It's an all too common problem: Roughly half of men with diabetes—and up to 25 percent of men overall—experience erectile dysfunction (ED) at some point in their lives. And it's a complicated problem, too, with diverse physical origins and complex emotional ramifications. Yet diabetes-related ED needn't be a no-sex sentence for men. There are ways to avoid this disorder and to treat it at any age. While much of the research on ED is still in its infancy, here is what science has to say so far.
Low testosterone represents another link between erectile dysfunction and heart disease. A man’s testosterone levels gradually diminish beginning at age 30. By the time he reaches his 70s, testosterone levels may have dropped to a tenth of youthful levels. Diminishing testosterone levels contribute to loss of muscle, increased body fat, and reduced libido. Fatigue is common, as is depression. Low testosterone levels can also result in reduced concentration, irritability, passivity, loss of interest in activities, and even hypochondria.
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55
Diuretics: Diuretics are also referred to as water pills. They can make the flow of blood to your penis less intense. This makes getting an erection difficult. Diuretics are also known to lower zinc levels, which can decrease the amount of testosterone your body makes. In turn, this can decrease your sex drive. It may also affect your muscle contraction.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Nitrates have only modest antianginal effects and offer no prognostic benefit for mild recurrent angina or unstable angina. Therefore, such anginal symptoms occurring after sildenafil use should be treated with other nonnitrate antianginal agents such as β-blockers.15x15Taylor, HA Jr. Sexual activity and the cardiovascular patient: guidelines. Am J Cardiol. 1999; 84: 6N–10N
Alprostadil is an ED drug that comes in two forms. One form (Caverject, Caverject Impulse, or Edex) is injected into the side of the penis to increase blood flow and cause an erection within 5 to 20 minutes. Its effects last 1 hour or less. The most common side effect is pain. Other side effects include bruising, redness, numbness, bleeding, and irritation.
PubMed | Google ScholarSee all References The risk of ED was 1.83 times higher in men with a total cholesterol level greater than 240 mg/dL as opposed to less than 180 mg/dL. Also, an HDL cholesterol level greater than 60 mg/dL was found to be protective against the development of ED. In the MMAS, HDL cholesterol levels were noted to have an inverse relationship with the presence of ED.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References Of 1774 patients with a history of myocardial infarction, only 2 who had experienced a myocardial infarction after sexual intercourse were able to exercise to at least 6 METs without symptoms.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
After adjusting for cardiovascular risk factors including diabetes, heart failure and stroke, those taking PDE5 inhibitors were found to be markedly less likely to die than those taking alprostadil or no erectile dysfunction drugs. Filling more prescriptions for PDE5 inhibitors appeared to be associated with a greater benefit, although Andersson said that trend should be interpreted with caution because the study was not large enough for a definitive dose-response analysis.
Talk with your doctor about your sexual health. Do not be shy or embarrassed. Your doctor has probably dealt with this issue before. If your doctor is an older man, he might even have ED. First, your doctor will figure out what is causing your ED, which can usually be done just by talking with you. Next, your doctor will look for risk factors for atherosclerosis (the Table) by asking you questions, checking your blood pressure, and performing a few blood tests. Identifying and successfully treating atherosclerotic risk factors can reduce the chance of developing major vascular events (heart attacks and strokes).
Crossref | PubMed | Scopus (23) | Google ScholarSee all References In some elderly men, tadalafil could be detected in the bloodstream 6 days after oral ingestion.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
Having chronically high blood pressure can affect overall satisfaction with sex and affect men’s ability to achieve a firm erection. Due to constant vessel damage as a result of high blood pressure, linings of the arteries begin to harden and narrow, a process called atherosclerosis. Because blood flow is limited to the affected regions of the body, arterial blood circulation to various organs—including the heart muscles, brain, and even the groin—can be compromised, with myocardial infarctions, strokes, and erectile difficulty being common in hypertensive patients. Studies show that approximately 30 percent of hypertensive patients reported having erectile dysfunction, and approximately 49 percent of men aged 40 to 79 had both high blood pressure and ED.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phosphodiesterase type 5 is found predominantly in the smooth muscle of the corpora cavernosa but can be found in smaller quantities in platelets and other vascular smooth muscle.56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.
Joel Fuhrman, M.D. is a board-certified family physician, six-time New York Times bestselling author and internationally recognized expert on nutrition and natural healing, who specializes in preventing and reversing disease through nutritional methods. Dr. Fuhrman coined the term “Nutritarian” to describe his longevity-promoting, nutrient dense, plant-rich eating style.
Nehra A, Jackson G, Miner M, Billups KL, Burnett AL, Buvat J, Carson CC, Cunningham GR, Ganz P, Goldstein I, Guay AT, Hackett G, Kloner RA, Kostis J, Montorsi P, Ramsey M, Rosen R, Sadovsky R, Seftel AD, Shabsigh R, Vlachopoulos C, Wu FC. The Princeton III Consensus recommendations for the management of erectile dysfunction and cardiovascular disease, Mayo Clin Proc , 2012, vol. 87 (pg. 766-778)https://doi.org/10.1016/j.mayocp.2012.06.015
27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
A follow-up study from the ExCEED database compared men with ED and prostate cancer to men with ED without prostate cancer and found that the prostate cancer survivors had worse erectile function but reported better quality of life than those without prostate cancer.37 The authors hypothesized that the prostate cancer survivors were able to “rationalize” away their sexual dysfunction with the knowledge that they may have been “cured” of their prostate cancer. Clearly, diabetic men could not use the same rationale.
Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).
*** High-risk patients include those with unstable or refractory angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction without intervention (<2 weeks), high-risk arrhythmia (exercise-induced ventricular tachycardia, implanted internal cardioverter defibrillator with frequent shocks, and poorly controlled atrial fibrillation), obstructive hypertrophic cardiomyopathy with severe symptoms, and moderate to severe valve disease, particularly aortic stenosis.
Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Crossref | PubMed | Scopus (47) | Google ScholarSee all References Because of this perceived increase in risk, many couples are concerned about resuming sexual activity in the setting of cardiac disease. A study that monitored male patients after coronary artery bypass grafting found that 17% of patients and 35% of their partners were afraid of resuming sexual activity.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.