Exercise regularly. Make it a priority to get outside or go to the gym to walk, run, swim, bike, or do strength training at least 4 times a week. According to a study conducted by Harvard, walking 30 minutes a day caused a 41% drop in risk for ED.[3] Getting regular exercise aids circulation, getting your blood pumping through your entire body. When it's time to sustain an erection, better circulation is key.[4]

In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Positron emission tomorgraphy (PET), and functional magnetic resonance imaging (fMRI) have led to a greater understanding to which center are activated during arousal. These imaging studies measure increases in cerebral blood flow or changes in cerebral activity on a real-time basis. Studies are performed when male subject are aroused by visual cues (usually sexual explicit photos or videos) and compared to images obtained during exposure to sexually neutral cues differences can be measured. Several studies have identified that the inferior frontal lobes, inferior temporal lobes and insular gyrus, and occipital lobes are involved with processing arousal cues, although each are likely to process different stimuli (20-23).
The truth is medication or psychosexual counselling are the first treatments a doctor will suggest because they’ve been proven to work. If a doctor has approved a medication for you then it’s safe. If you would still like to see if herbal supplements work for you, then there is a list below of supplements thought to work for erectile dysfunction. Just before you invest your money in them, remember they aren’t proven to work:
Erectile problems can happen to men of any age.  There are many factors that contribute to ED including poor health, untreated medical problems, medications and pornography use.  Many men struggle with understanding when they are experiencing situational sexual dysfunction verses when is your erectile issue an ongoing problem that requires medical help.
PDE5i for ED in patients with MS can be considered as reasonably effective and safe. Fowler et al. performed a randomized, multicenter, double-blind, flexible dose trial with open label extensions comparing sildenafil to placebo (75). A nearly 4-fold increase in effective erections was noted in the treatment arm, 96% vs. 24%. Sexual satisfaction and overall satisfaction were also improved in the treatment group based on IIEF scores, and quality of life assessments. Lombardi et al. evaluated tadalafil use in men with MS (71). Seventy eight percent of the men responded with improved erections, better quality of life with regards to sexual function, partner relationship and family life. Just less than half the men who responded to the tadalafil did so at the lower dosage of 10 mg. Subjects in either studies did not have any significant adverse side effects beyond flushing, and headache with PDE5i use.

Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.
Alprostadil (also known as prostaglandin E1 [PGE1]) is the prominent known smooth-muscle dilator of the corpus cavernosum. Its mechanism of action is believed to be the promotion of intracellular accumulation of cyclic adenosine monophosphate, thereby causing decreased intracellular accumulation of calcium and resulting smooth muscle relaxation. Alprostadil can be delivered to the erectile tissue either via an intraurethral suppository that is massaged and then absorbed across the corpus spongiosum of the urethra to the corpora cavernosa, or directly injected into the corpora cavernosa. When administered urethrally, doses are substantially higher than when directly injected (typical dosing is 500 mcg to 1 mg intraurethral compared with 2.5 mcg to 20 mcg intracavernosal).
Sildenafil has been previously suggested as a treatment option for ED in men with epilepsy (77,78). However, Matos et al. warned that PDE5i are potentially pro-convulsant and should be used with great caution in men with epilepsy (79). Animal studies in rat and mice overwhelmingly suggest PDE5i can reduce seizure threshold. In human trials, seizures were rare but reported. PDE5i exerted their proconvulsive effect by lower seizure threshold possibly by worsening sleep or obstructive sleep apnea, causing cardiovascular changes, or leading to EEG changes specifically with tadalafil use.
In comparison, 37% of men who had received external radiotherapy as their primary therapy reported the ability to attain functional erections suitable for intercourse, along with 43% of men who had received brachytherapy as primary treatment. Pretreatment sexual health-related quality of life score, age, serum prostate-specific antigen (PSA) level, race or ethnicity, body mass index, and intended treatment details were associated with functional erections 2 years after treatment. [45]

