Management of Sexual Dysfunction in Men and Women: An Interdisciplinary Approach 1st ed.

3. The Impact of the Environment on Sexual Health

James M. Dupree  and Gavin M. Langille2

(1)

Department of Urology, University of Michigan Medical Center, 3875 Taubman Center/SPC 5330, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-5330, USA

(2)

Dalhousie University, Saint John, NB, Canada

James M. Dupree

Email: jim.dupree@gmail.com

Keywords

ObesityDietExerciseSmokingAlcoholDrugsLifestyleTemperatureMaternal ageElectromagnetic radiationBuilt environmentFertilitySexual function

3.1 Introduction

There is a great deal of interest regarding environmental influences that potentially affect sexual health and fertility, as reflected by the large body of literature on the topic. Patients with sexual dysfunction or infertility are often quite motivated to assess and ameliorate these conditions, and the readily apparent nature of environmental factors in everyday life inevitably makes them a target for modification. Despite numerous studies examining environmental factors that may play a role in sexual health and fertility, widespread randomized controlled trials are limited. The issues contributing to this lack of robust data include difficulty controlling for environmental factors and a lack of consensus regarding suitable study end points. Widespread public interest in the impact of environmental factors fuels coverage from the lay press, often generating news based on inconclusive scientific discourse.

In this chapter, we review the impact of the environment on the sexual health of men and women. It is worth noting from the outset that sexual health is challenging to define, because what might be considered a healthy sexual lifestyle in one culture may be viewed as unhealthy in another [1]. Additionally, in women, sexual function is challenging to measure. Unlike female fecundity/fertility and hormones, measurement of “healthy” sexual functioning currently lacks the objective measures we use to assess the former metrics, in contrast to the availability of these measures in men. Nevertheless, in this chapter, we summarize the available literature on the impact of environment on sexual function in both genders; the majority of the female-specific discussion in this chapter will focus on fertility due to a paucity of research on the impact of the environment on sexual function, libido, and sexual satisfaction in women. In the studies discussed below, the terms fertility and fecundity are often used interchangeably, but in their classic definitions, fertility refers to the ability to produce a live offspring while fecundity refers to the ability to conceive [2].

3.2 Obesity

People with a body mass index (BMI) between 25 and 30 kg/m2 are defined as overweight, while those with a BMI >30 kg/m2 are obese [3]. As of 2010 in the United States, over one third of the population is obese [4].

There is a clear relationship between obesity in women and impaired fertility. Women with increased BMI have a higher risk of menstrual disorders, miscarriages, impaired fecundity, and pregnancy outcomes [5]. A study of women with a BMI >25 or a pregnancy weight >80 kg took twice as long to achieve a pregnancy [6]. Additionally, weight loss interventions have been shown to improve menstrual cycle regularity, ovulation, and fecundity [7].

Two studies have investigated the potential relationship between obesity and female sexual dysfunction. In the first, 45 obese women were age-matched to 30 healthy controls. The study found a negative correlation between BMI and orgasm and between weight and sexual satisfaction; women with higher BMI reported lower rates of orgasms (p = 0.007), and women with higher weights reported less satisfaction (p = 0.03) [8]. However, on the more global female sexual function index (FSFI) scale , there were no significant differences between obese and normal weight women (mean FSFI score of 22.1 ± 4.3 versus 23.1 ± 3.7, respectively, p = 0.74). The diagnosed rates of female sexual dysfunction (defined as an FSFI score of ≤26.55) were 86 % in obese women and 83 % in controls (no significant difference). A second study of 64 obese women and 27 age-matched controls similarly showed no significant differences in FSFI scores (p = 0.29) and rates of female sexual dysfunction of 50 % and 41 % in the obese and control groups, respectively (p = 0.34) [9].

Between 1981 and 2008, the global incidence of obesity rose from 4.8 to 9.8 % in men [10]. The rise in obesity rates in males beginning in childhood and extending into their reproductive years is especially troubling, and data regarding the effects of obesity on semen parameters are conflicting. A meta-analysis by MacDonald et al. showed no correlation between semen parameters and BMI [11]. However, a meta-analysis by Sermondade et al. demonstrated an increased chance of abnormal semen parameters in overweight and obese men [odds ratio (confidence interval) for azoospermia or oligospermia of 1.11 (1.01–1.21) for overweight, 1.28 (1.06–1.55) for obese, and 2.0 (1.59–2.62) for morbidly obese men] [12]. Data from the LIFE study by Eisenberg et al. showed an inverse correlation between waist circumference and semen volumes and concentrations [13].

