Ashwagandha (Withania somnifera), used widely in Ayurvedic medicine, holds a similar role to that of ginseng in Chinese medicine. Though unrelated to ginseng, it appears to share similar properties and actions. Ayurveda considers this herb to be a rasayana, or particularly powerful rejuvenative. The name ashwagandha means “like a horse,” connoting that it is regarded as a premier sexual tonic.
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 [6]. 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 [7]. A small proportion of autonomic nerves do not release either Ach or norepinephrine [8]. 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 [9]. 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 [10]. 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.
Yohimbe. Before Viagra and the other prescription erectile dysfunction drugs became available, doctors sometimes prescribed a derivative of the herb yohimbe (yohimbine hydrochloride) to their patients suffering from ED. But experts say the medication is not particularly effective, and it can cause jitteriness and other problems. "It's not a great drug," says McCullough. "And I suspect the herb is not as potent as the pharmaceutical version." What's more, evidence shows that yohimbe is associated with high blood pressure, anxiety, headache, and other health problems. Experts discourage its use.
The herb is particularly effective for those whose willy woes are based on other medications: An older study from the University of California found ginkgo biloba is 76% effective in treating sexual dysfunction caused by antidepressants. “Gingko helps counteract sexual dysfunction caused by certain antidepressants called SSRIs by blocking serotonin activity in the erectile centers of the brain, ultimately leading to better synthesis and bioavailability of nitric oxide,” Walker explains.
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
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The Claim: If you squint and have an excellent imagination, mature ginseng roots vaguely resemble a human body. That ties into folk ideas for finding medicines–in this case, the idea that a plant that looks like a person must contain materials that help sick people. Ginseng was traditionally used as a tonic to treat erectile dysfunction and low sexual drive in men (as well as many other complaints).
Many stores sell herbal supplements and health foods that claim to have sexual potency and fewer side effects. They’re also often cheaper than prescribed medications. But these options have little scientific research to back up the claims, and there’s no uniform method on testing their effectiveness. Most results from human trials rely on self-evaluation, which can be subjective and difficult to interpret.
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