Tobacco use is well-known to be a significant health concern. Nevertheless, millions of men and women around the world continue to use tobacco products. Most antitobacco education and advertising efforts have focused on the traditional warnings of lung cancer, heart disease, and pregnancy complications. However, in the last two decades, the link between smoking and impotence has been described by various authors.[1,2,3,4,5,6,7,8,9,10,11,12] Despite this, impotence is not well recognized by the general public or even by general practice medical providers as a potential consequence of smoking. Pharmacists and other health professions are missing an opportunity to teach smokers about another good reason to kick the habit.
Literature regarding smoking and impotence describes various mechanisms for the link. McVary et al. published a comprehensive review in 2001 that examined clinical and scientific studies. The investigators found evidence that impotence can be caused directly by smoking-induced reductions in nitric oxide concentrations, which impair endothelium-dependent relaxation of arteries, and indirectly by smoking-induced atherosclerosis.
The likelihood of impotence or erectile dysfunction (ED) in men who smoke has also been described by various authors. The review by McVary et al. indicated that smoking may increase the risk of moderate or complete impotence by two times that of nonsmokers and that smoking cessation may decrease impotence risk. Austoni et al. found that after adjustment for confounding variables, Italian men who smoked more than 10 cigarettes per day and former smokers had significantly higher risks (odds ratio [OR] 1.4 and 1.3, respectively; both p < 0.0001) for ED. Shiri et al. demonstrated similar but nonsignificant findings in Finnish men: OR 1.4 for smokers (95% CI, 0.9—2.3) and 1.3 for former smokers (95% CI, 0.9-1.9). Polsky et al. found that Canadian men with ED were twice as likely to be former smokers (OR 2.2; 95% CI, 1.2—3.9) but that current smoking did not significantly increase ED risk.
Recently, a U.S. epidemiologic study of 1329 white men (smokers and nonsmokers) showed that 15% reported suffering from impotence. The authors concluded that the relative OR of impotence in smokers or past smokers compared with nonsmokers was significant at 1.46 (95% CI, 1.05—2.02). When adjustments were made for age and for age and comorbidity, the relative OR became nonsignificant at 1.42 (95% CI, 1.00—2.02) and 1.38 (95% CI, 0.97—1.97), respectively. A dose—response relationship suggesting that men with a longer smoking history had a higher likelihood of impotence was also seen. In men with greater than a 29-pack-year history, the relative ORs of impotence were significant at 2.08 (95% CI, 1.41—3.08) compared with 1.34 (95% CI, 0.88—2.07) in those with a 12.6—29.0-pack-year history and 0.92 (95% CI, 0.58—1.46) in those with a 1—12.5-pack-year history. When adjustments were made for age and for age and comorbidity, the relative OR for the greater than 29-pack-year group was reduced but still significant at 1.69 (95% CI, 1.10—2.58) and 1.60 (95% CI, 1.04—2.46), respectively. Interestingly, when the authors stratified the data by age from current smokers and from men who formerly or never smoked, smokers in their 40s had the greatest relative OR of having impotence (2.74; 95% CI, 0.44—16.89).
Unfortunately, not only does smoking tobacco appear to increase impotence risk, data suggest it also predicts a poor response to popular pharmacologic treatment for impotence. Park et al. found that current smoking was significantly associated with sildenafil failure in men over the age of 60 years suffering from impotence (OR 1.34; 95% CI, 1.04—3.52; p = 0.015). The lack of effect was likely due to the failure of sildenafil to potentiate endogenous nitric oxide-mediated vascular responses—responses that are reduced in smokers. Since all phosphodiesterase inhibitors, such as sildenafil, exert their effect through nitric oxide modulation, this therapeutic failure may be a class effect.