Testosterone levels in obese men are lower compared to men with a lower BMI [14], attributed in part to an increase in aromatization of testosterone to estrogen in adipose tissue [15]. In addition, obesity contributes to a diagnosis of “metabolic syndrome” along with hypertension, insulin resistance, elevated triglycerides, and low levels of high-density lipoprotein, which has a negative impact on erectile function [1618]. Dyslipidemia has also been shown to negatively impact sperm morphology [19]. The adipose tissue surrounding the testes in obese patients may impair fertility through elevated scrotal temperatures, and surgical removal of the suprapubic fat pad in such patients has resulted in increased sperm concentration and motility in a series of 22 patients [20].

3.3 Diet

Due to complex cultural and financial considerations, many countries are shifting consumption toward a “western” diet characterized by large portions of refined grains, sugars, and red meats while being low in fresh fruits and vegetables, a combination widely considered unhealthy [21]. A healthy diet contributes to both physical and mental health and is important for avoidance of obesity, diabetes, and cardiovascular disease [22]. Obese patients have a significantly increased risk of developing depression [23], a well-known risk factor for sexual dysfunction [2425].

While some studies have suggested that a woman’s prepregnancy diet can affect fetal health [26], few studies have directly investigated potential links between female diet and fertility [22]. However, the first trimester is likely the time where the embryo’s health is most directly related to the mother’s diet and nutrition [22]. Numerous investigations of the impact of vitamins, particularly folic acid and other B-group vitamins on neural tube development, have led to an understanding of their impact on fetal health [27]. However, fewer studies about vitamins and their impact on fertility exist. The study of a large prospective cohort of 18,555 women did show that women taking folic acid and other B-group vitamins had a lower risk of infertility [28].

Erectile dysfunction (ED) is more commonly diagnosed in men with obesity, diabetes, and cardiovascular disease, as well as other comorbid conditions [29]. A randomized controlled trial of 145 obese men found a significant improvement in erectile function as assessed using the IIEF-5 questionnaire for those enrolled in a weight loss program employing diet and exercise [30]. In regard to male fertility, a case-control study of 30 men showed that infertile males had a lower intake of fruits and vegetables, with a higher intake of red meats [31]. Similarly, a study of 189 men showed an inverse relationship between red meat intake and total sperm count [32]. An observational study of 188 men showed that those who avoided a western diet had increased sperm motility [33].

3.4 Exercise

While exercise is generally considered a healthy endeavor, in excess, it can impair fertility in women. As far back as 1986, a population-based case-control study of 187 infertile women and 419 parous controls showed that vigorous exercise lasting more than 60 min per day could increase a women’s risk for infertility associated with abnormal ovulation [34]. Female athletes show significantly more menstrual cycle irregularity as compared to sedentary women (1–44 % irregular cycles versus 2–5 % irregular cycles, respectively) [5]. Additionally, being underweight (defined as a BMI < 19) has been shown to reduce a woman’s fecundity by up to fourfold [6]. In their study, Hassan and Killick found that underweight women took an average of 29 months to achieve a pregnancy, as compared to 6.8 months for women of normal weight [6]. However, for obese women with polycystic ovary syndrome , women engaging in moderate exercise were more likely to resume ovulation [35].

The Massachusetts Male Aging Study followed 593 men for 8 years; men who regularly exercised showed a 30 % decreased risk of developing ED [36]. Aerobic exercise has been shown to improve semen concentration, motility, and morphology as seen in a 14-week study of 60 men using a home treadmill routine of moderate intensity [37]. A study of 222 men aged 18–22 found that a higher ratio of exercise to television watching actually improved sperm concentration and total sperm count [37]. However, vigorous cycling was shown to increase reactive oxygen species and worsen semen parameters [38]. In obese men, regular exercise increased serum testosterone levels and improved erectile function [39].

Patients should be counseled that regular aerobic exercise of moderate intensity is likely beneficial for the maintenance of fertility and sexual function while a complete lack or excess of physical activity is likely to be detrimental.

3.5 Smoking

Although tobacco use in the western world has decreased over the past several decades, the smoking rate in the United States remains at almost 20 % [40]. Tobacco use has been associated with many health conditions including lung cancer, heart disease, and, more recently, infertility. However, public knowledge of smoking as a cause of infertility is significantly lower than knowledge about the link between smoking and lung cancer and heart disease [41]. Using a population-based sample, Hull and colleagues found that women who smoked were 54 % more likely to have a fecundity delay of greater than 12 months, as compared to nonsmokers [42]. This relationship also appears to be dose-dependent, with heavy smokers having worse fertility [6]. A review of 13 studies found that 12 of the 13 studies demonstrated a negative impact of smoking on fecundity [43]. Biologically, smoking has been associated with lowered ovarian reserve, lower estrogen levels, higher follicle-stimulating hormone levels, and earlier menopause in women, all likely contributing to the increased primary and secondary infertility seen among female smokers [44].

