This web only provides the extract of this article. If you want to read the figures and tables, please reference the PDF full text on Blackwell Synergy. Thank you.
- Review -
Do lifestyle changes work for improving erectile dysfunction?
Kaya Horasanli, Ugur Boylu, Muammer Kendirci, Cengiz Miroglu
The Second Urology Department, Sisli Etfal Training and Research Hospital, Sisli-34377, Istanbul, Turkey
The main cause of erectile dysfunction (ED) is organic in nature, with vascular etiologies being the most common
risk factors. Although there have been sufficient data on the relationship between ED and several well-recognized risk
factors, including aging, coronary artery disease, atherosclerosis, diabetes mellitus, dyslipidemia, high blood pressure,
and pelvic surgeries, little attention has been paid by the urologists to the role of lifestyle factors in ED. However,
accumulating data from basic science and clinical studies have determined a link between the occurrence of ED and
a number of lifestyle factors, such as smoking, obesity, alcohol consumption, and lack of physical activity. The
application of findings from animal and human studies to the clinical practice regarding the modification of lifestyle
factors could help improving ED as well as reducing the risks of developing cardiovascular diseases. This
communication addresses the impact of lifestyle factors on erectile function and the potential benefits of modifying these
factors to improve ED in respect to the current
evidence. (Asian J Androl 2008 Jan; 10: 28_35)
Keywords: erectile dysfunction; lifestyle; smoking; obesity; alcohol; sedentary life
Correspondence to: Dr Muammer Kendirci, Sisli Etfal Egitim ve Arastirma Hastanesi, 2. Uroloji Klinigi, Sisli-34377, Istanbul, Turkey.
Tel: +90-212-231-2209 ext. 1290 Fax: +90-212-233-9687
Erectile function is a complex phenomenon regulated by neural, hormonal, vascular and structural factors. Penile
erection is the end result of a chain of events that cause smooth muscle relaxation in the corpora cavernosa of the
penis. Upon sexual stimulation, nitric oxide (NO), the key mediator for the initiation and maintenance of
penile erection, is synthesized and released by the autonomic nerves and endothelium, serving the penile
arteries and nerve terminals of the corpus cavernosum . NO enters the cavernosal smooth muscle cell and activates soluble guanylate
cyclase (sGC), which promotes the formation of cyclic guanosine monophosphate (cGMP). Through a cascade of
events, cGMP reduces intracellular calcium levels, allowing for relaxation of smooth muscle cells of the vasculature.
Good erectile function depends on a delicate homeostasis between vascular constricting and relaxing factors through a
The vascular endothelium of the penis plays a pivotal role in modulating vascular tone and blood flow into the
penis in response to humoral, neural, and mechanical
stimuli. In endothelial dysfunction, the regulatory role of the
endothelium is hindered, resulting in decreased responsiveness to vasodilatory mediators and/or increased sensitivity to
various vasoconstricting agents. Well-recognized disease states and vascular risk factors, such
as diabetes mellitus, coronary artery disease, atherosclerosis, hypertension, and smoking, have long been known to impair penile
endothelial function, resulting in a decrease in endothelial-dependent corpora cavernosal smooth muscle relaxation through
decreased expression and activity of neuronal and endothelial NO synthase (nNOS and eNOS), impaired NO release,
and/or increased destruction or total loss of NO bioactivity in the penis .
Although the impact of abovementioned well-known risk factors and disease states on erectile function have been
extensively elucidated, little attention has been paid by the sexual medicine specialists to the role of lifestyle factors in
penile endothelial function and ED. As ED has a significant impact on quality-of-life by reducing self-esteem and
confidence, and by affecting interpersonal relationships to the point of termination, all aspects of the contributing
factors need to be evaluated. Recently accumulating evidences from basic science and clinical studies have
demonstrated the link between the occurrence of ED and a number of lifestyle factors, such as smoking, obesity, alcohol
consumption, and lack of physical activity (Figure 1) [3, 4]. More importantly, as ED and cardiovascular diseases
have epidemiologic and pathophysiologic associations, it
is crucial to ascertain these unfavorable lifestyle factors
not only for erectile function but also for a generalized
Current practice in ED treatment has been mainly
based on utilizing type 5 phosphodiesterase inhibitors
(PDE-5i) as the first-line approach for majority of cases,
because of their high efficacy, ease of use, and acceptable
safety profile. However, some ED patients may not be
eligible for PDE-5i due to a number of factors, including
lack of efficacy, side effects, contraindications, loss of
efficacy, advanced age, progression of the underlying
disease, and uncontrolled co-morbidities . Recent
evidence from clinical studies suggests that the
modification of lifestyle factors could help improving ED as
well as reducing the risks of developing cardiovascular
disease. Therefore, this communication addresses the
impact of lifestyle factors on erectile function and the
potential benefits of modifying these factors to improve
ED in respect to the current evidence.
