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Association of E-Cigarettes With Erectile Dysfunction: The Population Assessment of Tobacco and Health Study

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Introduction Smoking is independently associated with erectile dysfunction and cardiovascular disease. Given existing similarities in the constituents of e-cigarettes or ENDS and cigarettes, this study examines the association between ENDS use and erectile dysfunction. Methods Data from Wave 4 (2016–2018) of the Population Assessment of Tobacco and Health study were analyzed in 2020. Male participants aged ≥20 years who responded to the erectile dysfunction question were included. Multivariable logistic regression models examined the association of ENDS use with erectile dysfunction within the full sample and in a restricted sample (adults aged 20–65 years with no previous cardiovascular disease diagnosis) while adjusting for multiple risk factors. Results The proportion of erectile dysfunction varied from 20.7% (full sample) to 10.2% (restricted sample). The prevalence of current ENDS use within the full and restricted samples was 4.8% and 5.6%, respectively, with 2.1% and 2.5%, respectively, reporting daily use. Current daily ENDS users were more likely to report erectile dysfunction than never users in both the full (AOR=2.24, 95% CI=1.50, 3.34) and restricted (AOR=2.41, 95% CI=1.55, 3.74) samples. In the full sample, cardiovascular disease history (versus not present) and age ≥65 years (versus age 20–24 years) were associated with erectile dysfunction (AOR=1.39, 95% CI=1.10, 1.77; AOR= 17.4, 95% CI=12.15, 24.91), whereas physical activity was associated with lower odds of erectile dysfunction in both samples (AOR range=0.44−0.58). Conclusions The use of ENDS seems to be associated with erectile dysfunction independent of age, cardiovascular disease, and other risk factors. While ENDS remain under evaluation for harm reduction and smoking-cessation potential, ENDS users should be informed about the possible association between ENDS use and erectile dysfunction.

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What is known and objective Electronic nicotine delivery systems (ENDS) are battery‐powered devices that allow nicotine and/or other substances to be inhaled in aerosolized form. e‐Cigarettes (electronic cigarettes), the most commonly used ENDS, have been proposed to be smoking cessation aids. However, despite the rapid surge in their popularity, little is known about long‐term health consequences of e‐cigarette usage. We assess published data to see if they deliver what they promise. Comment e‐Cigarettes may contain uncertain quantities of various ingredients, and evidence of adulteration has been identified. Flavouring agents can alter the pharmacokinetics of nicotine and have uncertain impact on the nature of e‐cigarette use (eg ab initio use vs smoking cessation). What is new and conclusion Although e‐cigarettes have been proposed to be a safe approach to encouraging smoking cessation, there are inconsistencies in available data. And further data are needed regarding long‐term implications of primary and secondary exposure to e‐cigarette products.
Article
Background E-cigarettes are commonly used in attempts to stop smoking, but evidence is limited regarding their effectiveness as compared with that of nicotine products approved as smoking-cessation treatments. Methods We randomly assigned adults attending U.K. National Health Service stop-smoking services to either nicotine-replacement products of their choice, including product combinations, provided for up to 3 months, or an e-cigarette starter pack (a second-generation refillable e-cigarette with one bottle of nicotine e-liquid [18 mg per milliliter]), with a recommendation to purchase further e-liquids of the flavor and strength of their choice. Treatment included weekly behavioral support for at least 4 weeks. The primary outcome was sustained abstinence for 1 year, which was validated biochemically at the final visit. Participants who were lost to follow-up or did not provide biochemical validation were considered to not be abstinent. Secondary outcomes included participant-reported treatment usage and respiratory symptoms. Results A total of 886 participants underwent randomization. The 1-year abstinence rate was 18.0% in the e-cigarette group, as compared with 9.9% in the nicotine-replacement group (relative risk, 1.83; 95% confidence interval [CI], 1.30 to 2.58; P<0.001). Among participants with 1-year abstinence, those in the e-cigarette group were more likely than those in the nicotine-replacement group to use their assigned product at 52 weeks (80% [63 of 79 participants] vs. 9% [4 of 44 participants]). Overall, throat or mouth irritation was reported more frequently in the e-cigarette group (65.3%, vs. 51.2% in the nicotine-replacement group) and nausea more frequently in the nicotine-replacement group (37.9%, vs. 31.3% in the e-cigarette group). The e-cigarette group reported greater declines in the incidence of cough and phlegm production from baseline to 52 weeks than did the nicotine-replacement group (relative risk for cough, 0.8; 95% CI, 0.6 to 0.9; relative risk for phlegm, 0.7; 95% CI, 0.6 to 0.9). There were no significant between-group differences in the incidence of wheezing or shortness of breath. Conclusions E-cigarettes were more effective for smoking cessation than nicotine-replacement therapy, when both products were accompanied by behavioral support. (Funded by the National Institute for Health Research and Cancer Research UK; Current Controlled Trials number, ISRCTN60477608.)