Similarly, male smokers demonstrate impaired semen volume [45], concentration, motility [46], and morphology [46]. However, the effects of smoking in men on pregnancy rates have been more difficult to elucidate [47]. The mechanisms underlying the effects of tobacco on semen parameters are thought to be based on elevated nitric oxide, which results in an impaired acrosome reaction and lower sperm motility, while elevated lipid peroxidation compromises the sperm plasma membrane [48].

Smokers have a 40 % higher rate of ED than nonsmokers, which varies in a dose-dependent manner [49]. The increased risk of ED in smokers is derived from the endothelial and atherosclerotic insults resulting in end organ damage [50]. Former smokers have significantly less ED than active smokers, indicating that smoking cessation can result in improved erectile dysfunction [51].

3.6 Alcohol

When consumed by women during pregnancy, alcohol is well known to be a teratogen [22]. But separate from its effect on the fetus, both moderate (<100 g per week) and heavy (>100 g per week) alcohol consumptions have also been associated with female infertility. A multicenter case-control study of 1050 infertile women and 3833 parous controls found that both moderate and high alcohol intakes were associated with a 60 % increased risk of infertility [52]. It appeared that ovulatory dysfunction was the likely etiology of infertility among the women with heavy alcohol intake.

Regarding sexual function in women , there is a dose-dependent response between blood alcohol levels and genital response, with high blood alcohol levels associated with decreased genital responsiveness. Assessment of genital responsiveness, however, is complicated by an increased subjective sense of arousal in the setting of increased alcohol consumption, even when the objective genital response is impaired [53].

Although it has long been known that alcohol in moderate amounts can increase libido in men [54], when consumed in larger quantities, it causes ED [55]. Chronic alcohol use can induce ED by multiple factors including peripheral nerve damage and hypogonadism [56]. Central disruption of the gonadal axis has also been proposed [57]. Alcohol abuse and depression have been extensively linked, with alcohol being a known precipitant for depressive episodes [58]. In turn, depression is a known risk factor for erectile dysfunction [59]. The absolute effect of alcohol on semen parameters remains controversial in the literature to date. Ethanol intake has been shown to reversibly decrease sperm morphology, although pregnancy rates remain unaffected at the population level [60]. Among heavy drinkers (ethanol intake >80 g per day), 78.8 % had abnormal semen analyses [61].

3.7 Illicit Drugs

Marijuana and cocaine use have been associated with increased rates of infertility in women. In a case-control study of 150 infertile women, marijuana use increased the risk of infertility by about 70 %, especially when used in the year preceding attempted pregnancy [62]. Cocaine use also is also associated with increased infertility rates [62].

There are few published data about the impact of illicit drugs on sexual function in women. It is generally thought that chronic use of most illicit drugs leads to decreased sexual response in women [63]. Additionally, using illicit drugs has been associated with increased risky sexual behavior, as well as an increased risk of STIs and unwanted pregnancies [63].

Narcotic use and abuse in men has deleterious effects on testosterone levels and erectile function. Chronic narcotic use decreases serum testosterone, luteinizing hormone, follicle-stimulating hormone, and libido [64]. Erectile function is also negatively affected by narcotic use [65].

The legalization of marijuana in parts of the United States and elsewhere [66] highlights the importance for awareness of its deleterious effects on sperm motility [67], as well as decreased luteinizing hormone [68] and testosterone levels [69]. Interestingly, ED was not noted among a large cohort of marijuana users [70]. Cocaine has been shown to impair sperm concentration, motility, and morphology, and heroin has also been shown to negatively affect semen parameters [7172].

Testosterone supplementation is a well-known male contraceptive; an international study using intramuscular testosterone enanthate produced azoospermia in 65 % of men within 4 months [73]. Despite this, a survey of 387 urologists revealed that 25 % of respondents would actually prescribe testosterone in an attempt to ameliorate infertility, apparently unaware of the actual effects of testosterone on semen quality [74].

3.8 Male Gonads and Temperature

Elevated testicular temperature has a deleterious effect on testicular function [75]. Common causes for a hyperthermic testicular environment include febrile illness [76], saunas [77], warmer weather [78], and, as previously discussed, increased insulation of the testes by adipose tissue [79]. Heat exposure associated with sitting in an automobile for periods of >3 h per day also significantly prolonged the time to achieve a pregnancy [80]. The use of tight underwear, often a topic of inquiry from patients, does not appear to be detrimental to male fertility or sexual function [81]. The studies on these areas are a continued source of debate with little in the way of consensus on the role of temperature effects on male gonadal function.