Although there is much discussion regarding the role
of smoking on erectile function, most investigators still
consider smoking as a risk factor for vasculogenic ED
. However, the underlying pathophysiology of ED in
smokers remains poorly understood.
In Massachusetts Male Aging Study (MMAS), Feldman
et al.  found that smokers were more likely
to have ED than nonsmokers (24% vs. 14%, adjusted
odds ratio [OR], 1.97). Controlling for multiple confounders, Mannino
et al.  investigated whether cigarette smoking was associated with ED among
middle-aged men using a secondary analysis of a
cross-sectional survey of 4 462 US Army veterans from the
Vietnam era. The study sample consisted of 1 162 nonsmokers, 1 292 former smokers, and 2 008 current
smokers. The prevalence of ED was found to be 2.2%
among nonsmokers, 2.0% in former smokers, and 3.7%
in current smokers (P = 0.005). The unadjusted OR of
the association between smoking and reported ED was
1.8. They also demonstrated that neither the number
years of smoking nor the number of cigarettes smoked
daily were significant predictors of ED in current
smokers. After adjusting various risk factors, including
age, vascular disease, psychiatric disorders, hormonal
factors, substance abuse, marital status, and race, the
authors concluded that a higher percentage of cigarette
smokers reported ED than did nonsmokers.
Others have also demonstrated that the duration of
smoking, the number of cigarettes smoked per day, and
the number of years smoking directly correlated with
ED . The results of this study demonstrated not only
a higher prevalence, but also heightened severity of ED.
Clinically, there are strong parallels and shared risks
among smoking, coronary artery disease,
atherosclerosis and ED. Basic science studies provide strong
indirect evidence that smoking may affect penile erection by
the impairment of endothelium-dependent smooth muscle
relaxation. To establish a causal explanation, dose
response is one of the key components. Feldman
et al.  presented data of a gradient by showing the sequentially
increasing risk of ED in smokers with no exposure to
passive smoke, those with passive exposure only at home,
those with passive exposure at work and those with
passive exposure at both places. The adjusted ED incidences
were 14%, 23%, 28% and 33%, respectively . Other
researchers analyzed the role of smoking as a risk factor
for ED using data from a cross-sectional cohort in the
general population . In this study by Mirone
et al. , a total of 2 010 men older than 18 years were
randomly identified and interviewed by 143 general
practitioners. In comparison with nonsmokers, current
smokers had an OR of ED of 1.7 and ex-smokers of 1.6 of
developing ED. Of interest, they noted a true
association between smoking and ED risk in subjects without
any history of cardiovascular disease, cardiomyopathy,
hypertension, diabetes or neuropathy. These
researchers provide evidence that smoking influences the risk of
ED and the duration of the habit increased the risk.
A significant dose response relationship of smoking
and cavernous arterial occlusion was reported by Rosen
et al. . More recent studies supporting the evidence
revealed that cumulative smoking in pack-years suggests
a dose response pattern with the risk of ED  and as
in Boston Area Community Health (BACH) survey this
dose response association between smoking and ED is
significant with more than 20 pack-years of exposure
. Passive smoking remains unclear whether it causes
ED or not. In MMAS , passive exposure to cigarette
smoke predicted ED, whereas in the BACH survey, the
risk of ED was slightly but not significantly increased .
In addition to epidemiological studies, clinical and
animal studies support the concept that smoking causes
peripheral vascular disease and adversely affects erectile
function by impairing endothelium-dependent smooth
muscle relaxation . In one study, researchers
reviewed angiograms of the hypogastric-cavernous
arterial bed in young men with ED who had been referred for
selective pudendal angiography . Patients with
¡Ý 50% luminal diameter reduction were found to have smoked
more pack-years than patients without arterial disease.
This study showed that cigarette smoking was an
independent risk factor for the development of
atherosclerotic lesions of the internal pudendal arteries of young,
impotent men. Using a polysomnographic assessment,
Hirshkowitz et al.  examined the relationship between
cigarette smoking and erectile physiology in 314 men
with ED. The authors observed that penile rigidity
during nocturnal erections inversely correlated with the
number of cigarettes smoked per day and hypothesized that
smoking was associated with impairment of autonomic
function and measures of intracorporeal pressures. The
group of men who smoked the most (more than 40
cigarettes per day) had the shortest duration of nocturnal
tumescence and quickest period for detumescence. Short-term studies have demonstrated that impaired
nocturnal tumescence recording could be reversed by an
abrupt cessation of smoking .
