The Contribution of Diabetes

Mellitus in Developing Erectile

Dysfunction
Dena-Kay Walters

Abstract
Erectile Dysfunction (ED) is a condition in which a male is unable to maintain or to obtain an
erection. This dysfunction can be triggered by numerous factors, namely ageing, Diabetes
Mellitus (DM), etc. The disease, diabetes mellitus is diagnosed when there is an increased
glucose concentration present in the blood. Diabetes is classified as a risk factor of erectile
dysfunction; more than half the population of men with diabetes suffer from erectile dysfunction.
This research offers an explanation of how DM contributes to the development of erectile
dysfunction. The effects of a high blood sugar level in causing impotence are by virtue of the
damages sustained by the blood vessels, neurologic dysfunction and erectile smooth muscle
atrophy. The information collected were obtained through secondary sources, predominantly
scholarly sources such as peer reviewed journals. The information was then integrated to compile
this research essay. This research is of significance in developing treatment plans and
managerial strategies as well as preventative measures for diabetes associated erectile
dysfunction. The results of the research are viable and feasible claims. The proposed theories of
the contributing factors of diabetes associated erectile dysfunction are substantiated by
experimental evidence using animal models and human erectile tissue.

An increase in the blood sugar levels is the characteristic feature of Diabetes Mellitus
(DM). This metabolic and endocrinological disease is an occurrence of the impairment in one of
the bodys organs, the pancreas or the ineffectiveness of the insulin it secretes. There are four
categories of Diabetes Mellitus, namely Type I, Type II, Gestational, and other specified types,
with Type I and Type II being the most common types. Diabetes Mellitus has numerous
complications such as hypertension, atherosclerosis, obesity and erectile dysfunction (ED)
Inadequate penile erection and impotence are synonyms for erectile dysfunction, which is
defined as the incapability to successfully obtain or sustain a penile erection for intercourse
(Shamlouol and Ghanem 2012). The risk of developing erectile dysfunction increases with
diabetes mellitus but studies has not shown differentiation in either Type I or II as mentioned by
Penson and Wessels (2004). According to Gore and Rajfer (2004) more than 50% of diabetic
men suffer from erectile dysfunction. When compared with non-diabetic men, there is an
increased prevalence of erectile dysfunction at an earlier stage of life. In agreement is SantosLonghurst (2014), who stated that the National Institute of Diabetes and Digestive and Kidney
Diseases proposed that men with Diabetes Mellitus are 2-3 times more likely to develop erectile
dysfunction. This suggests, though erectile dysfunction is usually associated with men in later
years, age preference is not shown in diabetic males; an indicator that diabetes does contribute to
ED. Though DM is the second most common risk factor of ED (Shamlouol and Ghanem 2012),
it once was the most neglected condition until recent times where it is noted to be preventable.
Increased knowledge gained from extensive research and experiments conducted on animal
models and human tissue, in an effort to improve the quality of life of diabetic males (Penson
and Wessels 2004), has resulted in the projection of the malfunctions occurring in diabetes
associated erectile dysfunction. Invariably, the contributions of DM in developing ED are by
virtue of damages to blood vessels, neuropathy and smooth muscle dysfunction.
The male reproductive organ, like any other human organ is dependent upon the proper
functioning of the blood vessels. In individuals with DM the increased blood glucose levels
cause damage in the penile blood vessels as well as the surrounding vessels supplying it. The
physiology of these vessels is distorted by the destruction of the endothelial inner lining which
under normal circumstances secrete synthesized nitric oxide (NO). This NO is an important

