In modern medication of erectile dysfunction, the oral prescription medication of popular Viagra (Sildenafil) is effective, but in some men it is not compatible and Sildenafil works in less than 70% of men with various etiologies and has certain side effects23. The availability of Viagra has brought millions of couples to ED treatment. Oral testosterone can reduce ED in some men with low levels of natural testosterone, but it is often ineffective and may cause liver damage34. Other drugs such as Yohimbine, papaverine hydrochloride [used under careful medical supervision]5, phentolamine, and alprostadil (marketed as Caverject) widen blood vessels. However, this available modern medication for the ED in men is very expensive for most of the rural people in Ugandan and other developing countries. Yet, in traditional medicine, there are several medicinal plants that have been relied on for use in the treatment of ED. This ethnobotanical indigenous knowledge has not been earlier documented and scientifically validated for efficacy and safety, future drug discovery and development.
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.
Tribulus Terrestris is the fruit of the Zygophyllaceae plant and it grows primarily in North China. It is a well-known aphrodisiac with records that trace back to ancient times. There are plenty of animal experiments that verify the effectiveness of Tribulus for improving erectile function. These effects are mostly due to its androgen enhancing ability, namely increasing testosterone levels. Though testosterone doesn’t directly cause an erection, it does play a role. Erection is made possible by many factors, but mostly it's through receptors on cells lining our arteries that stimulate a chain reaction that relaxes the blood vessels that go to the penis, allowing blood flow to get in. Low testosterone is often associated with overall poor metabolic and cardiovascular health. When the test is low, estrogen is usually high, leading to oxidative stress and calcification of the arteries, including the penis, restricting blood flow to the penis. So, improving testosterone levels, and improving overall metabolic function, while reducing oxidative stress is a good plan for improving overall sexual function and erection.
The study was conducted between April 2000 and March 2003 in western Uganda. To collect this data indirect asking of questions and investigations that do not refer or offend anyone were used since nobody especially men can say openly that they have this problem. These methods are explained in the textbook of ethnobotany and others have been used in the field for this kind of studies in Uganda and elsewhere in the world10,12,13,14,21. These methods included visiting the traditional healers to document the indigenous knowledge (IK), regarding medicinal plants used, gender and socio-cultural aspects and where the plants are harvested. Informal and formal conversations, discussions and interviews, market surveys and field visits were conducted.
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 [13]. 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 [6]. 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.
Saw palmetto. Saw palmetto comes from the fruit of a small palm tree. It has been used to treat symptoms in men with an enlarged prostate gland, such as difficulty urinating, and it has been recommended to treat ED caused by an enlarged prostate. However, several recent clinical trials did not show that saw palmetto works any better on an enlarged prostate than a placebo does. "There is no evidence that saw palmetto should be used to treat erectile dysfunction," says Dr. Gilbert. Like ginkgo biloba, saw palmetto can interact with some prescription medications.
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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