Elise joined Lemonaid because she believes healthcare should be accessible and affordable to everyone! With extensive professional healthcare experience, Elise has spent the last decade as an advocate for the highest quality patient care in specialties like gynecology, internal medicine, and otolaryngology and has excelled in various roles such as office manager, surgery coordinator, and front office coordinator. She feels every patient should be treated with kindness and understanding, and she brings this attitude to work every day. Aside from her medical background, she’s also a professional musician and enjoys living life to the fullest with a smile on her face.
Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date. [4] Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.

Think of erectile dysfunction as your body’s “check engine light.” The blood vessels in the penis are smaller than other parts of the body, so underlying conditions like blocked arteries, heart disease, or high blood pressure usually show up as ED before something more serious like a heart attack or stroke. ED is your body’s way of saying, “Something is wrong.” And the list of things that cause erectile dysfunction can include:
The most common inflatable prosthesis is the three-piece penile prosthesis. It is composed of paired cylinders, which doctors surgically insert inside the penis. Patients can expand the cylinders using pressurized fluid (see figure 3). Tubes connect the cylinders to a fluid reservoir and pump, which doctors also surgically implant. The reservoir is usually in the pelvis. A doctor places the pump in the scrotum. By pressing on the pump, sterile fluid transfers from the reservoir into the cylinders in the penis. An erection is produced primarily by expansion of the width of the penis, however, one model can increase in length a small amount also. Lock-out valves in the tubing prevent the fluid from leaving the cylinder until a release valve is pressed. By pressing the relief valve and gently squeezing the penis, the fluid within the cylinders transfers back into the reservoir.
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 general medical history is important in identifying specific risk factors that may account for or contribute to the patient's erectile dysfunction. These include vascular risk factors such as hypertension, diabetes, smoking, coronary artery disease, peripheral vascular disorders, pelvic trauma or surgery, and blood lipid abnormalities. Decreased sexual desire or history suggesting a hypogonadal state could indicate a primary endocrine disorder. Neurologic causes may include a history of diabetes mellitus or alcoholism with associated peripheral neuropathy. Neurologic disorders such as multiple sclerosis, spinal injury, or cerebrovascular accidents are often obvious or well defined prior to presentation. It is essential to obtain a detailed medication and illicit drug history since an estimated 25 percent of cases of erectile dysfunction may be attributable to medications for other conditions. Past medical history can reveal important causes of erectile dysfunction, including radical pelvic surgery, radiation therapy, Peyronie's disease, penile or pelvic trauma, prostatitis, priapism, or voiding dysfunction. Information regarding prior evaluation or treatment for "impotence" should be obtained. A detailed sexual history, including current sexual techniques, is important in the general history obtained. It is also important to determine if there have been previous psychiatric illnesses such as depression or neuroses.
None of the ED drugs is safe to take with cardiac drugs called nitrates because it could cause a dangerous drop in blood pressure. Drugs that many men take for urinary symptoms, called alpha blockers, can also lower blood pressure, so take them at least four hours apart from ED drugs. Your doctor may start you on a smaller dose of the ED drug if you already take an alpha blocker, or may recommend the alpha blocker tamsulosin (Flomax), which affects blood pressure less.
You get to decide what is normal for you. That might include him still experiencing pleasure from you touching his penis even if he’s not hard. Some men can still orgasm without an erection. Or he may prefer not to have any touching while he is dealing with his erection problems. It is okay for you to orgasm even if he doesn’t. Reading about what might bring you pleasure, or considering how you think about sex can make this something enjoyable to explore together.
If you want to score points, this is the go-to line. I understand that when you can’t get hard, other sexy acts may be the last thing you want to do, but reciprocate the kindness your woman shows (unless you’re dating an asshole: If someone’s mean about an infrequent loss of boner, dump them.) Forget about your dick for a minute, and eat some pussy. Have you ever gotten head from a woman without getting her off? I thought so. You're taking the pressure off yourself, and giving her a grand gift. Bonus: A well-documented side effect of eating pussy is getting a boner, so this one is a win-win... win! Win!! WIN!!!!

Erectile dysfunction (ED) affects 50% of men older than 40 years, [4] exerting substantial effects on quality of life. [5] This common problem is complex and involves multiple pathways. Penile erections are produced by an integration of physiologic processes involving the central nervous, peripheral nervous, hormonal, and vascular systems. Any abnormality in these systems, whether from medication or disease, has a significant impact on the ability to develop and sustain an erection, ejaculate, and experience orgasm.

Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
The motivation and expectations of the patient and his partner and education of both are critical in determining which therapy is chosen and in optimizing its outcome. If single therapy is ineffective, combining two or more forms of therapy may be useful. Penile prostheses should be placed only after patients have been carefully screened and informed. Vascular surgery should be undertaken only in the setting of clinical investigation and extensive clinical experience. With any form of therapy for erectile dysfunction, long-term followup by health professionals is required to assist the patient and his partner with adjustment to the therapeutic intervention. This is particularly true for intracavernosal injection and vacuum constriction therapies. Followup should include continued patient education and support in therapy, careful determination of reasons for cessation of therapy if this occurs, and provision of other options if earlier therapies are unsuccessful.
Men with a rare heart condition known as long QT syndrome should not take vardenafil since this may lead to abnormal heart rhythms. The QT interval is the time it takes for the heart's muscle to recover after it has contracted. An electrocardiogram (EKG) measures the QT interval. Some people have longer than normal QT intervals, and they may develop potentially life-threatening abnormal heart rhythms, especially when given certain medications. Men with a family history of long QT syndrome should not take vardenafil, as it is possible to inherit long QT syndrome. Furthermore, vardenafil is not recommended for men who are taking medications that can affect the QT interval such as quinidine (Quinaglute, Quinidex), procainamide (Pronestyl, Procan-SR, Procanbid), amiodarone (Cordarone), and sotalol (Betapace).
The motivation and expectations of the patient and his partner and education of both are critical in determining which therapy is chosen and in optimizing its outcome. If single therapy is ineffective, combining two or more forms of therapy may be useful. Penile prostheses should be placed only after patients have been carefully screened and informed. Vascular surgery should be undertaken only in the setting of clinical investigation and extensive clinical experience. With any form of therapy for erectile dysfunction, long-term followup by health professionals is required to assist the patient and his partner with adjustment to the therapeutic intervention. This is particularly true for intracavernosal injection and vacuum constriction therapies. Followup should include continued patient education and support in therapy, careful determination of reasons for cessation of therapy if this occurs, and provision of other options if earlier therapies are unsuccessful.
When sexually stimulated there is a release of a chemical, nitric oxide (NO) in the blood vessels of the corpus cavernosum. The NO stimulates the production of a compound called cGMP, which causes relaxation of the smooth muscle in the blood vessels supplying the corpus cavernosum. PDE 5 is an enzyme that breaks down cGMP. By inhibiting the breakdown of cGMP by PDE5, these medications allow cGMP to build up in the penis. cGMP causes muscles in the corpora cavernosa of the penis to relax. When the muscle is relaxed, more blood can flow into the penis and fill the spaces in the penis. As the penis fills with blood, the veins in the penis are compressed, and this results a hard erection. When the effect on PDE5 decreases, the cGMP levels go down and the muscle in the penis contracts, causing less blood to flow into the penis and allowing the veins to open up and drain blood out of the penis.
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