Finally, gene therapy and stem cell research has widened the frontier of ED treatment proposed as possibility to even reverse ED. Specifically, gene therapy pertains to repairing the cause of ED by restoring defective gene function and/or altering the expression of the mutant gene (32). Most of the available data on gene therapy are in the animal model. However, a phase I clinical trial in men with ED undergoing intracavernous injection with a DNA plasmid carrying the alpha-subunit of the corporal smooth muscle Maxi-K channel showed promise in increased erectile function based on IIEF assessment sustained throughout the 3-month study period (122).

Despite how many men want to think that their dick has some autonomous powers of decision making, it all comes back to the brain, and if your brain is firing off stress signals, then your penis is going to need more than just mucho volition to come to life. Erections start in your head. Be it something you smell, feel, or see, it's all about the chemicals up top sending signals down there.
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
All devices that are currently approved by the FDA are considered safe for use in magnetic resonance imaging environments. However, 2 previously approved devices–the OmniPhase and the DuraPhase penile prostheses–are not considered safe in this environment. Other surgical procedures–including venous ligation to limit penile venous outflow and penile revascularization procedures–are rarely successful and are not recommended.19 These surgeries are only indicated when a patient demonstrates recent-onset ED and an occlusive lesion seen on angiogram or magnetic resonance angiography and should be performed only in centers of excellence for ED.
The most common treatment for erectile dysfunction is drugs known as phosphodiesterase-5 (PDE-5) inhibitors. These include tadalafil (Cialis), vardenafil (Levitra), and sildenafil citrate (Viagra). These are effective for about 75% of men with erectile dysfunction. They are tablets that are taken around an hour before sex, and last between 4 and 36 hours. Sexual stimulation is required before an erection will occur. The PDE-5 inhibitors cause dilation of blood vessels in the penis to allow erection to occur, and help it to stay rigid. Men using nitrate medication (e.g. GTN spray or sublingual tablets for angina) should not use PDE-5 inhibitors.
The primary nerve fibers to the penis are from the dorsal nerve of the penis, a branch of the pudendal nerve. The cavernosal nerves are a part of the autonomic nervous system and incorporate both sympathetic and parasympathetic fibers. They travel posterolaterally along the prostate and enter the corpora cavernosa and corpus spongiosum to regulate blood flow during erection and detumescence. The dorsal somatic nerves are also branches of the pudendal nerves. They are primarily responsible for penile sensation. [10]

Intraurethral alprostadil is contraindicated in individuals who have abnormal penile anatomy (for example, urethral stricture, severe hypospadias with penile curvature), patients with acute or chronic irritation/infection of the urethra, individuals prone to priapism such as those with sickle cell anemia, thrombocytopenia, polycythemia, multiple myeloma, or are prone to blood clots. Intraurethral alprostadil should not be used for sexual intercourse with a pregnant woman.
Melanocortin receptor agonists were found to induce erections serendipitously. A study investigating the dermatologic use of Melanotan-II (MT-II) was found to generate erections unexpectedly leading to the development of MTII derivatives for ED treatment (120). MT-II was initially used to induce pigment changes in the skin for artificial tanning but has been suspected to induce melanoma, however (121).

