixing in several drinks including locally made beer.
The Science: Chemicals inside these plants called ginsenosides are thought to ramp up the physiological pathway that makes nitric oxide, the neurotransmitter that gets the blood flowing during penile erection. Some studies support that idea: one found that ginsenoside-rich ginseng berry extracts relaxed smooth muscle inside rabbit erectile tissue. But so far there haven’t been high-quality double-blind and randomized trials of the chemicals’ effect on humans. The jury’s still out on whether ginsenosides have any effect on people at all, or (if they do) whether they work as well as medications like Viagra.
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.
Historically, it has been shown that herbal medicines may cure or prevent certain ailments. However, there are very little recorded data available to support the dose, efficacy, side effects and interactions. Because the safety and efficacy of herbal remedies have not been assessed, unlike synthetic drugs, well-controlled and randomized studies are warranted to establish the therapeutic efficy and safety of such products. Determination of side effects and interactions with prescription medicines are also needed. The amount of active ingredients in herbals may vary among preparations; thus, standardization of herbal medicines is required.
L-arginine, or arginine, is an amino acid found in red meat, poultry, fish, and dairy products that helps expand blood vessels and increase blood flow. “The body uses this semi-essential amino acid as the primary building block for nitric oxide,” explains Harry Fisch, M.D., clinical professor of urology and reproductive medicine at Weill Cornell Medical College/New York Presbyterian Hospital.
Dr. Niket Sonpal is the Associate Program Director of the Internal Medicine Residency at Brookdale Hospital Medical Center in Brooklyn and an Associate Professor at Touro College of Osteopathic Medicine. He's a practicing Gastroenterologist and Hepatologist with a focus on Men's and Women's Health, and a regular contributor to Women's health, Shape and Prevention Magazine.
There are so many potential reasons a man might develop erectile dysfunction (ED), it's nearly impossible to generalize the best ways to treat it. What works for one man may not work for another simply because they are having problems for different reasons. That said, it may encouraging to hear that there are a variety of options that may be considered, from psychological counseling to lifestyle changes, medications to treatments and devices.
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The search for a cure for erectile dysfunction (ED) dates back way before the introduction of Viagra in the 1990s. Natural aphrodisiacs, from ground rhinoceros horn topa chocolate, have long been used to increase libido, potency, or sexual pleasure. These natural remedies are also popular because they’re said to have fewer side effects than prescribed medications.