Article
Despite many advances over the last few decades, cardiovascular disease (CVD) remains the leading cause of death globally, with men afflicted at an earlier age than women. In a bid to reduce the global burden of morbidity and mortality due to CVD, emphasis has been placed on prevention, particularly on widespread promotion of ideal cardiovascular health behaviors and advancing strategies to identify and treat high-risk individuals who may benefit from aggressive preventive therapy. Erectile dysfunction is a highly prevalent condition that has been demonstrated to share the same risk factors as clinical CVD, and to have independent predictive value for future CVD events. Importantly, subclinical atherosclerosis appears to precede vascular ED by a decade or longer, with ED preceding clinical CVD such as myocardial infarction and stroke in temporal sequence by about 2–5 years. Crucially, since ED may represent the first presentation of otherwise “healthy” men to care providers, a clinical diagnosis of vascular ED may represent a unique opportunity to identify high risk individuals, intervene, and thus prevent progression to clinical CVD. This review summarizes up-to-date evidence of the relationship between ED and subclinical and clinical CVD, and details the position of current guidelines and clinical recommendations on the role of ED assessment in CVD prevention. Finally, this review proposes a clinical framework for the incorporation of ED into standard CVD risk assessment in middle-age men.
Article
Vascular erectile dysfunction (ED) and cardiovascular disease (CVD) share common risk factors including obesity, hypertension, metabolic syndrome, diabetes mellitus, and smoking. ED and CVD also have common underlying pathological mechanisms, including endothelial dysfunction, inflammation, and atherosclerosis.1 Despite these close relationships, the evidence documenting ED as an independent predictor of future CVD events is limited.We therefore leveraged the MESA study (Multi-Ethnic Study of Atherosclerosis), an ethnically diverse, community-based, multisite prospective cohort study, to examine the value of self-reported ED for predicting incident coronary heart disease (CHD) and CVD in those free of these CVD events at baseline. Details of MESA have been described previously.2 Male MESA participants who attended visit 5 and answered the single Massachusetts Male Aging Study question3 on ED symptoms were considered for our analysis (n=1914). A participant was considered to have ED if he responded "never able" or "sometimes able" to the Massachusetts Male Aging Study question. After excluding 155 participants with a CVD event before visit 5, 1757 participants were followed for 3.8 years (interquartile range, 3.5-4.2) and outcomes of hard CHD and CVD events were assessed. Hard CVD events included all hard CHD events (myocardial infarction, resuscitated cardiac arrest, and CHD death), plus stroke and stroke death. Participants provided informed consent, and each study site obtained approval from their institutional review board.
