From the researchers' point of view, the usage of herbal remedies in managing male sexual disorders is useful because of long cultural history of utilisation and the current renewed interest in natural products to sustain health globally. As a way recognising the values and roles of traditional medical knowledge in health care provision, further research into the efficacy and safety of herbal remedies in male sexual disorders is precious in Uganda and beyond. More so, the establishment of rapport between relevant government department in Ministry of Health, modern health workers through collaborative and networking ventures with traditional healers under close supervision and monitoring of herbal treatments is noble.
Size matters, so get slim and stay slim. A trim waistline is one good defense — a man with a 42-inch waist is 50% more likely to have ED than one with a 32-inch waist. Losing weight can help fight erectile dysfunction, so getting to a healthy weight and staying there is another good strategy for avoiding or fixing ED. Obesity raises risks for vascular disease and diabetes, two major causes of ED. And excess fat interferes with several hormones that may be part of the problem as well.
The medical ethnobotanical indigenous knowledge were collected by visiting traditional healers and documenting the medicinal plants used and other socio-cultural aspects allied with sexual impotence and erectile dysfunction. The methods used to collect the relevant information regarding the medicinal plants used included informal and formal discussions, field visits and focused semi-structured interviews.
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.
W somnifera (ashwagandha), also referred to as winter cherry (family Solanaceae), grows in Africa, the Mediterranean, India, Pakistan, Bangladesh, Afghanistan, South Africa, Egypt, Morocco, Congo and Jordan . The roots of the plant contain steroid alkaloids and steroidal lactone, which are the main constituents of ashwagandha; these compounds are referred to as withanolides. Among the various alkaloids, withnine is the main constituent. The other alkaloids are somniferin, somnine, somniferine, withananine, pseudowithanine, tropine, pseudotropine, cuscohygrine, anferine and anhydrine. Two acyl steryl glucosides (sitoindoside VII and sitoindoside VIII) have been isolated from the root. The withanolides contain a C28 steroidal nucleus with a C9 side chain and six-membered lactone rings. Ashwagandha root also contains flavonoids and many ingredients of the withanolide class. It has several medicinal applications (aphrodisiac, liver tonic, anti-inflammatory agent, astringent), and is used to treat bronchitis, asthma, ulcers, insomnia, senility and dementia. Clinical trials and studies involving animal models support the use of ashwagandha for anxiety, cognitive and neurological disorders, inflammation and Parkinson’s disease. It also provides cryoprotective benefits to patients undergoing radiation and chemotherapy, and shows beneficial effects for nervous exhaustion. W somnifera is used as an aphrodisiac, sedative and rejuvenative, and is also used to treat chronic fatigue, dehydration, bone weakness, muscle weakness, loose teeth, impotency, premature ejaculation, debility, constipation, senility, rheumatism, nervous exhaustion, memory loss, drug withdrawal symptoms, anxiety and arthritis pain in the knee. Extracts from W somnifera inhibit transcription factor nuclear factor kappa B (NF-κB); thus, it acts as an anti-inflammatory agent. This has been attributed to its ability to interact with IKKB, a kinase that is responsible for the nuclear translocation of NF-κB and activation of inflammatory signalling pathways .
Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.