Men with diabetes are two to three times more likely to have erectile dysfunction (ED) than those without diabetes. In fact, some studies show that ED may be the first manifestation. Erectile dysfunction is a condition in which a man is unable to maintain an erection.
“Sexual dysfunction is a common, underappreciated complication of diabetes. Male sexual dysfunction among diabetic patients can include disorders of libido, ejaculatory problems, and erectile dysfunction (ED). All three forms of male dysfunction can cause significant bother for diabetic patients and can affect their quality of life. Despite this, health care providers often do not specifically ask their male diabetic patients about sexual function. This results in considerable underdiagnosis because patients are often reluctant or embarrassed to initiate discussion of these issues themselves. By not recognizing sexual dysfunction as a common organic sequalae of diabetes that should be addressed and treated, providers are missing an important opportunity to improve their patients’ daily existence and quality of life.
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 men 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’, it may be a relief for patients to learn that their ED is physical, related to their diabetes, and treatable.”1
“Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. The prevalence in the USA is 10–20 million men. The male erectile response is a neurovascular event reliant on the complex interaction between neurological and vascular responses. Erectile dysfunction is multifactoral and has been typically classified by the primary presumed cause: vasculogenic, psychogenic, neurogenic and endocrinologic disease. Any condition or injury that impairs the transmission of impulses along the psychogenic or reflexogenic neurological pathway, may be associated with neurogenic erectile dysfunction.”2
The trigger of an erection can be physical or psychological. It can also be stimulated by physical contact to the nerves that collect the sensitivity of the penis. This will lead to a reaction from other nerves whose function is to give orders, in this case, to begin an erection.
The orders given by these nerves are vasodilation. Thus, it increases the caliber of the arteries that reach the penis (mainly the cavernous artery), having more blood reaching the area. The cavernous artery runs through the interior of the corpora cavernosa, which swell when they get more blood. Parallel to this process it’s also developing the vasoconstriction of the deep veins of the penis. The veins partially close and the blood that has reached the penis is unable to leave it. Thus, it accumulates inside.
In the long term there are two problems that diabetes causes in the body: neuropathy and angiopathy. Both problems affect directly the erection, the first in relation to the injury of small nerves and the second in relation to the injury of small blood vessels.
“Erectile dysfunction in patients with type 1 diabetes mellitus poses a major clinical problem and was associated with poorer diabetes-related quality of life in the DCCT/Epidemiology of Diabetes Interventions and Complications (EDIC) cohort, particularly in those with other complications including neuropathy. It is principally mediated by impaired cavernosal vasodilatation due to a non-adrenergic, non-cholinergic nerve signaling defect, penile endothelial dysfunction and veno-occlusive disease; however, the relative contributions of each may differ between type 1 and type 2 diabetes.
Most earlier studies have primarily reported on erectile dysfunction in men with type 2 diabetes, and have demonstrated abnormalities in quantitative sensory testing (QST) results and sympathetic skin responses. Recent studies in participants with type 1 diabetes from the DCCT and EDIC cohorts have also shown that cardiovascular autonomic neuropathy and peripheral neuropathy are major risk factors for erectile dysfunction. Furthermore, failure of erectile dysfunction therapy has been attributed to severe erectile dysfunction at presentation, worsening of endothelial dysfunction and the presence of a significant neuropathy.”3
Neuropathy is a long-term complication of poorly controlled diabetes. The destruction of nerves occurs due to exposure to high glucose levels. It is mostly a consequence of constant abrupt changes in blood glucose levels. Once the nerves are destroyed, in this case those related to the penis, the latter ceases to have sensitivity. Therefore, it stops responding to sexual stimuli. In the end the patient cannot start the erection or cannot maintain it. “Diabetes can affect numerous body systems, including the autonomic nervous system (ANS). The ANS is responsible for controlling many systems, including gastrointestinal, cardiovascular, and genitourinary. Damage to the ANS can result in a myriad of issues, including diabetic autonomic neuropathy (DAN) and sexual dysfunction (SD) […]
DAN has been described as a diverse disorder associated with the ANS and is considered a diagnosis of exclusion. This chronic illness can be defined as a combination of injuries or lesions to nerve fibers in the ANS that control both the sympathetic and parasympathetic systems. For patients with diabetes, risk factors for developing neuropathies are higher in those who have poor blood glucose control, longer duration of diabetes, and kidney disease, as well as in those who are obese, use alcohol, and who smoke. DAN typically coincides with other complications of diabetes, such as peripheral neuropathy, cardiovascular autonomic neuropathy, gastroparesis, and kidney disease. These complications have been associated with higher morbidity and mortality.
