We estimated the effects of smoking on the risk and prognosis of erectile dysfunction (ED), and of ED on smoking behavior. The follow-up sample consisted of the 1442 men aged 50–75 y, who responded to both baseline and follow-up questionnaires. We estimated the effect of smoking on the incidence of ED among the 1130 men free from ED, ED on risk to start smoking in the 502 nonsmokers, smoking on the prognosis of ED among the 312 with ED and ED on quitting smoking among the 292 current smokers at baseline. Risk of ED increased nonsignificantly with smoking (odds ratio (OR)=1.4), while ED recovery reduced (OR=0.6). Therefore, there was the ratio of 2.3 (1.4/0.6) describing the total effect of smoking on the risk of ED. Both quitting (OR=1.7) and starting (OR=1.9) smoking were rare and nonsignificantly higher in men with ED. Most of the OR estimates on smoking–ED relationships were not statistically significant, probably due to small numbers. There are two bidirectional relations between ED and smoking. Those who smoked had a higher risk of ED than nonsmokers. The men with ED were more likely to start smoking than those free from ED. The estimates of effects were not statistically significant, but they were consistent with each other and with the hypothesis that smoking causes ED and ED causes smoking. The recovery from ED was less in smokers than among nonsmokers, and current smokers with ED were more likely to stop smoking than men free from ED. Numbers were few and estimates of effects were not significant, but consistent with the hypothesis of smoking preventing recovery from ED and ED improving the success of smoking cessation. Such transitions in four directions explain indirectly the known positive association between the prevalence of smoking and the prevalence of ED.
Erectile dysfunction (ED) is a common public health problem affecting millions of men worldwide.1, 2 It has a strong negative effect on interpersonal relationship, well-being and quality of life.3, 4, 5, 6, 7, 8, 9, 10
Epidemiological findings would be obviously valuable for better understanding of ED and subsequently for developing appropriate service delivery and resource allocation modalities, as well as for developing prevention strategies when modifiable risk factors are established. Despite the recent interest on ED, there is still substantial gap in our knowledge of the etiology of ED.11, 12
The use of tobacco is a major public health problem worldwide, and its effect on sexual life is an often-used fact in anti-smoking campaigns. Association between smoking and ED has been assessed mainly in prevalence studies, which have considerable weaknesses for elucidating the etiology of ED.12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23 Only two longitudinal studies have evaluated the effect of smoking on erectile function. One has clearly shown that smoking does not have an effect on the incidence of ED,12 and the other has also found no effect in whole sample,11 while doubling of risk in a subgroup of men free from vascular diseases.14
Little is known about the frequency of spontaneous recovery, and no study has been published on the effect of smoking on the recovery from ED and the effect of ED on starting or stopping smoking. To better understand the mechanisms of causality between smoking and ED, we estimated the effects of smoking on the risk and prognosis of ED, and also the effect of ED on smoking behavior by means of a population-based follow-up study.
Materials and methods
This study is a population-based follow-up study in randomly selected cohorts of men who were born in 1924, 1934 or 1944, residing in the city of Tampere or 11 surrounding municipalities in Finland in 1994, identified from the Population Register Center. Information on the total population (3152) was collected by means of a mailed self-administered questionnaire, comprising items on sociodemographic status, life-style factors, medical conditions and medications, diet, physical activity, erectile capacity and concern about erection problems.
A total of 2198 men completed the baseline questionnaires (70% response proportion) during the first quarter of 1994. Of these, 257 were excluded from the study, 244 due to missing data regarding erectile function and 13 as the respondents were institutionalized or unable to respond independently. Hence, 1941 men (62% of the target population) were included in the study at baseline.
Similar questionnaires were sent 5 y later in May 1999 to 2864 men, with a reminder to the 1162 who did not respond to the first within 3 months. Between 1994 and 1999, 262 men had died, six had emigrated and 38 no longer had a permanent address in the Population Register. Overall, 1683 men (59% of those who were alive and eligible) responded to both the baseline and follow-up inquiries. Of them, 241 were excluded because of missing data on erection function and 1442 (50% of eligible survivors at follow-up) were included in the follow-up sample.
