But closer questioning often revealed a very different story—men would admit that struggles to achieve an erection usually preceded a heart attack or other cardiac event by one, two, or three years. Back then, the pattern of erectile dysfunction and cardiac disease was so widespread, that most in the medical profession attributed it to simple “aging,” as common as wrinkles and constipation.
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.
There have been some studies to suggest that a placebo effect that improves ED may work for some men. One study found that men taking an oral placebo pill showed as much improvement in ED symptoms as men who took actual medication to improve ED. Conversely, men who were given therapeutic suggestions to improve ED did not see signs of symptom improvement.
The same device is considered a vacuum erectile device (VED), when it is used to increase inflow of the blood to the penis without a constriction band. Regular use of VED in post-prostatectomy patient increases penile oxygenation and is accepted as a valid option in penile rehabilitation. Recent study reported transient increase in oxygenation to the glans penis and corporal bodies were detected by oximetry after VED was applied, providing proof for possible role for VED to counter the early penile hypoxia, cavernosal fibrosis and long-term ED after radical prostatectomy (9).
While all three forms of male sexual dysfunction can be found among diabetic men, this review will focus on the most common form, ED, because the literature is most mature in this area. Defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance, ED is highly prevalent in diabetic men1 and is almost always organic in its etiology. Given that many patients feel that their ED is “in their heads” and that “their provider will dismiss any sexual problems they might bring up,”2 it may be a relief for patients to learn that their ED is physical, related to their diabetes, and treatable. To this end, the goal of this article is to review the epidemiology, pathophysiology, quality of life effect, and treatment of ED in men with type 2 diabetes.
Cardiovascular disease and ED represent 2 common disease processes that are often intimately associated with one another. These common pathophysiological links necessitate a solid scientific and clinical understanding of these 2 disorders and a team effort between the cardiologist and urologist to provide effective management strategies for these patients.
Most importantly, herbal supplements are not well regulated in the United States. Studies have shown that 40-50% of herbal supplements do not even contain the supposed main ingredient, and many contain substances that are not listed which may have dangerous side effects2. Another study found that over two thirds of the products tested had substituted other plant species for the plants listed on the label, and a third of products also contained other fillers or contaminants3. A study by the New York State Attorney General of herbal products sold at GNC, Target, Walgreens, and Walmart found that four out of every five products didn’t contain the ingredient they claimed! Fourteen US states and territories have petitioned Congress to regulate the herbal supplements industry.
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
Higher consumption of fiber-rich vegetables, fruits and beans helps to keep blood pressure in the favorable range.10 Beans, nuts and seeds have unique cholesterol-lowering capabilities.11-13 Berries and the flavonoids they contain have a blood pressure-lowering effect, plus berries and pomegranate have potent antioxidant and anti-inflammatory effects that protect against the development of heart disease.14-18
Erectile dysfunction is an accurate predictor of heart attacks and strokes in the future. Psychogenic components play a role in erectile dysfunction, but the most common and primary cause in most men is organic vascular insufficiency, meaning not enough blood gets to the penis. Erectile dysfunction usually occurs one to five years before a male manifests overt signs of cardiovascular disease. The first sign may be death.
The study, which retrospectively tracked more than 43,000 men for an average of 3.3 years, found that men prescribed phosphodiesterase-5 (PDE5) inhibitors—the type of erectile dysfunction drug sold under the names Viagra, Levitra, Cialis and others—after their first heart attack were 38 percent less likely to die from any cause. No survival benefit was seen among men taking alprostadil, another type of erectile dysfunction drug that works through a different mechanism.
PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.
*all photos are models and not actual patients.If you are interested in a prescription product, Hims will assist in setting up a visit for you with an independent physician who will evaluate whether or not you are an appropriate candidate for the prescription product and if appropriate, may write you a prescription for the product which you can fill at the pharmacy of your choice.
Erectile dysfunction becomes more common with age. However, the condition is even more common among men who have diabetes. Over time, diabetes can damage the blood vessels and nerves that control erections. In addition, some of the other conditions that often occur with diabetes, such as coronary artery disease, can also contribute to the development of erectile dysfunction.
If you have several atherosclerotic risk factors or symptoms of heart disease, your doctor might do additional tests to look for atherosclerosis in the coronary arteries. A stress test involves monitoring the heart with an electrocardiogram or images before and after exercise. An angiogram, or cardiac catheterization, involves entering a blood vessel in the leg or wrist to pass instruments into the heart to directly visualize the coronary arteries. During this procedure, atherosclerosis can be treated by inflating a balloon or placing a metal stent in the coronary blood vessel to keep it open. If you and your doctor begin a treatment plan to prevent atherosclerosis at the first sign of ED, then you may significantly delay or prevent the need for these more invasive procedures.
Erectile dysfunction is defined as the inability to attain or maintain a penile erection sufficient for satisfactory sexual performance. Cases of ED may be classified as predominantly organic in nature, predominantly psychogenic, or mixed. Usual organic aetiologies are vasculogenic, hormonal, and neurogenic. Owing to the relationship of vasculogenic ED with CVD, it is important to distinguish men with predominantly vasculogenic ED from those with predominantly psychogenic ED or non-vasculogenic organic ED.
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.