The detection of diabetic neuropathy may occur as early as 1 year after the diagnosis of type 2 diabetes mellitus (T2DM) and within 2 years of the diagnosis of type 1 diabetes mellitus (T1DM). Typically, clinical symptoms may be subtle and unrecognizable by the provider and patient. Subclinical presentation of DAN is related to hyperglycemia resulting in minute neurovascular changes. This timeline reflects the gradual progression of DAN.”4
“Diabetes mellitus is associated with both macrovascular (including CVD) and microvascular (including retinopathy, nephropathy, and neuropathy) complications. People with diabetes are at a greater risk of developing CVDs, such as heart attack and stroke. The increased risk of CVD results, in part, from CVD risk factors that commonly accompany diabetes mellitus, as type 2 diabetes is associated with clustered risk factors for coronary heart diseases (CHD) including hypertension, elevated low-density lipoprotein-cholesterol (LDL), and obesity. Diabetic patients also have elevated risk for sight loss, foot and leg amputation, and renal failure, due to microvascular complications, which cause damage to the nerves and blood vessels.
Diabetes has been associated with sexual dysfunction both in men and in women. Diabetes is an established risk factor for sexual dysfunction in men; a threefold increased risk of erectile dysfunction (ED) was documented in diabetic compared with nondiabetic men. Among women, the evidence regarding the association between diabetes and sexual dysfunction is less conclusive, although most studies have reported a higher prevalence of female sexual dysfunction (FSD) in diabetic women as compared with nondiabetic women.
It is still not clear whether hyperglycemia, which is a main determinant of vascular diabetic complications, may participate in the pathogenetic mechanisms of sexual dysfunction in diabetes. On the other hand, diabetic people may present with several clinical conditions, including hypertension, overweight and obesity, metabolic syndrome, cigarette smoking, or atherogenic dyslipidemia, which are themselves risk factors for sexual dysfunction in both sexes.”5
The second major long-term complication of diabetes is angiopathy. It damages blood vessels as results from exposure to high glucose levels. Also by constant abrupt changes in blood glucose. However, in this case the blood vessels are not simply destroyed. What happens is that the endothelium (the innermost cell layer of the vessels, in contact with the blood) begins to proliferate. Thus, more and more cells appear “stuck” inside the vessel. It diminishes its caliber and with it the capacity of passage of blood through it. In this way, when angiopathy occurs in the cavernous artery less blood reaches the corpora cavernosa. It is then when it appears difficult to generate or maintain an erection.
“Cardiovascular complications are the leading cause of morbidity and mortality in patients with diabetes mellitus; up to 80% of deaths in patients with diabetes are closely associated with vascular disease. The ability of the organism to form a collateral network of blood vessels constitutes an important response to vascular occlusive disease and determines to a large part the clinical consequences and severity of tissue ischemia. The development of new vessels is significantly reduced in diabetic patients with coronary or peripheral artery disease. This probably contributes to the severe course of limb ischemia in diabetic patients, in which peripheral artery disease often results in foot ulceration and lower extremity amputation.”6
Another male sexual problem that frequently causes poorly controlled diabetes is retrograde ejaculation. This occurs because the damaged nervstimulate the urethral sphincter. This is responsible for letting go, or not, both urine and semen through the urethral orifice. Due to this erroneous stimulation, when ejaculating the sphincter is closed. In this way the semen, unable to go outside, goes to the bladder. Later, urinating eliminates both urine and semen.