Article
Introduction: The public health community is divided regarding electronic cigarettes. Skeptics emphasize potential vaping-induced increases in smoking among children and possible health hazards for adults. Enthusiasts consider e-cigarettes much less dangerous than smoking and believe they increase adult smoking cessation. We compare potential health benefits and costs to put these two perspectives in context. Methods: Using a dynamic model that tracks the US adult population's smoking status and smoking-related deaths over time, we simulate the effects of vaping-induced smoking initiation and cessation on life-years saved or lost to the year 2070. The base case assumes that vaping annually increases smoking initiation by 2% and smoking cessation by 10%. Sensitivity analyses raise the initiation rate increase to 6% while decreasing the cessation rate increase to 5%. Sensitivity analyses also test vaping's reducing the health benefits of quitting smoking by 10%. Results: With base-case assumptions, the population gains almost 3.3 million life-years by 2070. If all people who quit smoking by vaping lose 10% of the benefit of quitting smoking, the net life-year gain falls to 2.4 million. Under worst-case assumptions, in which vaping increases smoking initiation by 6% and cessation by 5%, and vaping-induced quitters lose 10% of the health benefits, the population gains over 580,000 life-years. Conclusion: Potential life-years gained as a result of vaping-induced smoking cessation are projected to exceed potential life-years lost due to vaping-induced smoking initiation. These results hold over a wide range of plausible parameters. Implications: Our analysis strongly suggests that the upside health benefit associated with e-cigarettes, in terms of their potential to increase adult smoking cessation, exceeds their downside risk to health as a result of their possibly increasing the number of youthful smoking initiators. Public messaging and policy should continue to strive to reduce young people's exposure to all nicotine and tobacco products. But they should not do so at the expense of limiting such products' potential to help adult smokers to quit.
Article
Introduction Erectile dysfunction (ED) is a common disorder that has many potential etiologies, including hormonal imbalances, psychogenic factors, neurologic disorders, vascular insufficiency, and other risk factors. Cigarette smoking has been well established as a risk factor for cardiovascular disease and stroke, but the relation between smoking and ED is less frequently considered. Aim To review the current literature that analyzes the association between cigarette smoking and ED. Methods The PubMed database was searched using the terms erectile dysfunction and smoking and erectile dysfunction and tobacco through December 2015. Main Outcome Measures Main outcome measures were significant changes in erectile function in relation to smoking status. Results Eighty-three studies and articles were reviewed. Multiple human studies, animal studies, case series, cross-sectional, and cohort studies analyzed the relation between smoking or nicotine and ED. Conclusion There is substantial evidence showing that cigarette smoking is a risk factor for ED. Multiple human, animal, case series, cross-sectional, and cohort studies support this conclusion. A positive dose-response relation also is suggested such that increased quantity and duration of smoking correlate with a higher risk of ED. Smoking cessation can lead to recovery of erectile function, but only if limited lifetime smoking exposure exists. Smoking contributes to ED in different ways, especially by causing penile vasospasm and increased sympathetic nervous system tone.
Article
Sexual problems are highly prevalent in both men and women and are affected by, among other factors, mood state, interpersonal functioning, and psychotropic medications.The incidence of antidepressant-induced sexual dysfunction is difficult to estimate because of the potentially confounding effects of the illness itself, social and interpersonal comorbidities, medication effects, and design and assessment problems in most studies. Estimates of sexual dysfunction vary from a small percentage to more than 80%. This article reviews current evidence regarding sexual side effects of selective serotonin reuptake inhibitors (SSRIs). Among the sexual side effects most commonly associated with SSRIs are delayed ejaculation and absent or delayed orgasm. Sexual desire (libido) and arousal difficulties are also frequently reported, although the specific association of these disorders to SSRI use has not been consistently shown. The effects of SSRIs on sexual functioning seem strongly dose-related and may vary among the group according to serotonin and dopamine reuptake mechanisms, induction of prolactin release, anticholinergic effects, inhibition of nitric oxide synthetase, and propensity for accumulation over time. A variety of strategies have been reported in the management of SSRI-induced sexual dysfunction, including waiting for tolerance to develop, dosage reduction, drug holidays, substitution of another antidepressant drug, and various augmentation strategies with 5-hydroxytryptamine-2 (5-HT2), 5-HT3, and [small alpha, Greek]2 adrenergic receptor antagonists, 5-HT1A and dopamine receptor agonists, and phosphodiesterase (PDE5) enzyme inhibitors. Sexual side effects of SSRIs should not be viewed as entirely negative; some studies have shown improved control of premature ejaculation in men. The impacts of sexual side effects of SSRIs on treatment compliance and on patients' quality of life are important clinical considerations. (J Clin Psychopharmacol 1999;19:67-85)
Article
Cigarette smoking is a leading cause of preventable morbidity and mortality in the United States. Although public policies have resulted in a decreased number of new smokers, smoking rates remain stubbornly high in certain demographics with 20% of all American middle-aged men smoking. In addition to the well-established harmful effects of smoking (i.e. coronary artery disease and lung cancer), the past three decades have led to a compendium of evidence being compiled into the development of a relationship between cigarette smoking and erectile dysfunction. The main physiologic mechanism that appears to be affected includes the nitric oxide signal transduction pathway. This review details the recent literature linking cigarette smoking to erectile dysfunction, epidemiological associations, dose dependency and the effects of smoking cessation on improving erectile quality.