While it is known that chronic smoking damages the
endothelium, nicotine can acutely cause significant
vasospasm of the penile arteries . Juenemann
et al.  assessed the effects of 7 to 12 minutes of acute
smoke exposure on penile erection in dogs. After
inhalation of cigarette smoke, five of six did not achieve
erection with neurostimulation. Arterial inflow and
veno-occlusion were impaired with almost complete abolition of
venous restriction. Moreover, chronic smoking has been
documented to be associated with ultrastructural
damage to the corpora cavernosa and to decrease cavernous NOS
levels . Other animal studies have shown
ultrastructural, enzymatic and morphological changes in the
endothelium of smoke-exposed animals [20, 21]. The
effects are illustrated in Figure 2. Free radicals and
aromatic compounds decrease the endothelial synthesis of
NO, causing impaired endothelium-dependent relaxation
of arteries, which is the earliest clinical sign of
endothelial dysfunction . The impaired
endothelium-dependent relaxation of saphenous vein rings appears to be
caused by decreased activity of eNOS, which is
attributable to an inadequate supply of the coenzyme
tetrahydrobiopterin . Cigarette smoke extracts can cause
smooth muscle contraction by the superoxide anion-mediated degradation of NO .
Reversal of ED by cessation of smoking may work
for treatment without medications or when medications
fail. Supporting data from Mannino et al.  revealed
that former smokers have significantly low rate of ED
compared to current smokers (2% vs. 3.7%). In a
prospective study, Guay et al.  reported significant and
rapid improvement in penile tumescence and rigidity
after cessation of smoking in patients smoking over 30
packs-year. Contrary to these, in the Health Professionals
Follow-up Study (HPFS)  including 22 086 men revealed, although there remains a small difference,
current and past smokers had a significant increased risk of
ED (current smokers' relative risk [RR]: 1.5; 95% CI:
1.3_1.7; past smokers' RR: 1.2, 95% CI, 1.1_1.3). Additionally, Derby
et al.  reported reassessment of the MMAS population regarding the modifiable risk
factors. By design, the analysis sample excluded men
with baseline ED, diabetes, heart disease and prostate
cancer, which are medical diseases or treatments that
may overwhelm any association of smoking with ED.
However, in this 8-year analysis, 50% of smokers stopped
smoking; nevertheless, no status change in ED was
observed among the quitters. Thus, smoking cessation in
middle-aged men did not significantly decrease the risk
of ED. Therefore, risk factors for ED may require
earlier intervention or a prolonged period for reversal,
similar to that in the differences in reversibility in coronary
artery disease and death from myocardial infarction.
3 Obesity and dyslipidemia
High low-density lipoprotein (LDL) and total cholesterol, and low high-density lipoprotein (HDL)
cholesterol are known risk factors for vascular disease.
Because of higher saturated fats in diets and sedentary
lifestyle, the prevalence of obesity is increasing in the
modern world. Population-based studies demonstrate
that dyslipidemia and obesity are major risk factors for
ED. Among men with ED, 26% were found to have elevated serum cholesterol levels . Recent studies
have shown that the prevalence of hypertension and
hyperlipidemia in ED patients being between 40%_80% .
In the original MMAS study, having any degree of
ED was not dependent upon the body mass index (BMI),
but the probability of having ED was inversely related to
the HDL levels. The moderate and complete ED rates
were 25% and 16%, respectively, for the High-density
lipoproteins (HDL) levels of 30 mg/dL, while it was 7%
and 0% for the moderate and complete ED, respectively,
when the HDL levels were considered to be 90 mg/dL
. In 1994, Wei et al.  reported the OR of
developing ED for every mmol/L increase in cholesterol was
1.32 (95% CI, 1.04_1.68), while every mmol/L of increase in HDL cholesterol was associated with 0.38 times
increased risk for ED (95% CI, 0.18_0.80). This article
supports the MMAS data regarding the importance of
the HDL cholesterol. In addition to the longitudinal
population-based studies, Chung et al.  investigated 325
men who were diagnosed with ED regarding the effect
of intracavernosal injections on the erectile response as
graded on a scale from 0 to 4 . They showed
significantly better mean erectile responses in patients with
> 120% ideal body weight than in < 120% ideal body
weight (1.62 vs. 1.32) after intracavernosal
Using a nationally representative managed care
database claims that covered 51 health plans with 28 million
lives between 1995 and 2002, Seftel et al.  found
that 42.4% of men with ED had hyperlipidemia. This
rate is 5.4% higher than the rate in the study of Solomon
et al.  for hyperlipidemia. The Rancho Bernardo
Study assessed age, smoking, hypertension, diabetes,
hypercholesterolemia and obesity in 1 810 men from 1972
to 1974, and 25 years later 570 surviving males
completed the International Index of Erectile Function
(IIEF-5) questionnaire. In a cumulative logit model, age,
hypercholesterolemia and obesity were found to be independent
predictors of increased ED severity . Roumeguere
et al.  demonstrated the prevalence of
hypercholesterolemia as 70.6% in 216 ED patients, whereas this value
was only 52% in controls with normal erectile function.
In another case-control study by Nikoobakht et al.
