would appear that even without outright vasculopathy, a

history of smoking represents the presence of a silent vas-

cular insult that persists over time.

However, not all of the damage appears to be perma-

nent. There is currently mounting evidence that some

damage is reversible if smoking is stopped prior to mid-

dle age and is not restarted (Pourmand

et al.

, 2004; Sigh-

inolF

et al.

, 2007; Harte & Meston, 2008; Chan

et al.

2010).

Interestingly, a short smoking abstinence period of

–

36 hours in heavy smokers can allow for signiFcant

improvements in tumescence (Guay

et al.

, 1998; Harte &

Meston, 2012) and vascular erectile parameters (SighinolF

et al.

, 2007). Along this vein, in a cohort of 143 men with

ED who quit smoking,

50% reported improvements in

erectile function at 6 months

–

double the rate of those

who were unable to quit (Chan

et al.

, 2010). Effects per-

sisted for at least 1 year (Chan

et al.

, 2010). Among

patients with no other risk factors, successful smoking

cessation via an 8-week trial of nicotine replacement ther-

apy signiFcantly improved erectile function at a 1-year

follow-up (Pourmand

et al.

, 2004).

It appears, however, that age modiFes the chances of

regaining erectile function. In the study by Pourmand

et al.

(2004), improvements were conFned to patients

50 years old. Likewise, in another study by Chew

et al.

(2009), those who quit and were under 50 years of age

did not show increased risks of ED. A slightly higher age

of 60 years was shown by Austoni

et al.

(2005) to delin-

eate better ORs for former smokers compared to current

smokers of similar ages.

±urthermore, the severity of a patient’s ED may also pre-

dict one’s response to quitting. In the study by Pourmand

et al.

(2004), of those men who regained erectile function

after quitting smoking, 49% had only mild ED at baseline.

No men with severe ED regained function

–

a worrisome

statistic as many former smokers are more likely to have

severe ED (Chew

et al.

, 2009). The presence of other vas-

cular risk factors such as hypertension or diabetes further

increased the odds of ED in former smokers. ±urthermore,

men with these comorbidities did not show beneFts to

quitting smoking, suggesting that smoking may not pres-

ent an additional vascular risk if vascular damage from

hypertension, hyperlipidaemia, diabetes and cardiovascular

disease is already present (Austoni

et al.

, 2005).

In summary, large epidemiologic studies do not appear

to show a return to baseline risk in men who are

smokers. Smaller studies, however, do show that younger

men (

50 years old) have a better chance of erectile

improvement after quitting. Early cessation is necessary

to increase the chances of erectile improvement. There

also appears to be a physiologic set point where the pres-

ence of severe cardiovascular disease and ED does not

respond to smoking cessation.

Conclusions

In the general population, over half of men over the age

of 40 will have some varying degree of ED. Smokers are

at even higher risk of developing ED independent of age

and comorbidities. There is overwhelming evidence in the

literature to support the claim that smoking worsens

erectile function through vascular mechanisms (primarily

depletion of nitric oxide). It is yet unclear whether, at a

population level, quitting smoking will improve ED rates;

however, in controlled trials, gains in erectile function are

made by men who do. Unfortunately, the current litera-

ture suggests that this improvement is limited to younger

men with a more minor smoking history and a lack of

comorbidities.

Acknowledgements

JRK and RR are NIH K12 Scholars supported by a Male

Reproductive Health Research Career (MHRH) Develop-

ment Physician-Scientist Award (HD073917-01) from the

Eunice Kennedy Shriver National Institute of Child

Health and Human Development (NICHD) Program.

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