Article
IntroductionSome original studies and a recent meta-analysis suggested that smoking could be associated with the risk of erectile dysfunction (ED), but the dose–response relationship between them was unclear.AimThe aim of this study was to investigate the potential association between quantity and duration of smoking and the risk of ED.Methods We conducted a literature search of PubMed, Embase, Web of Science, and Scopus from these databases' inception through March 2014 for observational epidemiological studies examining the association between smoking and risk of ED. Random-effects meta-analyses were used to combine the results of included studies.Main Outcome MeasureQuantitative review of published observational epidemiological studies on the association between smoking and risk of ED was the main outcome measure.ResultsOne cohort study and nine cross-sectional studies were eligible for inclusion in the meta-analysis (50,360 participants and 12,218 cases with ED). No evidence of a curve linear association was observed between smoking and risk of ED. The summary odds ratio of ED for an increase of 10 cigarettes smoked per day was 1.14 (95% confidence interval 1.09 to 1.18), with moderate heterogeneity (P = 0.061, I2 = 44.7%). For an increment of 10 years of smoking, the combined odds ratios of ED was 1.15 (95% confidence interval 1.10 to 1.19), without substantial heterogeneity (P = 0.522, I2 = 0.0%).Conclusions Evidence from observational studies suggests that there is a positive dose–response association between quantity and duration of smoking and risk of ED. Cao S, Gan Y, Dong X, Liu J, and Lu Z. Association of quantity and duration of smoking with erectile dysfunction: A dose–response meta-analysis. J Sex Med **;**:**–**.
Article
Electronic cigarettes (e-cigarettes) are products that deliver a nicotine-containing aerosol (commonly called vapor) to users by heating a solution typically made up of propylene glycol or glycerol (glycerin), nicotine, and flavoring agents (Figure 1) invented in their current form by Chinese pharmacist Hon Lik in the early 2000s.1 The US patent application describes the e-cigarette device as “an electronic atomization cigarette that functions as substitutes [sic] for quitting smoking and cigarette substitutes” (patent No. 8,490,628 B2). By 2013, the major multinational tobacco companies had entered the e-cigarette market. E-cigarettes are marketed via television, the Internet, and print advertisements (that often feature celebrities)2 as healthier alternatives to tobacco smoking, as useful for quitting smoking and reducing cigarette consumption, and as a way to circumvent smoke-free laws by enabling users to “smoke anywhere.”3
Article
Context β-Blocker therapy remains substantially underused in cardiac patients despite its proven mortality benefits. Reluctance to prescribe these agents may derive from concerns about their association with symptoms of depression, fatigue, and sexual dysfunction.Objective To determine the association of β-blockers with depressive symptoms, fatigue, and sexual dysfunction by performing a quantitative review of randomized trials that tested β-blockers in myocardial infarction, heart failure, and hypertension.Data Sources Randomized trials of β-blockers used in the treatment of myocardial infarction, heart failure, or hypertension were identified by searching the MEDLINE database for English-language articles (1966-2001). In addition, we searched the reference lists of previously published trials and reviews of β-blockers for additional studies.Study Selection Criteria for inclusion of trials in the review were: random allocation of study treatments, placebo control, noncrossover design, enrollment of at least 100 patients, and a minimum of 6 months of follow-up. The initial search produced 475 articles, 42 of which met these criteria. Fifteen of these trials reported on depressive symptoms, fatigue, or sexual dysfunction and were selected for inclusion.Data Extraction For each trial, 1 author abstracted the frequency of adverse events in the β-blocker and placebo groups and the numbers of patients randomized to the treatment groups. Two other authors verified the counts of events, and all authors