The followed-up population was similar to those who responded to baseline survey with respect to education, marital status, residence, alcohol consumption and most of the chronic diseases. They were slightly older (on average 1 y). The 499 men without follow-up information were older than the followed-up sample (Table 1), more frequently reported to have ED, heart disease (25 vs 15%), cerebrovascular disease (9 vs 5%) and diabetes (10 vs 6%), and were more often current smokers (31 vs 20%).
ED was defined according to the National Institutes of Health Consensus Panel on ED as the inability to achieve or maintain an erection sufficient for satisfactory sexual function.2 ED was assessed by two questions on subjects' erectile capacity: ‘Have you had problems getting an erection before intercourse begins?’ and ‘Have you had problems maintaining an erection once intercourse has begun?’ The two questions were combined to classify the severity of ED. No difficulty in achieving and maintaining erection was defined as normal erectile function. Some difficulties in achieving and/or maintaining was classified as minimal ED and fairly frequent difficulties as moderate ED. Complete ED was defined when intercourse did not succeed at all. ED was categorized as none or minimal vs moderate or complete for the analysis.
Self-reported smoking history was obtained from the questionnaire. Men were defined as current smokers, if their history of smoking had lasted for at least 1 y, and ex-smokers if they had smoked at least 1 y in their life and were not current smokers, and nonsmokers if they had never smoked or smoked less than 1 y.
The 1130 men free from ED, 312 with ED, 502 nonsmokers and 292 current smokers at baseline were included in this analysis (Table 2). The number of cases who started to smoke during the follow-up period was very few and only crude odds ratios (ORs) were estimated. The statistical significance (two-tailed P-value≤0.05) was assessed by a χ2 test, and multivariate logistic regression model used with the SPSS software computer package.
The local ethical review committees approved the study protocol.
A total of 203 men (18%) developed ED during the 5-y follow-up period among the 1130 men free from ED at baseline. The incidence of ED increased with age and with smoking (Table 3). The increase with age was stronger (OR=2.3 and 4.5 for 60–65 and 70–75 y, respectively compared with 50–55 y) than with smoking (OR=1.4, 95% CI 0.9–2.3), which was nonsignificant. Among the current smokers, no dose–response effect was detected for the duration of smoking. The OR for each 10-y increment in the number of years spent smoking was 1.0 (95% CI 0.6–1.6). There was an interaction only between smoking and fecal incontinence (OR=7.2, 95% CI 2.2–24.7). However, the number of cases was few and estimate based on only 12 cases. The OR for the effect of fecal incontinence itself on ED was 5.3 (95% CI 1.9–14.9).
The men with ED were older and more often ex-smokers (Table 2). Among the 312 men with ED at baseline, 61 (20%) had spontaneous recovery (Table 3). Recovery was more rare with advancing age (OR=0.6, 95% CI 0.3–1.3 and 0.5, 95% CI 0.2–1.3 for 60–65 and 70–75 y, respectively) and was less in smokers (OR=0.7, 95% CI 0.3–1.3 and 0.6, 95% CI 0.2–1.4 for ex- and current smokers, respectively, compared with nonsmokers). Among those who had ED, 12% (n=37) reported that they had sought treatment during the follow-up period. Younger men sought treatment more often than older (P=0.017). Only four men (11%) reported to have improvement by ED treatment, and recovery was less common among those who had ED treatment (OR=0.4, 95% CI 0.1–1.2).
A total of 43 men (15%) in the 292 current smokers at baseline stopped smoking during the follow-up period (Table 4). Quitting was higher in the 70–75-y-old men (OR=1.9, 95% CI 0.6–6.3) and in those who had ED (OR=1.7, 95% CI 0.8–3.9).