“This results in a low-volume ejaculate and a low or absent sperm count with subsequent subfertility. The condition can occur as a result of congenital abnormality, spinal trauma, retroperitoneal lymph node dissection, diabetes mellitus, and bladder neck surgery or can be idiopathic. Retrograde ejaculation accounts for less than 2% of cases of subfertility presenting to a fertility clinic. Treatment methods aim to restore antegrade ejaculation either medically or with surgery or to retrieve spermatozoa from the urine. Medical management aims at increasing tone of the bladder neck and therefore preventing retrograde flow of semen into the bladder by either stimulating sympathetic activity or blocking parasympathetic stimulation. Surgical interventions in the management of retrograde ejaculation aim at restoring integrity of the bladder neck. Urinary sperm retrieval aims to extract sufficient viable sperm from the postejaculatory urine for insemination, IVF, or intracytoplasmic sperm injection (ICSI).”7
Pathology of Diabetic ED
“The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels. Autonomic neuropathy is a major contributor to the high incidence of ED in people with diabetes. Norepinephrine and acetylcholine-positive fibers in the corpus cavernosum have also been shown to be reduced in people with diabetes. This results in loss of the autonomic nerve–mediated muscle relaxation that is essential for erections.
The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
Nonsustained erection with detumescence after penetration is most commonly caused by anxiety or the vascular steel syndrome. In the vascular steel syndrome, blood is diverted from the engorged corpora cavernosae to accommodate the oxygen requirements of the thrusting pelvis. Questions should be asked regarding the presence or absence of nocturnal or morning erections and the ability to masturbate. Complete loss of nocturnal erections and the ability to masturbate are signs of neurological or vascular disease. It is important to remember that sexual desire is not lost with ED—only the ability to act on those emotions.”8
The best prevention that exists is the adequate control of the glycemia of the diabetic patient. In this way there will not be, or will be less, the damage produced in the blood vessels and nerves of the person. As for the treatment once the erectile dysfunction has appeared, the famous Viagra could be administered, whose active principle is sildenafil. Also other inhibitors of phosphodiesterase-5.
(1) Penson, D. F., & Wessells, H. (2004). Erectile dysfunction in diabetic patients. Diabetes Spectrum, 17(4), 225-230. Available online at http://spectrum.diabetesjournals.org/content/17/4/225
(2) Bleustein, C. B., Arezzo, J. C., Eckholdt, H., & Melman, A. (2002). The neuropathy of erectile dysfunction. International journal of impotence research, 14(6), 433. Available online at https://www.nature.com/articles/3900907
(3) Azmi, S., Ferdousi, M., Alam, U., Petropoulos, I. N., Ponirakis, G., Marshall, A., … & Boulton, A. J. (2017). Small-fibre neuropathy in men with type 1 diabetes and erectile dysfunction: a cross-sectional study. Diabetologia, 60(6), 1094-1101. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423985/
(4) Wooton, A. K., & Melchior, L. M. (2018). Diabetic autonomic neuropathy resulting in sexual dysfunction. The Nurse Practitioner, 43(11), 39-45. Available online at https://journals.lww.com/tnpj/Fulltext/2018/11000/Diabetic_autonomic_neuropathy_resulting_in_sexual.7.aspx
(5) Maiorino, M. I., Bellastella, G., & Esposito, K. (2014). Diabetes and sexual dysfunction: current perspectives. Diabetes, metabolic syndrome and obesity: targets and therapy, 7, 95. Available online at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949699/
(6) Silvestre, J. S., & Lévy, B. I. (2006). Molecular basis of angiopathy in diabetes mellitus. Available online at https://www.ahajournals.org/doi/pdf/10.1161/01.RES.0000200396.90220.41
(7) Jefferys, A., Siassakos, D., & Wardle, P. (2012). The management of retrograde ejaculation: a systematic review and update. Fertility and sterility, 97(2), 306-312. Available online at https://www.fertstert.org/article/S0015-0282(11)02795-6/pdf
(8) Chu, N. V., & Edelman, S. V. (2001). Diabetes and erectile dysfunction. Clinical diabetes, 19(1), 45-47. Available online at http://clinical.diabetesjournals.org/content/diaclin/19/1/45.full.pdf