adjudicated any discrepancies. Two different types of information on adverse events were abstracted: patient-reported symptoms and withdrawal of therapy due to a specified symptom. We categorized the tested β-blockers by generation (early vs late) and lipid solubility (high vs low to moderate).Data Synthesis The 15 trials involved more than 35 000 subjects. β-Blocker therapy was not associated with a significant absolute annual increase in risk of reported depressive symptoms (6 per 1000 patients; 95% confidence interval [CI], –7 to 19). β-Blockers were associated with a small significant annual increase in risk of reported fatigue (18 per 1000 patients; 95% CI, 5-30), equivalent to 1 additional report of fatigue for every 57 patients treated per year with β-blockers. β-Blockers were also associated with a small, significant annual increase in risk of reported sexual dysfunction (5 per 1000 patients; 95% CI, 2-8), equivalent to one additional report for every 199 patients treated per year. None of the risks of adverse effects differed significantly by degree of β-blocker lipid solubility. The risk associated with reported fatigue was significantly higher for early-generation than for late-generation β-blockers (P = .04).Conclusion The conventional wisdom that β-blocker therapy is associated with substantial risks of depressive symptoms, fatigue, and sexual dysfunction is not supported by data from clinical trials. There is no significant increased risk of depressive symptoms and only small increased risks of fatigue and sexual dysfunction. The risks of these adverse effects should be put in the context of the documented benefits of these medications. The use of β-blockers after myocardial infarction (MI) reduces mortality by approximately 20%.1 Long-term β-blocker therapy has also emerged as a valuable treatment in heart failure (HF), resulting in lower mortality and morbidity.2 Despite the importance of these agents, they are underused in appropriate patients.3 The reluctance of physicians to prescribe these agents may derive, in part, from concerns about the development of common symptoms, including depression, fatigue, and sexual dysfunction. Although these conditions have been considered to be strongly associated with β-blockers,4- 7 the evidence supporting these associations is limited.8- 10 To investigate the association of β-blocker therapy with depressive symptoms, fatigue, and sexual dysfunction, we performed a quantitative review of randomized trials. In addition, we categorized the β-blockers by generation and lipid solubility to determine whether the risks of adverse effects differed by these factors.
Article
Significance: Electronic cigarettes, also known as e-cigarettes, are devices designed to imitate regular cigarettes and deliver nicotine via inhalation without combusting tobacco. They are purported to deliver nicotine without other toxicants and to be a safer alternative to regular cigarettes. However, little toxicity testing has been performed to evaluate the chemical nature of vapour generated from e-cigarettes. The aim of this study was to screen e-cigarette vapours for content of four groups of potentially toxic and carcinogenic compounds: carbonyls, volatile organic compounds, nitrosamines and heavy metals. Materials and methods: Vapours were generated from 12 brands of e-cigarettes and the reference product, the medicinal nicotine inhaler, in controlled conditions using a modified smoking machine. The selected toxic compounds were extracted from vapours into a solid or liquid phase and analysed with chromatographic and spectroscopy methods. Results: We found that the e-cigarette vapours contained some toxic substances. The levels of the toxicants were 9-450 times lower than in cigarette smoke and were, in many cases, comparable with trace amounts found in the reference product. Conclusions: Our findings are consistent with the idea that substituting tobacco cigarettes with e-cigarettes may substantially reduce exposure to selected tobacco-specific toxicants. E-cigarettes as a harm reduction strategy among smokers unwilling to quit, warrants further study. (To view this abstract in Polish and German, please see the supplementary files online.).
Article
Context: Electronic cigarettes (e-cigarettes) are becoming increasingly popular yet their effects on health remain unknown. Objective: To conduct the first comprehensive and standardized assessment of the acute impact of active and passive e-cigarette smoking on serum cotinine and lung function, as compared to active and passive tobacco cigarette smoking. Materials and methods: Fifteen smokers (≥15 cigarettes/day; seven females; eight males) and 15 never-smokers (seven females; eight males) completed this repeated-measures controlled study. Smokers underwent a control session, an active tobacco cigarette (their favorite brand) smoking session and an active e-cigarette smoking session. Never-smokers underwent a control session, a passive tobacco cigarette smoking session and a passive e-cigarette smoking session. Serum cotinine, lung function, exhaled carbon monoxide and nitric oxide were assessed. The level of significance was set at p ≤ 0.001 to adjust for multiple comparisons. Results: e-Cigarettes and tobacco cigarettes generated similar (p > 0.001) effects on serum cotinine levels after active (60.6 ± 34.3 versus 61.3 ± 36.6 ng/ml) and passive (2.4 ± 0.9 versus 2.6 ± 0.6 ng/ml) smoking. Neither a brief session of active e-cigarette smoking (indicative: 3% reduction in FEV1/FVC) nor a 1 h passive e-cigarette smoking (indicative: 2.3% reduction in FEV1/FVC) significantly affected the lung function (p > 0.001). In contrast, active (indicative: 7.2% reduction in FEV1/FVC; p < 0.001) but not passive (indicative: 3.4% reduction in FEV1/FVC; p = 0.005) tobacco cigarette smoking undermined lung function. Conclusion: Regarding short-term usage, the studied e-cigarettes generate smaller changes in lung function but similar nicotinergic impact to tobacco cigarettes. Future research should target the health effects of long-term e-cigarette usage, including the effects of nicotine dosage.
Article
Unlabelled: Electronic cigarette consumption ('vaping') is marketed as an alternative to conventional tobacco smoking. Technically, a mixture of chemicals containing carrier liquids, flavors, and optionally nicotine is vaporized and inhaled. The present study aims at the determination of the release of volatile organic compounds (VOC) and (ultra)fine particles (FP/UFP) from an e-cigarette under near-to-real-use conditions in an 8-m(3) emission test chamber. Furthermore, the inhaled mixture is analyzed in small chambers. An increase in FP/UFP and VOC could be determined after the use of the e-cigarette. Prominent components in the gas-phase are 1,2-propanediol, 1,2,3-propanetriol, diacetin, flavorings, and traces of nicotine. As a consequence, 'passive vaping' must be expected from the consumption of e-cigarettes. Furthermore, the inhaled aerosol undergoes changes in the human lung that is assumed to be attributed to deposition and evaporation. Practical implications: The consumption of e-cigarettes marks a new source for chemical and aerosol exposure in the indoor environment. To evaluate the impact of e-cigarettes on indoor air quality and to estimate the possible effect of passive vaping, information about the chemical characteristics of the released vapor is needed.
Article
To assess the profile, utilization patterns, satisfaction and perceived effects among users of electronic cigarettes ('e-cigarettes'). Internet survey in English and French in 2010. Online questionnaire. Visitors of websites and online discussion forums dedicated to e-cigarettes and to smoking cessation. There were 3587 participants (70% former tobacco smokers, 61% men, mean age 41 years). The median duration of electronic cigarette use was 3 months, users drew 120 puffs/day and used five refills/day. Almost all (97%) used e-cigarettes containing nicotine. Daily users spent $33 per month on these products. Most (96%) said the e-cigarette helped them to quit smoking or reduce their smoking (92%). Reasons for using the e-cigarette included the perception that it was less toxic than tobacco (84%), to deal with craving for tobacco (79%) and withdrawal symptoms (67%), to quit smoking or avoid relapsing (77%), because it was cheaper than smoking (57%) and to deal with situations where smoking was prohibited (39%). Most ex-smokers (79%) feared they might relapse to smoking if they stopped using the e-cigarette. Users of nicotine-containing e-cigarettes reported better relief of withdrawal and a greater effect on smoking cessation than those using non-nicotine e-cigarettes. E-cigarettes were used much as people would use nicotine replacement medications: by former smokers to avoid relapse or as an aid to cut down or quit smoking. Further research should evaluate the safety and efficacy of e-cigarettes for administration of nicotine and other substances, and for quitting and relapse prevention.
Article
The distribution of four main arterial risk factors (ARF) (diabetes, smoking, hyperlipidaemia (HLP), and hypertension) was investigated in 440 impotent men (mean age 46.8) in whom the penile blood-pressure index (PBPI) (ie, the ratio of the lowest systolic pressure in one of the four main arteries of the penis to the systolic pressure in the arm) was measured. In 222 the cause (organic or functional) of impotence was sought by further investigations, such as cavernosonography. 80% of this subgroup had organic impairment of erection. In 53% of these there was evidence of an arterial lesion. Smoking (64%), diabetes (30%), and HLP (34%) were all significantly more common in the 440 impotent men than in the general male population of a similar age. Whenever two or more ARFs were present mean PBPI was significantly lower. The frequency of organic impotence increased from 49% in the absence of any ARF to 100% in patients with 3 or 4 ARFs. It is concluded that increase in the frequency of impotence with age is mainly related to arteriosclerotic changes for the arteries of the penis and that the ARF and PBPI should be evaluated first in any patient complaining of impotence.
Article
Forty-two male cigarette smokers, age 18 to 44, were randomly assigned to high-nicotine, low-nicotine, or control groups in a study relating cigarette smoking to sexual response. Subjects watched erotic film segments while their penile diameters, heart rates, and finger pulse amplitudes were continuously recorded by a polygraph. Subjects in the smoking groups smoked relatively high-nicotine (.9 mg) or very low-nicotine (.002 mg) cigarettes prior to watching the last two films, while control subjects ate candy. Smoking two high-nicotine cigarettes in immediate succession significantly decreased the rate of penile diameter change relative to the other conditions. These effects were not seen after a single cigarette was smoked. High-nicotine cigarettes caused significantly more vasoconstriction and heart rate increase than did low-nicotine cigarettes, which did not differ from control conditions.
Article
The authors sought to determine whether current cigarette smoking was associated with impotence among middle-aged men. This is a secondary analysis of a cross-sectional survey of 4,462 US Army Vietnam-era veterans aged 31-49 years who took part in the Vietnam Experience Study in 1985-1986. The main outcome measurement was the odds ratio for reported impotence, which was calculated by comparing current smokers with nonsmokers while controlling for multiple confounders. The study sample consisted of 1,162 never smokers, 1,292 former smokers, and 2,008 current smokers. The prevalence of impotence was 2.2% among never smokers, 2.0% among former smokers, and 3.7% among current smokers (p = 0.005). The unadjusted odds ratio (OR) of the association between smoking and reported impotence was 1.8 (95% confidence interval (CI) 1.2-2.6). The association held even after adjustments were made for confounders, including vascular disease, psychiatric disease, hormonal factors, substance abuse, marital status, race, and age (OR = 1.5, 95% CI 1.0-2.2). Neither years smoked nor cigarettes smoked daily were significant predictors of impotence in current smokers. The authors concluded that, among the men in this study, a higher percentage of cigarette smokers reported impotence than did nonsmokers. This observation could not be totally explained by comorbidity factors related to smoking.
Article
Erectile dysfunction (ED, formerly referred to as impotence, is a common (especially in diabetic and older men) and distressing condition. Several risk factors have been identified; among these are smoking, hyperlipidaemia, hypertension and diabetes mellitus. These risk factors are shared with atherosclerotic vascular disease (e.g. ischaemic heart disease). This observation underlies a common vascular pathology. Smoking may cause ED by several mechanisms, including adversely affecting intrapenile blood flow. It is important to be aware of the link between smoking and ED since this information may motivate some male smokers to quit. In this context, it is important to be aware of the link between smoking and ED since this information may motivate smokers to quit. In this context, it is relevant that there is evidence that quitting may restore/improve erectile function.