Only 15 men (3%) among the 502 nonsmokers at baseline had started to smoke during a period of 5 y (Table 4). Risk to start smoking was higher in men with ED (OR=1.9, 95% CI 0.6–6.1). The numbers were very few and the relative risk estimate was not statistically significant.
In our study, smokers had a higher risk and a lower recovery from ED than nonsmokers. Quitting smoking and risk to start smoking were higher among men with ED. Although the relative risks were nonsignificant, our findings were consistent with the hypothesis that there are two bidirectional associations between ED and smoking. Firstly, smoking causes ED and ED causes smoking. Secondly, smoking reduces recovery from ED and ED makes men more vulnerable to start smoking. Our original population-based sample was more than 3000, but follow-up and stratification resulted in much smaller populations with only few incident cases of outcome. Therefore, there was substantial random variation and the estimated incidence ORs were not statistically significant. These four associations and their relative importance result in the common finding of association between the prevalence of smoking and the prevalence of ED.
The use of tobacco is a major public health problem worldwide, and the available evidence on the role of smoking on erectile function is equivocal.12, 13, 14, 15, 16 Anti-tobacco advertisements now feature the risk of ED as a reason to avoid or cease tobacco use. As warnings of cancer and heart disease have lost their ability to alarm, tobacco control has turned to the risk of ED. The causal association of starting cigarette smoking with incidence of ED cannot be established by randomized controlled experiments due to ethical restraints.
Cross-sectional prevalence studies are easier to conduct, but they cannot disclose the complex four-direction causal pathways and they are more likely to suffer different biases. There is still lack of knowledge about the risk factors of ED. It is difficult to collect valid information from a representative sample. Most studies are biased towards the population of responders who agree to talk readily about sexual matters. Few population-based follow-up studies are available concerning risk factors. Our follow-up of men without ED at baseline is free of such bias.
Prevalence of smoking has been associated with ED in some14, 17, 22, 24, 25 but not all previous studies.11, 13, 19, 26 Higher prevalence of ED has been reported both among current and ex-smokers.20, 21, 22, 25, 27, 28, 29, 30, 31 In some studies only heavy smoking (30 cigarettes or more/day) was significantly associated with ED,18, 23 while another study found that smoking was related to the prevalence of complete ED only in current smokers with treated heart disease, hypertension and arthritis.13 Some studies suggest that the prevalence of ED increases with the number of years of smoking,18, 20, 25, 31 while others have failed to detect a relationship between years smoked or cigarettes smoked daily and ED.13, 22 Passive exposure to cigarette smoke both at home and at work also increased the incidence of ED in one study.14 Meta-analyses have shown that impotent men are significantly more likely to be current smokers than men in the general population (prevalence of smoking 40 vs 28%).15, 16 Yet, the results of studies have been completely equivocal.
Temporal relationship is an essential aspect of causality. For smoking to be a cause of ED, it clearly has to precede ED onset. The relationship between smoking and ED has been found mostly based on cross-sectional studies, which have a major limitation in establishing the time sequence of events. Measurements of smoking and ED in cross-sectional studies are made at the same time, and it cannot be assumed that smoking preceded the appearance of ED.
A reverse causal direction is quite credible. Quality of life effect caused by ED may be attempted to get relieved by smoking. To the best of our knowledge, such hypothesis was never empirically verified. The time frame for ED onset and recovery from ED after cessation of smoking is neither known and it is not clearly associated with the time from stopping, suggesting a lasting effect of smoking on ED.31 It may be markedly different from associations with other endothelial diseases such as coronary heart disease. The rate of decreasing risk is related to the underlying pathophysiology and it is relatively dependent upon population age.15
The response rate was comparable to that for other epidemiological studies on sexual function. Characteristics of the incidence sample were relatively similar to those who were included at baseline sample. Those without information at follow-up survey were slightly older, had more often ED and vascular diseases, and were more frequently current smokers than those who were included to the follow-up sample. The prevalence of smoking in the followed-up sample was similar to that among Finnish men of these ages in general, which suggests representativeness of the study population.32 If such selective forces were undifferential, the relative risks are not biased.