, mean plasma cholesterol and low-density lipoprotein
(LDL) levels in individuals suffering from ED were
significantly higher than controls. However, no difference
in the mean plasma triglyceride and HDL levels was
reported . In the health professionals follow-up study
(HPFS) , BMI > 28.7 kg/m2 remained independently
associated with ED (RR, 1.2; 95% CI, 1.0_1.5). One
drawback of this study was that assessment of ED was
based on a single question. Blanker et al. 
demonstrated that BMI > 30 kg/m2 was associated with ED on
univariate and multivariate analyses (OR, 3.0, 95% CI,
1.7_5.4). Unfortunately this study did not include
important factors such as hypertension and diabetes on
The association between hyperlipidemia and ED was
originally attributed to atherosclerosis in the
hypogastric-cavernosal arterial vascular bed, resulting in a
decline in penile blood flow. Impairment of
endothelium-dependent relaxation in various vascular beds of men with
hypercholesterolemia has been well established [37, 38].
Several researchers have attempted to locate
biochemical mediators that reverse the endothelial effects of
hyperlipidemia, which interferes with cavernous smooth
muscle relaxation. Oxidized LDL (ox-LDL) is found in
plaque formation to the endothelium and is a major cause
of impaired relaxation . Ox-LDL, the production of
superoxide radicals, and functional impairment of eNOS
are postulated to be the prime mechanisms for the
development of ED in the early stages of hyperlipidemia
[40_42]. Endothelin-1 has also been demonstrated to be
increased in hyperlipidemic patients, although the exact
mechanism of activation has not been fully elucidated .
In an animal model, Gholami et al.  revealed that
hypercholesterolemic rats had lower nerve content, fewer
endothelial cells, and higher smooth muscle content than
rats maintained with normal cholesterol levels. In this
study, rats placed on high-cholesterol diets showed
hypermyelination, severe atrophy of axons, a decrease
in the number and size of non-myelinated axons,
disarray of the smooth muscle cells with scant myofilaments
and foamy cytoplasm, and denuded endothelial lining of
the sinusoids covered by numerous platelets. The
authors concluded that a high-fat diet caused ED with
accompanying neurological and vascular changes, and
theorized that a vascular endothelial growth factor (VEGF)
and adeno-associated virus-mediated brain-derived nerve
growth factor (AAV-BDNF) could reverse some of the
underlying vascular pathology in hypercholesterolemia.
In another animal study, intracavernous injections of
VEGF were noted to protect the corporal endothelium
from hypercholesterolemia-induced injury, thus
preserving endothelial-dependent corporal smooth muscle
relaxation in the hypercholesterolemic rabbit .
In histological evaluations, Juenemann et
al.  demonstrated significant cavernous smooth muscle cell
degeneration with a loss of intercellular contacts in
rabbits put on high-cholesterol diets. Their data imply that
impaired lipid metabolism causes cavernous smooth muscle degeneration, which plays a major role in the
pathogenesis of ED. Ox-LDL, a thromboxane A2
receptor antagonist, produced a protective metabolic effect
on the erectile tissue of these hypercholesterolemic
rabbits. This is another avenue of therapy worthy of
Clinical studies performed in ED men contributed
what was found in the animal studies. Atahan et
al.  evaluated the relationship between the lipid levels and
electromyography of the corpora cavernosa (CC-EMG) in
39 patients with ED following intracavernous
papaverine injections. The authors demonstrated a correlation
between the presence of vasculogenic ED and the
cholesterol levels. On CC-EMG, there was a significant
difference in pre- and post-injection amplitudes between those
patients with vasculogenic and non-vasculogenic ED.
Although the effect of lipid-lowering drugs on
erectile function remains undefined at this stage, recent
evidence supports the benefit of using lipid-lowering
approaches. Saltzman et al.  studied the use of statins
to lower cholesterol and improve erectile function in men
who had hypercholesterolemia as the only risk factor for
ED. These investigators found that eight of the nine
men in the study reported improved erections adequate
for sexual intercourse as measured by nocturnal penile
tumescence and rigidity (Rigiscan) testing after using
atorvastatin with a mean 3.7 months of treatment. They
found a significant decrease in mean total and LDL
cholesterol after treatment and showed an increase in
erectile-function-domain scores from 14.2 to 20.7 as
measured by the Sexual Health Inventory of Male (SHIM)
questionnaire. Objective measurement using RigiScan
showed an increase in mean penile rigidity at both the
base and tip. The authors concluded that erectile
function improved in men with hypercholesterolemia as the
only risk factor for ED when treated with atorvastatin.
Additionally, in a case-control study, contrary to
Derby et al. , loosing weight was proven to be
independently associated with changes in the IIEF scores.
Esposito et al.  carried out a randomized clinical trial
of 110 obese ED men who did not have diabetes, hypertension, or hyperlipidemia. Men in the intervention
group received detailed advice regarding loosing 10% or
more of their total body weight by reducing caloric
intake and increasing physical activity, while men in the
control group were given general information about
healthy food choices and exercise. These investigators
demonstrated significantly decreased BMI and increased
mean IIEF scores in the intervention group within 2 years.