3.9 Testicular Exposure to Electromagnetic Radiation

There is evidence that the ) radiofrequency electromagnetic radiation (RF-EMR) produced by cellular telephones can adversely affect sperm motility and morphology [82]. In a study of ten men, the level of sperm DNA fragmentation was increased in men using cellular telephones for more than 4 h per day, exacerbated by storage of the phone in the trouser pocket [83]. A study by Agarwal et al. demonstrated decreased motility of ejaculated sperm after exposure to RF-EMR [84]. Although robust randomized controlled trials are lacking, the available data suggest that minimization of gonadal RF-EMR exposure is advisable.

3.10 Maternal Age

The age of first maternity is increasing. According to the Centers for Disease Control and Prevention, the average age of first birth for women increased from 21.4 years in 1970 to 25.0 years in 2006 [85]. This is thought to result from a variety of factors including changes in marriage patterns, educational and career opportunities, and contraceptive use [86]. Increasing age is a clear risk factor for infertility, with women over 35 often taking significantly longer to achieve a pregnancy [87], thought to be related to higher menstrual cycle irregularity, chromosomal abnormalities, and a decrease in oocyte quality as women age [87].

3.11 The Built Environment

Although the literature is very limited, a brief discussion of the impact of the built environment on sexual health is necessary. The built environment refers to the physical structures that people live in and around, as well as the neighborhood environment [88]. “Riskscapes ” describe geographic areas with low incomes and an excess of poor land use, neighborhood stressors, and limited access to healthcare resources or healthy land uses such as parks and open spaces [88]. Research into the effect of the built environment has found that adolescent residents of riskscapes have higher rates of sexually transmitted infections (STIs) , unprotected sexual activities, and unintended pregnancies [88]. Additionally, women in these areas are at increased risk for sexual assault [88]. Riskscapes may also be associated with increased stress and fatigue among women for these reasons, and any environmental condition that induces stress or fatigue can lower sexual desire [1].

3.12 Conclusion

There exists a breadth of environmental influences on male and female sexual function and reproductive health. The available literature supports promotion of sexual and reproductive function through a healthy lifestyle with attention to diet and exercise while limiting tobacco, alcohol, and illicit drugs that negatively impact sexual function when possible. Future trials of higher quality are required to further elucidate the role of additional environmental factors on sexual and reproductive health.

References

1.

Bancroft J. Impact of environment, stress, occupational, and other hazards on sexuality and sexual behavior. Environ Health Perspect. 1993;101 Suppl 2:101–7.CrossRefPubMedPubMedCentral

2.

Buck GM, Sever LE, Batt RE, Mendola P. Life-style factors and female infertility. Epidemiology. 1997;8:435–41.CrossRefPubMed

3.

Bray GA. Overweight is risking fate. Definition, classification, prevalence, and risks. Ann N Y Acad Sci. 1987;499:14–28.CrossRefPubMed

4.

Moyer VA, U.S. Preventive Services Task Force. Screening for and management of obesity in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2012;157:373–8.PubMed

5.

Kelly-Weeder S, O’Connor A. Modifiable risk factors for impaired fertility in women: what nurse practitioners need to know. J Am Acad Nurse Pract. 2006;18:268–76.CrossRefPubMed

6.

Hassan MA, Killick SR. Negative lifestyle is associated with a significant reduction in fecundity. Fertil Steril. 2004;81:384–92.CrossRefPubMed

7.

Norman RJ, et al. Improving reproductive performance in overweight/obese women with effective weight management. Hum Reprod Update. 2004;10:267–80.CrossRefPubMed

8.

Yaylali GF, Tekekoglu S, Akin F. Sexual dysfunction in obese and overweight women. Int J Impot Res. 2010;22:220–6.CrossRefPubMed

9.

Kadioglu P, et al. Obesity might not be a risk factor for female sexual dysfunction. BJU Int. 2010;106:1357–61.CrossRefPubMed

10.

Finucane MM, et al. National, regional, and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants. Lancet. 2011;377:557–67.CrossRefPubMedPubMedCentral

11.

MacDonald AA, Herbison GP, Showell M, Farquhar CM. The impact of body mass index on semen parameters and reproductive hormones in human males: a systematic review with meta-analysis. Hum Reprod Update. 2010;16:293–311.CrossRefPubMed

12.