component in acquiring and sustaining a successful erection as it is required for the relaxation of
erectile tissue that leads to the compression of the veins present. Compression causes occlusion,
thus impeding local venous return and increase the arterial pressure within the erectile tissue as
Chu and Edelman (2001) explained. In other words, as Dubois (2013) simplified, the release of
NO causes the smooth erectile muscle to relax which then chokes the vein preventing the blood
from leaving the penis. This preposition is plausible as NO is a known vasodilator which will in
turn increase blood flow to the male genitals and a sufficient increase in arterial pressure will
cause an erection to occur. Venous occlusive dysfunctions may not only be a result of the
reduction in the synthesis, release and activity of NO but also the leakage of blood from within
the erectile tissues, corpus cavernosa (Nunes 2012). This venous leakage is due to the
compromise in the drainage system. If there is blood leakage from the erectile tissue this
therefore implies that there is insufficient pressure needed to obtain a penile erection
successfully, therefore impotent.
Additionally, atherosclerosis is a vasculogenic factor in DM. Atherosclerosis is the
accumulation of lipid plaques within the blood vessel resulting in a smaller lumen. This
blockage in the penile artery or in pudendal arteries supplying the genitals obstructs blood flow
to the penis (Chu and Edelman 2001; Moore and Wang 2006). Chu and Edelman (2001); Moore
and Wang (2006), in extension implored that the close association of DM with atherosclerosis is
a result of the development of Advanced Glycated End-products (AGEs) in diabetic individuals.
AGEs are non- enzymatic reactions of glucose with proteins, lipids or nucleic acids to form
irreversible product build up known as Schiff bases (Moore and Wang 2006). This is a logical
claim as the lingering glucose that remains in the blood of diabetics after a meal will result in the
reaction of this sugar with proteins, acids and lipids present, forming plaques within these
vasculatures. Obstructed blood flow into the corpus cavernosa, again will elicit an inadequate
penile erection.
The normal mechanism of a penile erection would be regarded as a multi-systematic
process since a successful erection is achieved when there is healthy blood vessels, nerves, and
muscles are required along with proper cognitive functions. In persons with diabetes, it has been
proven that there is an impairment of the neurological system. Like the blood vessels, the nerves
produce NO, the main neurotransmitter which brings about smooth muscle relaxation required

for an erection. Damages to the nerves disallow the synthesis of NO, thus depressing its activity
leading to a maintained flaccidity. Furthermore, the elevated levels of AGEs in diabetics destroys
the myelin sheaths of nerve fibres and this disruption causes a delay in the transmission of nerve
impulses (Gore and Rajfer 2004; Nunes 2012). It can then be inferred that this delay will cause a
delay in penile erection and would thus present signs of erectile dysfunction. The
interrelationship between nerve and blood vessels is an implication that damages to the blood
vessels will also impact on the nerves. Essential for the survival of the cavernosal nerve cells is
the blood supply from respective so damages to these vessels will ultimately lead to nerve cell
death. A plausible explanation presented by Gore and Rajfer (2004); Nunes (2012). Simply put,
nerves in a similar manner to blood vessels are damaged by the high concentration of blood
glucose. Consequently, nerve damage affects both sensation and nerve signalling involved in
erection, Dubois (2013) revealed.
Equally important to the nerves and blood vessels, is the smooth erectile muscle for
normal penile erection. In diabetic male patients this muscle becomes dysfunctional as a
consequence of the impaired blood vessels supplying this muscle and by the high blood glucose
levels. The muscle cells now being insufficiently supplied with nutrients leads to early apoptosis
of smooth muscle cells, resulting in the death of the entire muscle (Nunes 2012). In addition
Nunes (2012) mentioned that the NO produced by the endothelium and nerves may react with
free oxygen radicals converting NO to nitrogen dioxide (NO2). The oxidation of NO to NO2 will
eliminate the effect of NO in causing penile smooth muscle relaxation. This is a feasible proposal
by Nunes (2012) as AGEs compounds do release oxygen radicals in the blood and if the penile
muscle is not relaxed, the mechanism to produce an erection is skewed. On the other hand,
though Penson and Wessels (2004) are in agreement with Nunes (2012) that AGEs affect smooth
erectile muscle, they suggested that abnormal levels of AGEs change the structure of smooth
erectile muscle such as increasing the collagen content of the muscle. The structural changes are
promoters of rigidity and decreases contractility of the muscle. Penile contractile muscle is
important for an erection hence this claim is also viable as decreased contraction of the smooth
muscle will result in erectile dysfunction.
Conclusively, diabetes mellitus increases the risk of developing erectile dysfunction. The
factors of diabetes associated erectile dysfunction are ultimately related to the vasculogenic and

neurogenic factors as well as smooth muscle dysfunction. This evident as it has been tested and
proven, with the use of animal models and human tissue, that the complete health and wellness
of the blood vessels, nerves and penile muscle is essential in obtaining an erection as the
mechanism is described as multi-systematic. Knowledge of the particular systems affecting
penile erection in diabetic males and how it is affected may help developing treatment to
improve their quality of life.

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