Article
To project the likely worldwide increase in the prevalence of erectile dysfunction (ED) over the next 25 years, and to identify and discuss some possible health-policy consequences using the recent developments in the UK as a case study. Using the United Nations projected male population distributions by quinquennial age groups for 2025, the prevalence rates for ED were applied from the Massachusetts Male Aging Study (MMAS) to calculate the likely incidence of ED. The MMAS has the advantage of being the first study to provide population-based rates rather than rates based on clinical samples. All the projections were age-adjusted. It is estimated that in 1995 there were over 152 million men worldwide who experienced ED; the projections for 2025 show a prevalence of approximately 322 million with ED, an increase of nearly 170 million men. The largest projected increases were in the developing world, i.e. Africa, Asia and South America. The likely worldwide increase in the prevalence of ED (associated with rapidly ageing populations) combined with newly available and highly publicized medical treatments, will raise challenging policy issues in nearly all countries. Already under-funded national health systems will be confronted with unanticipated resource requests and challenges to existing government funding priorities. The projected trends represent a serious challenge for healthcare policy makers to develop and implement policies to prevent or alleviate ED.
Article
We estimated the incidence of erectile dysfunction in men 40 to 69 years old at study entry during an average 8.8-year followup, and determined how risk varied with age, socioeconomic status and medical conditions. Data from a randomly sampled population based longitudinal study of Massachusetts men were analyzed. A total of 1,709 men completed the baseline interview during 1987 to 1989 and 1,156 survivors completed followup from 1995 to 1997. The analysis sample consisted of 847 men without erectile dysfunction at baseline and with complete followup information. Erectile dysfunction was assessed by discriminant analysis of 13 questions from a self-administered sexual function questionnaire and a single global self-rating question. The crude incidence rate for erectile dysfunction was 25.9 cases per 1,000 man-years (95% confidence interval [CI] 22.5 to 29.9). The annual incidence rate increased with each decade of age and was 12.4 cases per 1,000 man-years (95% CI 9.0 to 16.9), 29.8 (24.0 to 37.0) and 46.4 (36.9 to 58.4) for men 40 to 49, 50 to 59 and 60 to 69 years old, respectively. The age adjusted risk of erectile dysfunction was higher for men with lower education, diabetes, heart disease and hypertension. Population projections for men 40 to 69 years old suggest that 17,781 new cases of erectile dysfunction in Massachusetts and 617,715 in the United States (white males only) are expected annually. Although prevalence estimates and cross-sectional correlates of erectile dysfunction have recently been established, incidence estimates were lacking. Incidence is necessary to assess risk, and plan treatment and prevention strategies. The risk of erectile dysfunction was about 26 cases per 1,000 men annually, and increased with age, lower education, diabetes, heart disease and hypertension.
Article
It is estimated that as many as 30 million men in the United States suffer from erectile dysfunction (ED). Because ED is so widespread, especially among the older population, it is imperative that this disorder be recognized as an important and manageable health problem.
Article
Despite the fact that the epidemiological evidence linking cigarette smoking with cardiovascular disease is overwhelming, the precise components of cigarette smoke responsible for this relationship and the mechanisms by which they exert their effect have not yet been elucidated. There are however, some promising pointers as a result of recent developments and this review concentrates on new evidence since earlier reviews of this topic. It is now known that the endothelium has a vastly more important role than was ever thought to be the case a decade ago. Its role in health and disease is increasingly understood, as is the relationship between endothelial injury and the development of atherosclerosis. There is considerable evidence that cigarette smoking can result in both morphological and biochemical disturbances to the endothelium both in vivo and in cell culture systems. Cigarette smoke is a complex mixture and only a few components have been extensively studied. Nicotine and carbon monoxide are much less damaging than is whole smoke. However the free radical components of cigarette smoke have been shown to cause damage in model systems. Further work will be necessary to consolidate the evidence base but the data reported in this review suggest that the free radical components of cigarette smoke may be responsible for the morphological and functional damage to endothelium that has been observed in model systems.