In one study, men with a Vitamin D deficiency were nearly 33% more likely to have ED. But you don’t need that much sun exposure to get a healthy amount of Vitamin D. As little as 15–20 minutes a day is enough. Taking Vitamin D is a good idea, especially if you are over 65. Vitamin D can also help if you’re obese or dark-skinned (dark skin limits the amount of Vitamin D you naturally, produce)
In diabetes, vasoconstrictors and vasoactive factors are increased in addition to structural changes and attenuation of relaxation responses in the corpus cavernosum. A shifting of the balance of vasoactive factors occurs such that relaxation factors (eg, nitric oxide [NO]) are inhibited and contractile factors are induced in microvascular disease. With epidemiological predictions suggesting that the incidence of diabetes mellitus will increase to 300 million by 2025, management of diabetes-induced ED is increasingly important.

Between 2001–2006, one-third of the US population had insufficient amounts of vitamin D, according to the Institute of Medicine. Risk factors for vitamin D deficiency include obesity and high BMI, not enough sun exposure or outdoor activity, having darker skin and suffering from certain from inflammatory conditions like Crohn’s disease. You can get a blood test to find out if you’re vitamin D deficient.
Sildenafil citrate, tadalafil and vardenafil hydrochloride are contraindicated in patients with a known hypersensitivity to any organic nitrates (oral, sublingual, transdermal or by inhalation) due to the risk of developing potentially life-threatening hypotension. Concomitant use of PDE-5 inhibitors is contraindicated with HIV protease inhihibitors (indinavir, ritinovir, saquinavir) as well as ketoconazole, itraconazole, cimetidine and erythromycin, because these drugs are potent inhibitors of cytochrome P450 3A4 and can raise the plasma levels of PDE-5 inhibitors. Coadministration of PDE-5 inhibitors to patients taking alpha-adrenergic blockers such as alfluzocin or tamsulosin may lead to symptomatic postural hypotension, including dizziness and lighheadedness in some individuals.
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Unsurprisingly, the two online outlets are fully stocked with sketchy solutions for the age-old issue of reinvigorating the male libido. Regardless of their packaging and marketing, when you read the fine print, you can see that these products contain alternative medicine staples like Cordyceps, Ashwagandha, and Maca. But do any of these herbs actually work?  
Ashwagandha’s reputation as a sexual enhancement herb is supported by research. One animal study showed that extracts of ashwagandha increased production of sex hormones and sperm, presumably by exerting a testosterone-like effect. In another clinical trial, the herb (taken at a dose of 3 gm per day for 1 year) was given to healthy male adults 50–59 years of age. Among benefits noted: serum cholesterol levels decreased, gray hair was reduced, and a vast majority (over 70%) reported improvement in sexual performance.
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. 
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 [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.
Dadder seed (Tusizi): there are 2 species i.e., (I) Cuscuta chinensis Lam and (II) Cuscuta japonica. The ripe seeds are collected in autumn, and then they are dried in the sun or boiled. Used to treat deficient kidneys manifesting as impotence, nocturnal emissions, premature ejaculation; Dadder seed (Tusizi) can be used with Schisandra fruit (Wuweizi), Cnidium fruit (Shechuangzi), Flattened milkvetch seed (Shayuanzi) and Grossy privet fruit (Nuzhenzi) for impotence.

A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.
Erectile dysfunction is a common problem in men of all ages than publicly perceived. Since, I started the research in reproductive health care; the commonest question asked by men is related with medicinal plants that empower male sexuality. So far, several males have been consulting on the treatment of ED using herbal remedies, either by themselves or through friends12.
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.
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. 
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