Finally, as both obesity and dyslipidemia promote
atherosclerosis, which are independent risks for
development of ED, a detailed analysis of these conditions are
crucial in clinical settings. A number of studies showing
evidence for the link among obesity and/or dyslipidemia
and ED is summarized in Tables 1 and 2.
4 Alcohol consumption
Excess alcohol consumption has long been regarded
as a risk factor for ED. Although it is considered to
improve erection and sexual drive when utilized small
amounts because of its vasodilatory effect and
suppression of anxiety, large amounts can cause central sedation,
decreased libido and ED .
In MMAS, the adjusted incidence for ED was 16% in
men with < 1 drink/day, 16% in those with 1_3
drinks/day and 15% in those with more than 4 drinks/day . This
incidence was adjusted for age, smoking, cholesterol,
hypertension, physical activity, fat intake, and obesity,
testosterone, depression and antihypertensive medications.
In the cross-sectional HPFS study, the multivariate
adjusted RRs for ED were decreased with moderate levels
of alcohol consumption. The RRs were 1.0, 0.9, 0.8
and 1.0 for 0.1_4.9, 5.0_14.9, 15_29.9, > 30 g/day of
alcohol consumption, respectively . In the HPFS
prospective cohort study, no significant difference in the
risk of developing ED was found in all categories of
alcohol consumption. The multivariate RRs for 0.1_4.9,
5.0_14.9, 15.0_29.9 and > 30 g/day of alcohol was 1.0,
1.0, 1.0 and 1.1 . However, Derby et
al.  prospectively evaluated the effect of alcohol consumption
on erectile function and were unable to find any
relationship between heavy drinking and ED. Similar results
were observed in the study by Paick et al. . In
contrast, Polsky et al.  reported a significantly higher
OR with > 8 drinks/day than 1_7 drinks/day (2.09
vs. 1.96) after adjusting age, the education levels, presence of
diabetes and smoking
Interestingly, a recent meta-analysis which included
11 cross-sectional studies found that regular alcohol
consumption was negatively correlated with ED (OR,
0.79; 99% CI, 0.67_0.92) . Although any
association was observed between less alcohol consumption
(1_7 drinks/week) and ED, the authors reported that
consumption of 8 or more drinks/week significantly reduced
the risk of ED (OR, 0.85; 99% CI, 0.73_0.99). These
contradictory results from epidemiological studies are not
sufficient to make a conclusion regarding the role of
alcohol consumption in ED. Therefore, further basic
science and clinical research is needed by evaluating the
amount, the duration and the type of alcohol consumed
in order to delineate whether alcohol is a contributor or
protector for ED.
5 Physical activity
Given the similar risk factor profiles for ED and
cardiovascular diseases, it can be hypothesized that they
may share similar protective factors including physical
activity. Recently, there have been explosion of data
regarding the benefit of physical activity on erectile and
cardiovascular function. In a number of independent
cross-sectional and cohort studies, regular exercise has
been shown to be beneficial on erectile function.
In MMAS , the adjusted incidence of ED was found to be lower in those with > 200 kcal/day of
physical activity compared to those with < 200 kcal/day of
physical activity (15% vs. 19%). Another supporting
data from Derby et al.  clearly demonstrated the
reduced risk of ED in men with a sedentary lifestyle at
baseline when they became physically active during the
course of the study. Men who initiated physical activity
in midlife had a 70% reduced risk for ED relative to those
who remained sedentary. The highest risk for ED was
among men who were sedentary both at the baseline visit
and follow-up. In this study, reduction in smoking,
obesity and the amount of alcohol consumption were also
found to be associated with a lower overall incidence of
ED, although not as strongly as the levels of physical
Other cross-sectional studies have also shown
significantly reduced rate of ED when higher levels of
physical activity were employed. In HPFS , physical
activity was associated with lower risk for ED; the multivariate
relative risk was 0.7 (95% CI, 0.6_0.7) for >
32.6 metabolic equivalent hours of exercise per week
vs. 0 to 2.7 metabolic equivalent hours of exercise per week. In 2006,
Bacon et al.  investigated the impact of health
behaviors on development of ED among 22 086 participants.
They found that 3 905 men reported occurrences of ED
within 14-year-follow-up period. These investigators
reported that higher levels of physical activity were
associated with a reduced risk of ED. They also found
that higher levels of sedentary behavior were a positive
predictor for ED.
Nicolosi et al.  conducted a study in 2 412 men
aged 40 to 70 in Brazil, Italy, Japan and Malaysia to
examine the relationship between the lifestyle factors and
ED. Of these men, 1 335 had no diagnosis of
cardiovascular or prostate diseases, diabetes, ulcer or depression.
They demonstrated an inverse correlation between ED
and the levels of physical activity. Among study
participants, 13.9% of men with greater than average levels of
physical activity had ED, while 17.5% of men with
average levels of physical activity demonstrated ED; this rate
was 31.8% in men with less than average physical activity.
