Erectile dysfunction (ED) is defined as the “inability to reach and maintain erection during the intercourse” (1) leading to the victim’s experience of inadequate libido, inefficient orgasm and retarded or premature ejaculation. In Recent times, ED has been labeled as the most common sexual problem among pleasure-seeking males and a complaint of all men irrespective of their age, race and culture but age is the most important risk factor for ED (2). It is reported that nearly 100 million people around the world are living with erectile dysfunction. Yet, only 10% of these 100 million, i.e., 10 million are opting for treatment, despite enormous advancements and treatment facilities in all parts of the world (2). To cite a few countries, in China and Korea only 9% and 30% males voluntarily admit to having ED (2) and in most of the other countries in Asia, it is still considered very sensitive with considerable social stigma and secretly will resort to herbal remedies and tonics before seeking conventional medical help.
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.
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 .
Epimedium extract (Horny Goat Weed) (11), (Figure 9): the Chinese refer to this herb as ‘yin yang huo’, which has been loosely translated as ‘licentious goat plant’; hence, its common name is well known as ‘horny goat weed’ by many Western cultures. Scientifically, studies have shown that Epimedium may restore low levels of both testosterone and thyroid hormone, bringing low levels back to their normal levels (5), which may account for some of its benefits in improving sexual libido. Other benefits to Epimedium involve increased muscle mass. Used for fatigue and aging, And vasodilatation effect; thus, most frequently used in treatment of sexual dysfunction in Traditional Chinese Medicine (12). The active substance from horny goat weed was reported by Xin Zhong Cheng at Beijing Medical University as Icarin—acts by increasing sexual activities and ICP levels in castrated rats after long term oral administration. It has no effects on serum testosterone level in castrated rats after long term oral administration. Instead Icariin increases nNOS and iNOS mRNA and protein expression in the corpus cavernosum after long term oral administration and hence may have long term efficacy on erectile dysfunction after oral administration.
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.
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.
It should be noted that Panax ginseng doeshave one major side effect: insomnia. However, compared to the side effects of other erectile dysfunction medications have, such as Viagra, many may consider this side effect to be worth it. Also, ginseng may react negatively if you’re taking any other medications, and with caffeine, so you should always talk to your doctor about your options before taking this step.
If you’re stressed about not being able to maintain an erection, there are more reliable and scientifically tested methods out there. Drinking less alcohol, eating healthier foods, staying away from sugar, and doing pelvic exercises have all been proven to partially help with ED. The best part to these alternatives to the “alternative”? They are inexpensive and don’t require a shaman.
For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact.