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.
There are two kinds of surgery for ED: one involves implantation of a penile prosthesis; the other attempts vascular reconstruction. Expert opinion about surgical implants has changed during recent years; today, surgery is no longer so widely recommended. There are many less-invasive and less-expensive options, and surgery should be considered only as a last resort.
The bad news: Men with diabetes are three times more likely to report having problems with sex than non-diabetic men. The most common sexual problem is Erectile Dysfunction, or ED, sometimes called impotence. Even worse, because ED is such a private issue, many men feel embarrassed to discuss the problem with their doctor, or even their partner, so the problem is never addressed.
When it comes to boosting sexual performance, many men will walk all over God’s green earth looking for ways to maintain a good sex life. Luckily men, all you have to do is walk — not run — 2 miles a day. This, along with other healthier lifestyle interventions can help obese men reduce their risk of ED, or even “reverse” current impotence, according to a 2005 study. This comes of importance, since maintaining a trim waistline is a good defense for ED, as men with a 42-inch waist are 50 percent more likely to have ED than those with a 32-inch waist. Getting to a healthy weight and maintaining it is a good strategy for preventing and treating ED.
As men age they require more stimulation up front to get and maintain an erection firm enough for sex. Engaging in some foreplay either on you or on your partner is a great way to get your arousal levels up and get an erection that is firm enough for sex. Many men begin to rush the process of sex once they experience ED. They worry that they will lose their erection so they rush rather than go slow understanding that rushing will only make the problem worse.
The somatosensory pathways for erections originate in the penile skin, glans and urethra. Glans afferent sensory free nerve endings are 10-fold more than their corpuscular receptors, and are derived from Aδ and unmyelinated C fibers. The nerve endings coalesce to form the dorsal penile nerve along with other sensory nerve fibers. Through the pudendal nerve they enter the S2-4 nerve roots to terminate on spinal neurons and interneurons. The dorsal nerve is not purely somatic, however. Nerve bundles within the dorsal nerve contain nitric oxide (NO) synthase, found typically in autonomic nerves, and stimulation of the sympathetic chain can leak to evoked potentials from the dorsal nerve and vice versa (10-12).
You can also consider using a cock ring or penis ring if you are able to get an erection but have trouble maintaining it. Cock rings work by trapping the blood inside your penis so it remains harder for longer. You can purchase one in a sex store or online for about $5 and you put in on over your penis and testicles when you are half hard and keep it on until you are finished with sex. It’s a great cheap fix for erectile issues.
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).
When lifestyle changes alone don’t work, drug therapy (Viagra®, Cialis®, Levitra®, etc.) is normally the next step. Most of these medications work similarly to enhance a natural chemical in your body that relaxes the muscles in your penis. The goal of this medication is to increase your response to sexual stimulation by increasing the blood flow in your penis allowing you to get an erection.22
Clinical experience in switching medications to improve ED has been disappointing in that improvement does not often occur. Nonetheless, it is important to try to discontinue possible offending medications before proceeding to more invasive ED treatment options. Oral ED medications have changed the way clinicians discontinue medications in patients with ED and has improved the approach. For example, a patient may develop ED on a thiazide diuretic. The diuretic may be withdrawn, but a trial of oral ED therapy can be initiated during the observation period while the patient is waiting to see if any spontaneous improvement in ED occurs after drug withdrawal. Alternatively, if diuretic therapy is effective, well tolerated, and controlling blood pressure, oral ED therapy can be used on an ongoing basis to treat the side effect of ED.
Conditions associated with reduced nerve and endothelium function (eg, aging, hypertension, smoking, hypercholesterolemia, and diabetes) alter the balance between contraction and relaxation factors (see Pathophysiology). These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.
Since endothelial dysfunction, CVD and ED are closely associated in epidemiological studies, the question for clinicians is whether to recommend the man presenting with ED undergo a cardiovascular (CV) evaluation. Clearly, based on numerous studies, ED can be considered at least a ‘marker’ for possible further vascular disease or CVD.15 In their report, Vlachopoulos and coworkers make the point that the man presenting with ED, the clinician, is offered an opportunity to attempt to improve the health of the man by addressing lifestyle modification, and consider further vascular evaluation owing to the clear relationship between endothelial dysfunction, ED and CVD.19
On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.
Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.
Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.
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medicines called alpha-blockers such as Hytrin (terazosin HCl), Flomax (tamsulosin HCl), Cardura (doxazosin mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl), Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin). Alpha-blockers are sometimes prescribed for prostate problems or high blood pressure. In some patients, the use of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
ED is defined as the inability to achieve a full erection or the inability to maintain an erection adequate for sexual intimacy. Other types of sexual dysfunction such as premature ejaculation and low libido may occur; however, the most common and disruptive problem in men is ED. Although most men will experience periodic episodes of ED, these episodes tend to become more frequent with advancing age.
As is true in so many medical conditions, lifestyle modifications, considered first-line therapy, can have a salutary effect in ED management, and men should be encouraged to make the necessary changes to the benefit of their sexual function and to their overall health as well. Despite the benefits of behaviour modification, men presenting with ED want the physician to help with measures that can have an immediate impact.
There are many alternative impotence treatments available but many of them are neither licensed nor legitimate, Beware of sellers offering “herbal” impotence treatments - these remedies do not work and are often sold illegally. You should also be wary of online sellers who offer Viagra and other prescription drugs without asking you for a prescription. Illegal pharmacies often sell counterfeit or fake medication and buying from them could put your health at risk.
Somatomotor penile innervation originates in Onuf’s nucleus in the S2-4 spinal segments. These nerves travel to the ischiocavernosus and bulbocavernosus muscles when activated lead to contraction necessary for the rigid-erection phase. Several animal studies show that stimulation of the somatomotor pathways may also be under sympathetic control, and adrenergic stimulation may lead to contraction of these muscles during ejaculation (13,14). Somatomotor spinal reflexes may also be initiated by genital stimulation. For instance, the well-known bulbocavernosus reflex is evidence this reflex exists; however the clinical significance of its absence in the neurological assessment of ED has not been substantiated (15).