In a multivariate regression analysis, Esposito
et al.  showed that physical activity as well as BMI and
C-reactive proteins independently predicted the IIEF scores.
A recent meta-analysis by Cheng et al. 
including 7 cross-sectional studies evaluated the impact of
physical activity on erectile function. The analysis revealed
that the presence of ED was negatively associated with
physical activity. These investigators reported a dose
response relationship between ED and physical activity,
with higher physical activity conferring lower risks for
ED (OR = 1 for low activity, OR = 0.63 for moderate
activity and OR = 0.42 for high activity). They
concluded that, although causality cannot be demonstrated
from cross-sectional studies, the apparent protective
effect of physical activity on ED should be further
investigated using large-scale cohort studies or randomized
Many men with ED have underlying vascular risk factors, such as diabetes, hypertension, coronary artery
disease, smoking, and lipid abnormalities. Controlling
these risk factors with lifestyle changes and/or proper
medications may improve the chance of success with
available ED treatments . ED patients taking
medications known to have adverse sexual side effects can
be switched to an alternative drug or drug class when
appropriate. For example, patients who are taking
propranolol or metoprolol, which are known to aggravate
sexual dysfunction, might be changed to atenolol, while
patients receiving anti-hypertensive medications may
substitute another class of drug altogether, such as
angiotensin-converting enzyme inhibitors (ACEIs) or
angiotensin-receptor blockers (ARBs). Losartan (an
angiotensin II receptor antagonist), in particular, has been
shown to have a beneficial effect on erectile function
. Similarly, antidepressive medications known to
worsen erectile function can be switched those with less
or no deleterious effects on erectile function.
Controlling blood sugar with diet and antidiabetic medications
may also help improve erectile and vascular endothelial
Clinical studies provide evidence that an organic
etiology is responsible for more than 80% of patients with
ED. Although there have been sufficient data on the
relationship between ED and several well-recognized risk
factors, including aging, coronary artery disease,
atherosclerosis, diabetes mellitus, high blood pressure,
and pelvic surgeries, less attention has been paid by the
sexual medicine specialists to the role of the lifestyle
factors in ED. Recent basic science and clinical studies
have determined a link between the occurrence of ED
and a number of lifestyle factors, such as smoking,
obesity, alcohol consumption, and lack of physical activity.
Efforts focusing on the modification of these lifestyle
factors could help improving ED, as well as reducing the
risks of developing cardiovascular disease. Further
research is needed to elucidate the exact pathophysiology
of these lifestyle factors on erectile function and
potential benefits of modifying these unfavorable risk factors
on improving erectile function.
1 Kim N, Azadzoi KM, Goldstein I, Saenz de Tejada I. A nitric
oxide-like factor mediates nonadrenergic-noncholinergic
neurogenic relaxation of penile corpus cavernosum smooth muscle. J
Clin Invest 1991; 88: 112_8.
2 Kendirci M, Hellstrom WJ. Role of Endothelium in Erectile
Function and Dysfunction. In: Aird WC, editor. Endothelial
Biomedicine: A Comprehensive Reference. Cambridge, New York:
Cambridge University Press; 2007. p1541_8.
3 Bacon C, Mittleman M, Kawachi I, Giovannucci E, Glasser D,
Rimm E. A prospective study of risk factors for erectile
dysfunction. J Urol 2006; 176: 217_21.
4 Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R,
D'Andrea F, et al. Effect of lifestyle changes on erectile
dysfunction in obese men: a randomized controlled trial. JAMA 2004;
5 Kendirci M, Tanriverdi O, Trost L, Hellstrom WJ. Management
of sildenafil treatment failures. Curr Opin Urol 2006; 16: 449_59.
6. Sullivan ME, Keoghane SR, Miller MA. Vascular risk factors and
erectile dysfunction. BJU Int 2001; 87: 838_45.
7 Feldman HA, Johannes CB, Derby CA, Kleinman KP, Mohr BA,
Araujo AB, et al. Erectile dysfunction and coronary risk factors:
prospective results from the Massachusetts male aging study.
Prev Med 2000; 30: 328_38.
8 Mannino DM, Klevens RM, Flanders WD. Cigarette smoking: an
independent risk factor for impotence? Am J Epidemiol 1994;
9 El-sakka AI. Characteristics of erectile dysfunction in Saudi
patients. Int J Impot Res 2004; 16: 13_20.
10 Mirone V, Imbimbo C, Bortolotti A, Di Cintio E, Colli E, Landoni M,
et al. Cigarette smoking as risk factor for erectile dysfunction: results
from an Italian epidemiological study. Eur Urol 2002; 41: 294_7.
11 Rosen MP, Greenfield AJ, Walker TG, Grant P, Dubrow J, Bettmann
MA, et al. Cigarette smoking: an independent risk factor for
atherosclerosis in the hypogastric-cavernous arterial bed of men with
arteriogenic impotence. J Urol 1991; 145: 759_63.