Effect of Smoking Cessation on Impotence
Data are mixed regarding the usefulness of smoking cessation in smokers to improve erectile function or reverse ED. Some studies have indicated that men who are former smokers are still more likely to have ED than nonsmokers.[9,11,12] Shiri et al. indicated that recovery from ED is reduced in those currently smoking (adjusted OR 0.6; 95% CI, 0.2—1.4) and in former smokers (adjusted OR 0.7; 95% CI, 0.3—1.3) compared with nonsmokers, but the results were not statistically significant and the overall number of patients in this analysis was low. However, results from a study by Derby et al. suggested that smoking cessation in young adulthood (versus later in life) may be necessary to reduce the risk of ED.
A small, prospective study by Guay et al. indicated that smoking cessation significantly decreases the risk of ED. This study evaluated acute changes in smoking status in 10 smokers (ages 32—62 years) using the RigiScan portable home monitor (Dacomed/Urohealth, Minneapolis, MN), which measures penile tumescence and rigidity. At the time of the study, all patients were smoking at least one pack of cigarettes per day and had smoked for at least 30 pack-years. Men were monitored for two nights: one when they smoked and one when they did not smoke for 24 hours. In addition, four men were monitored after smoking cessation (using nicotine patches) for one month. Results of the study showed that after not smoking for 24 hours, the men had a statistically significant improvement in penile tumescence and rigidity (p < 0.05 for all measures). In addition, sustained improvement in ED was found in the four men who were monitored after one month of nicotine replacement and smoking cessation, indicating that nicotine may not be the only mediator of ED from smoking.
A long-term prospective study evaluating whether smoking cessation can improve ED in smokers was recently published. Pourmand et al. evaluated smokers ages 30—60 years who requested nicotine replacement therapy (NRT) for smoking cessation and who also complained of ED starting at least five years after starting to smoke. Of the 2837 smokers, 22.5% (n = 637) reported having ED and 54.3% (n = 346) of those with ED had no other risk factors for ED besides smoking. Those patients without other ED risk factors were followed for one year after stopping NRT. They were then classified as current smokers (those who continued to smoke) or as former smokers (those who stopped smoking with NRT). Results indicated there was a relatively significant correlation between pack-years of smoking and ED status in all patients (Spearman's correlation coefficient, 0.533). At follow-up, there were 118 former smokers and 163 current smokers. The ED status improved by at least one grade in 30 (25%) of the former smokers but in none of the current smokers. Moreover, more current smokers had deterioration in their erectile function: 3 (2.5%) former smokers versus 11 (7%) current smokers. Overall, former smokers tended to have a significantly better ED status after follow-up compared with current smokers (p = 0.09).
In addition to potentially benefiting the health and erectile status of men with ED, smoking cessation may also affect their treatment for ED. Park et al. suggested that stopping or reducing the consumption of cigarettes may ensure better efficacy with sildenafil for the treatment of ED.
Tobacco Education and Advertising Regarding Impotence
Two U.S. states and some countries have strived to increase the public's knowledge of the detrimental effects of tobacco on erectile function in an attempt to reduce smoking. In the late 1990s, the California Department of Health Services introduced a one-year marketing campaign targeting the link between smoking and impotence. Newspaper headlines read "The Marlboro Man needs Viagra" and "What Viagra may give, tobacco taketh away." Hawaii followed suit with the "limp" television campaign geared toward 1824-yearold men. These campaigns were not the first to target impotence as a reason to stop smoking, but they were the most impressive. Unfortunately, published data describing the effects of these advertising campaigns are not available (Stevens CM, personal communication, 2005 Aug 29). However, a 2006 news release from the California Department of Health Services indicates that smoking rates in California have continued to decline since 1996 and are currently at an all-time low of 14%, 25% less than the rest of the nation.