The current findings showed that both past and current smokers were at higher risk of ED. Only 4% of those who suffered from ED improved annually and spontaneous recovery was lower in smokers. In view of the fact that the risk of ED increased and recovery reduced with age, the effect of age on ED becomes stronger (OR=3.8 (2.3/0.6) for 60–65 y and 9.0 (4.5/0.5) for 70–75 compared with 50–55 y). The increase in the risk of ED with smoking was relatively small (OR=1.4 only, compared, for example, to the strength of health education level on this relationship). As smoking seems to prevent recovery from ED (OR=0.6), the overall association becomes stronger (1.4/0.6=2.3). On the basis of our results, it is impossible to conclude whether smoking causes ED through vascular diseases and those diseases are on a causal pathway between smoking and ED, or whether smoking independently causes ED and chronic diseases.
This study showed that ED is also likely to precede smoking, especially in young men. In fact, our results were consistent with the hypothesis that never-smoked men with ED are likely to start smoking and smokers who suffered from ED are also likely to stop smoking. The mechanisms of such actions are obviously psychosocial and demonstrate the importance of ED on the quality of life for men. In principle, it is possible that ED causes stress, anxiety, depression, loss of self-esteem, dissatisfaction and anger that the men assume to be relieved by smoking. It is also possible that the known etiological role of smoking on ED increases quitting smoking in those who suffer from ED in the hope of recovery. Our samples were too few, especially on the effect of ED on starting smoking to confirm any associations.
Our results are consistent with the hypothesis that there are two bidirectional relationships between ED and smoking. Those who smoked had a higher risk of ED than nonsmokers, and the men with ED were more likely to start smoking than those free from ED. The estimates of effects were not statistically significant, while they were consistent with each other and with the hypothesis that smoking causes ED and ED causes smoking. The incidence of recovery from ED was less among smokers than nonsmokers. The current smokers who suffered from ED were more likely to stop smoking than men free from ED. Numbers were few and the estimates of effects were not significant but consistent with the hypothesis of smoking preventing recovery from ED and ED increasing the success of smoking cessation. Such transitions in four directions result in known positive association between the prevalence of smoking and the prevalence of ED.
Ayta IA, McKinlay JB, Krane RJ . The likely worldwide increase in erectile dysfunction between 1995 and 2025 and some possible policy consequences. BJU Int 1999; 84: 50–56.
National Institutes of Health Consensus Conference. Impotence: National Institutes of Health Development Panel on impotence. JAMA 1993; 270: 83–90.
Laumann EO, Paik A, Rosen RC . Sexual dysfunction in the United States: prevalence and predictors. JAMA 1999; 281: 537–544.
Melman A, Gingell JC . The epidemiology and pathophysiology of erectile dysfunction. J Urol 1999; 161: 5–11.
Fugl-Meyer AR, Lodnert G, Branholm IB, Fugl-Meyer KS . Life satisfaction in male erectile dysfunction. Int J Impot Res 1997; 9: 141–148.
Jonler M et al. The effect of age, ethnicity and geographical location on impotence and quality of life. Br J Urol 1995; 75: 651–655.
Kaiser FE . Sexuality in the elderly. Urol Clin North Am 1996; 23: 99–109.
Wiley D, Bortz WM . Sexuality and aging: usual and successful. J Gerontol A: Biol Sci Med Sci 1996; 51: M142–M146.
MacDonagh R, Ewings P, Porter T . The effect of erectile dysfunction on quality of life: psychometric testing of a new quality of life measure for patients with erectile dysfunction. J Urol 2002; 167: 212–217.
Ansong KS, Lewis C, Jenkins P, Bell J . Help-seeking decisions among men with impotence. Urology 1998; 52: 834–837.
Moreira Jr ED et al. Incidence of erectile dysfunction in men 40 to 69 years old: results from a population-based cohort study in Brazil. Urology 2003; 61: 431–436.