12 Polsky J, Aronson K, Heaton J, Adams M. Smoking and other
lifestyle factors in relation to erectile dysfunction. BJU Int 2005;
13 Kupelian V, Link C, McKinlay J. Association between smoking,
passive smoking, and erectile dysfunction: results from the
Boston Area Community Health (BACH) Survey. Eur Urol 2007;
14 McVary KT, Carrier S, Wessells H. Subcommittee on Smoking and
Erectile Dysfunction Socioeconomic Committee, Sexual
Medicine Society of North America. Smoking and erectile dysfunction:
evidence based analysis. J Urol 2001; 166: 1624_32.
15 Hirshkowitz M, Karacan I, Arcasoy MO, Acik G, Narter EM,
Williams RL. Prevalence of sleep apnea in men with erectile
dysfunction. Urology 1990; 36: 232_4.
16 Guay AT, Perez JB, Heatley GJ. Cessation of smoking rapidly
decreases erectile dysfunction. Endocr Pract 1998; 4: 23_6.
17 Jacobs MC, Lenders JW, Kapma JA, Smits P, Thien T. Effect of
chronic smoking on endothelium-dependent vascular relaxation
in humans. Clin Sci (Lond) 1993; 85: 51_5.
18 Juenemann KP, Lue TF, Luo JA, Benowitz NL, Abozeid M,
Tanagho EA. The effect of cigarette smoking on penile erection.
J Urol 1987; 138: 438_41.
19 Mersdorf A, Goldsmith PC, Diederichs W, Padula CA, Lue TF,
Fishman IJ, et al. Ultrastructural changes in impotent penile
tissue: a comparison of 65 patients. J Urol 1991; 145: 749-58.
20 Jorge PA, Ozaki MR, Almeida EA. Endothelial dysfunction in
coronary vessels and thoracic aorta of rats exposed to cigarette
smoke. Clin Exp Pharmacol Physiol 1995; 22: 410_3.
21 Pittilo RM, Mackie IJ, Rowles PM, Machin SJ, Woolf N. Effects of
cigarette smoking on the ultrastructure of rat thoracic aorta and its
ability to produce prostacyclin. Thromb Haemost 1982; 48: 173_6.
22 Powell JT. Vascular damage from smoking: disease mechanisms
at the arterial wall. Vasc Med 1998; 3: 21_8.
23 Higman DJ, Strachan AM, Buttery L, Hicks RC, Springall DR,
Greenhalgh RM, et al. Smoking impairs the activity of
endothelial nitric oxide synthase in saphenous vein. Arterioscler Thromb
Vasc Biol 1996; 16: 546_52.
24 Murohara T, Kugiyama K, Ohgushi M, Sugiyama S, Yasue H.
Cigarette smoke extract contracts isolated porcine coronary
arteries by superoxide anion-mediated degradation of EDRF. Am J
Physiol 1994; 266: H874_80.
25 Derby CA, Mohr BA, Goldstein I, Feldman HA, Johannes CB,
McKinlay JB. Modifiable risk factors and erectile dysfunction:
can lifestyle changes modify risk? Urology 2000; 56: 302_6.
26 Rosen RC, Fisher WA, Eardley I, Niederberger C, Nadel A, Sand
M. Men's Attitudes to Life Events and Sexuality (MALES) Study.
The multinational Men's Attitudes to Life Events and Sexuality
(MALES) study: I. Prevalence of erectile dysfunction and related
health concerns in the general population. Curr Med Res Opin
2004; 20: 607_17.
27 Seftel AD, Sun P, Swindle R. The prevalence of hypertension,
hyperlipidemia, diabetes mellitus and depression in men with
erectile dysfunction. J Urol 2004; 171: 2341_5.
28 Feldman HA, Goldstein I, Hatzichristou DG, Krane RJ, McKinlay
JB. Impotence and its medical and psychosocial correlates: results
of the Massachusetts Male Aging Study. J Urol 1994; 151: 54_61.
29 Wei M, Macera CA, Davis DR, Hornung CA, Nankin HR, Blair
SN. Total cholesterol and high density lipoprotein cholesterol as
important predictors of erectile dysfunction. Am J Epidemiol
1994; 140: 930_7.
30 Chung WS, Sohn JH, Park YY. Is obesity an underlying factor in
erectile dysfunction? Eur Urol 1999; 36: 68_70.
31 Solomon H, Man J, Wierzbicki AS, O'Brien T, Jackson G.
Erectile dysfunction: cardiovascular risk and the role of the cardiologist.
Int J Clin Pract 2003; 57: 96_9.
32 Fung MM, Bettencourt R, Barrett-Connor E. Heart disease risk
factors predict erectile dysfunction 25 years later: the Rancho
Bernardo Study. J Am Coll Cardiol 2004; 43: 1405_11.
