The association between smoking and erectile dysfunction was evaluated in a cohort of 2,115 Caucasian men, aged 40-79 years, randomly selected from Olmsted County, Minnesota. Smoking status was assessed by questionnaire; during the fourth biennial examination, erectile dysfunction was assessed with the Brief Male Sexual Function Inventory. Of the 1,329 men with a regular sexual partner, 173 were current smokers, 836 had previously smoked, and 203 reported erectile dysfunction. Compared with former and never smokers, current smokers in their forties had the greatest relative odds of erectile dysfunction, 2.74 (95% confidence interval (CI): 0.44, 16.89), compared with 1.38 (95% CI: 0.51, 3.74), 1.70 (95% CI: 0.82, 3.51), and 0.77 (95% CI: 0.27, 2.21) for men in their fifties, sixties, and seventies, respectively. Compared with men who never smoked, men who smoked at some time had a greater likelihood of erectile dysfunction (age-adjusted odds ratio = 1.42, 95% CI: 1.00, 2.02), and there was a dose response. Although the causal pathway underlying this association is not clear, this study contributes to the growing literature describing an association between smoking and erectile dysfunction.

ABSTRACT:Carboxylesterases are important in the metabolism of cocaine, catalyzing the hydrolysis of cocaine to its two major metabolites, benzoylecgonine and ecgonine methyl ester. In the presence of ethanol, some cocaine undergoes transesterification with ethanol instead of hydrolysis with water producing the active metabolite, cocaethylene. The metabolic fate of cocaethylene is unknown, but given its structural similarity to cocaine, it was hypothesized that cocaethylene would also be metabolized by carboxylesterases and its elimination decreased in the presence of ethanol, as is cocaine's. Dogs were given cocaine alone, cocaethylene alone, cocaine and ethanol, cocaethylene and ethanol, and cocaine and cocaethylene on separate study days and sequential blood sam- Most cocaine users also ingest ethanol (McCance-Katz et al., 1993). This combination results in a decrease in the clearance of cocaine and the formation of the pharmacologically active metabolite, cocaethylene (Perez-Reyes et al., 1994;Hart et al., 2000). These alterations in the metabolic disposition of cocaine are mediated through the effects of ethanol on carboxylesterase. In humans, two carboxylesterase enzymes have been identified, carboxylesterase 1 (hCE1 1 ) and carboxylesterase 2 (hCE2) that participate in the metabolism of cocaine (Dean et. al., 1991;Brzezinski et. al., 1997). Although present in many tissues including heart, stomach, kidney, colon, and others, they are most abundant in the liver (Riddles et al., 1991;Schwer et al., 1997). Carboxylesterases are located in the endoplasmic reticulum and catalyze the hydrolysis of lipophilic esters to their more water-soluble alcohol and acyl substituents. There is evidence for the involvement of carboxylesterases in the metabolism of endogenous substrates such as lipids and steroids, but their primary function seems to be protecting the body from foreign substances encountered through the diet and other routes (Satoh et al., 2002). The carboxylesterases hCE1 and hCE2 are low affinity, high capacity enzymes able to hydrolyze a wide variety of structurally dissimilar esters (Kroetz et al., 1993;Satoh et al., 2002).Perhaps the best-known and most thoroughly studied substrate of hCE1 and hCE2 is cocaine. Cocaine is primarily eliminated by hydrolysis to benzoylecgonine by hCE1 and to ecgonine methyl ester by hCE2 with subsequent renal elimination. When ethanol is consumed with cocaine, a new metabolite is produced, cocaethylene (Rafla and Epstein, 1979;Boyer and Petersen, 1992;Bourland et al., 1997). Its formation results from hCE1 catalyzed transesterification between cocaine and ethanol as opposed to the normal reaction with water (hydrolysis) that produces the inactive metabolite, benzoylecgonine (Dean et al., 1991;Boyer and Petersen, 1992;Brzezinski et al., 1994;Bourland et al., 1997). Structurally, cocaine and cocaethylene differ only in the substitution of ethyl in place of the methyl ester [i.e., the ecgonine methyl ester (cocaine) is metabolized to ethyl ester (cocaethylene)]. Because of the...

Introduction-Severe obstructive sleep apnea has been associated with sexual dysfunction; however, it is unclear whether milder forms of sleep disturbances might also be associated with sexual problems.

Introduction-The presence of erectile or ejaculatory dysfunction may indicate physical problems; however, individual perceptions (e.g., sexual satisfaction) may reflect the degree of concern about these changes. Long-term data showing how changes in multiple sexual function domains track together may be useful in understanding the importance of physical declines vs. sexual satisfaction.

Few studies have examined the association between sex hormone serum levels, erectile function, and sex drive. Using data from the Olmsted County Study of Urinary Symptoms and Health Status among Men we examined the associations between sex hormone serum levels, erectile function, and sex drive. During 1989-1991, Caucasian men ages 40-79 years were randomly selected from Olmsted County, MN, and in the sixth year of follow-up questions on sexual function from the Brief Male Sexual Function Inventory were added and included biennially thereafter with assays for estradiol, testosterone, and bioavailable testosterone levels. Out of 414 men, 294 had a regular sexual partner and androgen measurements at the fourteenth year of follow-up. These cross-sectional results suggest the relationship between sex hormones and sexual function is complex. Total testosterone and erectile function were significantly correlated even after adjustment for age (r = 0.12, p = 0.04). Conversely, total testosterone was not significantly correlated with sex drive (r = 0.08, p = 0.17). Bioavailable testosterone was significantly correlated with both erectile function and sex drive (r = 0.16, p = 0.01 and r = 0.20, p = 0.001, respectively). However, these associations disappeared after age-adjustment (r = 0.04 and r = 0.09). This suggests that the age-related decline in sexual function may be due to age-related declines in levels of bioavailable testosterone rather than total testosterone levels.