Johannes CB et al. Incidence of erectile dysfunction in men 40 to 69 years old: longitudinal results from the Massachusetts Male Ageing Study. J Urol 2000; 163: 460–463.
Feldman HA et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994; 151: 54–61.
Feldman HA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med 2000; 30: 328–338.
McVary KT, Carrier S, Wessells H . Smoking and erectile dysfunction: evidence based analysis. J Urol 2001; 166: 1624–1632.
Tengs TO, Osgood ND . The link between smoking and impotence: two decades of evidence. Prev Med 2001; 32: 447–452.
Morales AM et al. Prevalence and independent risk factors for erectile dysfunction in Spain. Results of the epidemiologia de la dysfunction erectile masculine study. J Urol 2001; 166: 569–574.
Nicolosi A et al. Epidemiology of erectile dysfunction in four countries: cross-national study of the prevalence and correlates of erectile dysfunction. Urology 2003; 61: 201–206.
Akkus E et al. Prevalence and correlates of erectile dysfunction in Turkey: a population-based study. Eur Urol 2002; 41: 298–304.
Green JS et al. An investigation of erectile dysfunction in Gwent, Wales. BJU Int 2001; 88: 551–553.
Parazzini F et al. Frequency and determinants of erectile dysfunction in Italy. Eur Urol 2000; 37: 43–49.
Mannino DM, Klevens RM, Flanders WD . Cigarette smoking: an independent risk factor for impotence? Am J Epidemiol 1994; 140: 1003–1008.
Moreira Jr ED, Bestane WJ, Bartolo EB, Fittipaldi JA . Prevalence and determinants of erectile dysfunction in Santos, southeastern Brazil. Sao Paulo Med J 2002; 120: 49–54.
Pinnock CB, Stapleton AM, Marshall VR . Erectile dysfunction in the community: a prevalence study. Med J Aust 1999; 171: 353–357.
Safarinejad MR . Prevalence and risk factors for erectile dysfunction in a population-based study in Iran. Int J Impot Res 2003; 15: 246–252.
Jeremy JY, Mikhailidis DP . Cigarette smoking and erectile dysfunction. J R Soc Health 1998; 118: 151–155.
Bortolotti A, Parazzini F, Colli E, Landoni M . The epidemiology of erectile dysfunction and risk factors. Int J Androl 1997; 20: 323–334.
Fried LP, Moore RD, Pearson TA . Long-term effects of cigarette smoking and moderate alcohol consumption on coronary artery diameter: mechanism of coronary artery disease independent of arteriosclerosis or thrombosis? Am J Med 1986; 80: 37–44.
Shabsigh R, Fishaman IJ, Schum C, Dunn JK . Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology 1991; 38: 227–231.
Mikhailidis DP, Jeremy JY . Smoking and erectile impotence. Int Angiol 1993; 12: 297–298.
Mirone V et al. Cigarette smoking as risk factor for erectile dysfunction: Results from an Italian epidemiological study. Eur Urol 2002; 41: 294–297.
Helakorpi S, Berg M-A, Uutela A, Puska P . Health Behavior Among Finnish Adult Population, Vol B8. National Public Health Institute, Helsinki, 1994 pp 13–95.
About this article
Cite this article
Shiri, R., Hakama, M., Häkkinen, J. et al. Relationship between smoking and erectile dysfunction. Int J Impot Res 17, 164–169 (2005) doi:10.1038/sj.ijir.3901280
- erectile dysfunction
- risk factors
Prevalence of erectile dysfunction and associated factors among diabetic men attending the diabetic clinic at Felege Hiwot Referral Hospital, Bahir Dar, North West Ethiopia, 2016
BMC Research Notes (2018)
Sexual Medicine Reviews (2016)
Health-Related Characteristics and Unmet Needs of Men with Erectile Dysfunction: A Survey in Five European Countries
The Journal of Sexual Medicine (2014)
Smoking and Risk of Erectile Dysfunction: Systematic Review of Observational Studies with Meta-Analysis
PLoS ONE (2013)