33 Roumeguere T, Wespes E, Carpentier Y, Hoffmann P, Schulman
CC. Erectile dysfunction is associated with a high prevalence of
hyperlipidemia and coronary heart disease risk. Eur Urol 2003;
34 Nikoobakht M, Pourkasmaee M, Nasseh H. The Relationship
between Lipid Profile and Erectile Dysfunction. Urol J 2005; 2: 40_4.
35 Bacon CG, Mittleman MA, Kawachi I, Giovannucci E, Glasser
DB, Rimm EB. Sexual function in men older than 50 years of
age: results from the health professionals follow-up study. Ann
Intern Med 2003; 139: 161_8.
36 Blanker MH, Bohnen AM, Groeneveld FP, Bernsen RM, Prins A,
Thomas S, et al. Correlates for erectile and ejaculatory
dysfunction in older Dutch men: a community-based study. J Am Geriatr
Soc 2001; 49: 436_42.
37 Kugiyama K, Kerns SA, Morrisett JD, Roberts R, Henry PD.
Impairment of endothelium-dependent arterial relaxation by
lysolecithin in modified low-density lipoproteins. Nature 1990;
38 Rosenfeld ME. Oxidized LDL affects multiple atherogenic
cellular responses. Circulation 1991; 83: 2137_40.
39 Rubbo H, Trostchansky A, Botti H, Batthyany C. Interactions of
nitric oxide and peroxynitrite with low-density lipoprotein. Biol
Chem 2002; 383: 547_52.
40 Kim SC. Hyperlipidemia and erectile dysfunction. Asian J Androl
2000; 2: 161_6.
41 Kim SC, Kim IK, Seo KK, Baek KJ, Lee MY. Involvement of
superoxide radical in the impaired endothelium-dependent
relaxation of cavernous smooth muscle in hypercholesterolemic
rabbits. Urol Res 1997; 25: 341_6.
42 Liao L, Aw TY, Kvietys PR, Granger DN. Oxidized LDL-induced
microvascular dysfunction. Dependence on oxidation procedure.
Arterioscler Thromb Vasc Biol 1995; 15: 2305_11.
43 Saenz de Tejada I, Goldstein I, Azadzoi K, Krane RJ, Cohen RA.
Impaired neurogenic and endothelium-mediated relaxation of
penile smooth muscle from diabetic men with impotence. N Engl
J Med 1989; 320: 1025_30.
44 Gholami SS, Rogers R, Chang J, Ho HC, Grazziottin T, Lin CS,
et al. The effect of vascular endothelial growth factor and
adeno-associated virus mediated brain derived neurotrophic factor on
neurogenic and vasculogenic erectile dysfunction induced by
hyperlipidemia. J Urol 2003; 169: 1577_81.
45 Henry GD, Byrne R, Hunyh TT, Abraham V, Annex BH, Hagen
PO, et al. Intracavernosal injections of vascular endothelial growth
factor protects endothelial dependent corpora cavernosal smooth
muscle relaxation in the hypercholesterolemic rabbit: a
preliminary study. Int J Impot Res 2000; 12: 334_9.
46 Junemann KP, Aufenanger J, Konrad T, Pill J, Berle B,
Persson-Junemann C, et al. The effect of impaired lipid metabolism on
the smooth muscle cells of rabbits. Urol Res 1991; 19: 271_5.
47 Atahan O, Kayigil O, Metin A. Electrical activity of corpus
cavernosum in vasculogenic and non-vasculogenic erectile
dysfunction. Scand J Urol Nephrol 1997; 31: 549_54.
48 Saltzman EA, Guay AT, Jacobson J. Improvement in erectile
function in men with organic erectile dysfunction by correction
of elevated cholesterol levels: a clinical observation. J Urol 2004;
49 Miller NS, Gold MS. The human sexual response and alcohol and
drugs. J Subst Abuse Treat 1988; 5: 171_7.
50 Paick JS, Yang JH, Kim SW, Ku JH. Severity of erectile
dysfunction in married impotent patients: interrelationship with
anthropometry, hormones, metabolic profiles and lifestyle. Int J
Urol 2007; 14: 48_53.
51 Cheng JY, Ng EM, Chen RY, Ko JS. Alcohol consumption and
erectile dysfunction: meta-analysis of population-based studies.
Int J Impot Res 2007; 19: 343_52.
52 Nicolosi A, Moreira E, Villa M, Glasser D. A population study of
the association between sexual function, sexual satisfaction and
depressive symptoms in men. J Affect Disord 2004; 82: 235_43.
53 Cheng JY, Ng EM, Ko JS, Chen RY. Physical activity and
erectile dysfunction: meta-analysis of population-based studies. Int J
Impot Res 2007; 19: 245_52.
54 Kendirci M, Nowfar S, Hellstrom WJ. The impact of vascular risk
factors on erectile function. Drugs Today (Barc) 2005; 41: 65_74.
55 Khan MA, Morgan RJ, Mikhailidis DP. The choice of
antihypertensive drugs in patients with erectile dysfunction. Curr Med Res
Opin 2002; 18: 103_7.