Of particularly concern are antihypertensive medications for CVD (eg, digoxin, disopyramide [Norpace], gemfibrozil [Lopid]), anxiety, depression (eg, lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants), or psychosis (eg, chlorpromazine, haloperidol, pimozide [Orap], thioridazine, thiothixene). Antihypertensive drugs, such as diuretics (eg, spironolactone, thiazides) and beta blockers, may be associated with ED. Discontinuation or switching to alternative drugs, such as angiotensin-converting enzyme inhibitors or calcium channel blockers (eg, diltiazem, nifedipine, amlodipine), may reduce ED. The newer angiotensin II receptor antagonists may be less problematic with respect to ED, but long-term data is needed to evaluate this.
Can apple cider vinegar treat erectile dysfunction? Apple cider vinegar is thought to have many health benefits, but can it help treat erectile dysfunction (ED)? ED can result from cardiovascular problems, diabetes, and other factors. Apple cider vinegar may help improve symptoms of conditions related to ED. Find out how it may help, and how to use it safely. Read now
Garlic is considered to help effectively in dealing with the impotence and ED problems because it has high levels of allicin which can help to improve blood flow and blood circulation. A small research of Dr. Graham Jackson, consultant cardiologist at Guys and St Thomas’ NHS Trust discovered that consuming  4 cloves of garlic every day for 3 months can help much in improving the erection in 6 out of 7 volunteers struggling with impotence.
If a trial of oral therapy and withdrawal of offending medications do not restore erectile function or if a patient has medical or financial contraindications to pharmacologic therapy, most primary care practitioners should consider referring the patient to a specialist for additional evaluation and discussion of alternative treatment options. However, some primary care practitioners may recommend vacuum constriction devices.
Implantation of penile prosthesis remains an important option for men with ED if medical treatment fails or is inappropriate. Prostheses are available as a saline-filled silicone device or a malleable device. The benefit of the former is a more natural appearance in the deflated state, closely approximating the appearance of a flaccid penis. The trade-off is a higher mechanical failure rate and higher cost. Satisfaction rates for patients who underwent penile prosthesis surgery have been reported to be near 90%.36 However, in the majority of patients who receive this treatment, less invasive alternatives have failed and therefore satisfaction with this treatment would be expected to be higher in this subset of patients. Risks of these devices include surgical and anesthetic risk, device infection, and device malfunction. Mechanical failure rates depend on the specific device being investigated. Overall, the percentage of devices that are free from mechanical failure at 5 years ranges from 84% to 94%.19 Infection rates in the era of coated devices and improved techniques are reported to be less than 1%.37
The sympathetic pathway originates from the 11th thoracic to the 2nd lumbar spinal segments and goes via the white rami to enter the sympathetic chain ganglia. Subsequently nerves travel through the lumbar splanchnic to inferior mesenteric and superior hypogastric nerves to the pelvic plexus. The T10 through T12 segments are most often the origin of sympathetic fibers, and the sympathetic chain ganglia that innervate the penis are located in the sacral and caudal ganglia (3).

Side effects include lightheadedness, fainting, priapism, urethral bleeding (intraurethral), dyspareunia in the partner (intraurethral), hematoma (intracavernosal) or penile curvature secondary to scar (intracavernosal). Efficacy of intraurethral alprostadil has been demonstrated to be around 50% ("able to have intercourse") in randomized controlled trials.31,32 For intracorporeal injection, typically alprostadil is tried alone, or compounded with papaverine (nonspecific phosphodiesterase inhibitor that increases intracellular cyclic adenosine monophosphate and cGMP) and/or phentolamine (competitive, non-selective alpha1- and alpha2-adrenoreceptor blocker). Pinsky et al33 reported an extensive review of the benefits and drawbacks of the combinations of these drugs.


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. 
Look, ED can have many causes. Most of the time, it’s physiological. But there are also lots of psychological reasons why someone may experience ED. Treating ED isn’t all about medication. Dealing with some of these psychological issues can help you battle ED, too. I’m talking about depression, anxiety, loss of desire, sense of inadequacy, guilt, fatigue, anger, relationship dysfunction. Working through these types of psychological challenges can help you achieve the happy, healthy manhood you deserve.

The main surgical treatment of ED involves insertion of a penile implant (also called penile prostheses). Because penile vascular surgery is not recommended for aging males who have failed oral PDE5 inhibitors, ICI or IU therapies, implants are the next step for these patients. Although placement of a penile implant is a surgery which carries risks, they have the highest rates of success and satisfaction among ED treatment options.
×