In 2000, Thailand became the first country to go beyond advertising by placing impotence warnings and pictures on cigarette labeling. Subsequently, Canada and Brazil implemented similar warnings on their cigarette packages.[22,23] Currently, the United Kingdom is considering adding various picture warnings to cigarette packages, some of which say that "smoking may reduce the blood flow and causes impotence." Data regarding the results of cigarette labeling indicate that graphic cigarette warning labels reach their intended audience and serve as an effective population-based smoking-cessation intervention. Unfortunately, U.S. requirements are lagging behind other countries, as cigarette manufacturers are only required to include traditional warnings from the U.S. Surgeon General regarding heart disease, lung cancer, emphysema, and complications with pregnancy.
Threat of impotence as a Motivator for Smoking Cessation.
On the basis of the association between smoking and impotence and data supporting the benefits of smoking cessation on impotence, it seems logical that this topic be included in smoking-cessation programs. Moreover, data support that there is a need for this information to be communicated to smokers, as a majority of men appear to be unaware that smoking increases ED risk. In a survey of Hong Kong men, only 13.9% were aware of the link between impotence and smoking, and only 12% of British smokers were aware in a 1999 survey. Results of a study conducted by Shiri et al. indicated that smokers with ED were more likely to stop smoking than smokers without ED (23% versus 12.6% stopped, respectively), but the results were not statistically significant likely because of the low numbers of patients in the analysis.
Recently, a small survey in the United States investigated the issue of using impotence as a motivator for smoking cessation. Male smokers ages 18 years and older were surveyed at a local health fair in Denver, Colorado, in April 2004. Surveys were voluntary and anonymous. Participants were surveyed to determine if they knew that smoking increases impotence risk and that regular smoking may reduce impotence drug-treatment response and to assess what effect the risk of impotence would have on their decision to continue smoking.
Sixty-two surveys were completed. Most of the men surveyed were middle age (65% ages 41—60 years) and white (76%). Smoking habits were evenly distributed among 6—10, 11—20, and 21—30 cigarettes smoked per day. The majority of men had attempted to quit smoking at least once, with over one quarter attempting six or more times.
Thirty-four men (55%) stated they were aware that smoking tobacco increases impotence risk, and 56% of the surveyed men maintained that they would be "somewhat more likely" or "much more likely" to stop smoking because of the link between smoking and impotence. Of the men who stated they were unaware of the increased risk of impotence due to smoking, 57% stated they would be somewhat more likely or much more likely to stop smoking. Overall, 39%, 37%, and 19% stated the relationship between smoking and impotence had no effect on their decision to continue smoking, made them somewhat more likely to stop smoking, and made them much more likely to stop smoking, respectively. Three men did not respond to this question.
In total, six men (10%) stated they suffered from impotence; of these, one smoked 6—10 cigarettes per day, two smoked 11—20 cigarettes per day, and three smoked 21—30 cigarettes per day. Three of the impotent men stated they were unaware of the link between impotence and smoking, and five stated that the link made them somewhat more likely or much more likely to stop smoking. Only one impotent man stated that impotence would not affect his decision to continue smoking. Thus, 96% of the men (23 of 24) who planned to continue smoking were not impotent. Overall, 23 men (37%) stated they were aware that smoking could potentially reduce the effects of pharmacologic agents (i.e., sildenafil, vardenafil, and tadalafil) used to treat impotence.
Implications for Pharmacists
Pharmacists and other health care providers involved in smoking-cessation programs are ideally situated to educate patients about the association between smoking and impotence. A majority of men will likely respond to smoking-cessation education that is focused on impotence risk, especially if they are already impotent. Younger smokers may be more likely to alter their smoking habits on the basis of potential impotence risk rather than remote threats of heart and lung disease. Moreover, health education programs in schools could incorporate impotence into their discussions of tobacco risks to encourage youths to avoid tobacco altogether.
The link between smoking and impotence should be used by pharmacists and other health providers to help motivate men to quit smoking.
Am J Health Syst Pharm. 2006;63(24):2509-2512. © 2006 American Society of Health-System Pharmacists
Cite this: Tobacco Education: Emphasizing Impotence as a Consequence of Smoking - Medscape - Dec 01, 2006.