Sermondade N, et al. BMI in relation to sperm count: an updated systematic review and collaborative meta-analysis. Hum Reprod Update. 2013;19:221–31.CrossRefPubMed

13.

Eisenberg ML, et al. The relationship between male BMI and waist circumference on semen quality: data from the LIFE study. Hum Reprod. 2014;29:193–200.CrossRefPubMed

14.

Zumoff B, et al. Plasma free and non-sex-hormone-binding-globulin-bound testosterone are decreased in obese men in proportion to their degree of obesity. J Clin Endocrinol Metab. 1990;71:929–31.CrossRefPubMed

15.

Cohen PG. Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. Med Hypotheses. 2001;56:702–8.CrossRefPubMed

16.

Montorsi F, et al. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease. Eur Urol. 2003;44:360–4; Discussion 364–5.

17.

Roumeguere T, Wespes E, Carpentier Y, Hoffmann P, Schulman CC. Erectile dysfunction is associated with a high prevalence of hyperlipidemia and coronary heart disease risk. Eur Urol. 2003;44:355–9.CrossRefPubMed

18.

Gorgel SN, Gorgel A, Sefik E. Sexual function in male patients with metabolic syndrome and effective parameters on erectile dysfunction. Int Braz J Urol. 2014;40:56–61.PubMed

19.

Schisterman EF, et al. Lipid concentrations and semen quality: the LIFE study. Andrology. 2014;2:408–15.CrossRefPubMedPubMedCentral

20.

Shafik A, Olfat S. Lipectomy in the treatment of scrotal lipomatosis. Br J Urol. 1981;53:55–61.CrossRefPubMed

21.

Bonaccio M, Iacoviello L, de Gaetano G, Moli-Sani I. The Mediterranean diet: the reasons for a success. Thromb Res. 2012;129:401–4.PubMed

22.

Homan GF, Davies M, Norman R. The impact of lifestyle factors on reproductive performance in the general population and those undergoing infertility treatment: a review. Hum Reprod Update. 2007;13:209–23.CrossRefPubMed

23.

Hryhorczuk C, Sharma S, Fulton SE. Metabolic disturbances connecting obesity and depression. Front Neurosci. 2013;7:177.CrossRefPubMedPubMedCentral

24.

Kennedy SH, Rizvi S. Sexual dysfunction, depression, and the impact of antidepressants. J Clin Psychopharmacol. 2009;29:157–64.CrossRefPubMed

25.

Mathew RJ, Weinman ML. Sexual dysfunctions in depression. Arch Sex Behav. 1982;11:323–8.CrossRefPubMed

26.

Moore VM, Davies MJ. Diet during pregnancy, neonatal outcomes and later health. Reprod Fertil Dev. 2005;17:341–8.CrossRefPubMed

27.

Anderson K, Nisenblat V, Norman R. Lifestyle factors in people seeking infertility treatment – a review. Aust N Z J Obstet Gynaecol. 2010;50:8–20.CrossRefPubMed

28.

Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Diet and lifestyle in the prevention of ovulatory disorder infertility. Obstet Gynecol. 2007;110:1050–8.CrossRefPubMed

29.

Meldrum DR, et al. Lifestyle and metabolic approaches to maximizing erectile and vascular health. Int J Impot Res. 2012;24:61–8.CrossRefPubMed

30.

Collins CE, et al. Improvement in erectile function following weight loss in obese men: the SHED-IT randomized controlled trial. Obes Res Clin Pract. 2013;7:e450–4.CrossRefPubMed

31.

Mendiola J, et al. Food intake and its relationship with semen quality: a case-control study. Fertil Steril. 2009;91:812–18.CrossRefPubMed

32.

Afeiche MC, et al. Meat intake and reproductive parameters among young men. Epidemiology. 2014;25:323–30.CrossRefPubMedPubMedCentral

33.

Gaskins AJ, Colaci DS, Mendiola J, Swan SH, Chavarro JE. Dietary patterns and semen quality in young men. Hum Reprod. 2012;27:2899–907.CrossRefPubMedPubMedCentral

34.

Green BB, Daling JR, Weiss NS, Liff JM, Koepsell T. Exercise as a risk factor for infertility with ovulatory dysfunction. Am J Public Health. 1986;76:1432–6.CrossRefPubMedPubMedCentral

35.

Huber-Buchholz MM, Carey DG, Norman RJ. Restoration of reproductive potential by lifestyle modification in obese polycystic ovary syndrome: role of insulin sensitivity and luteinizing hormone. J Clin Endocrinol Metab. 1999;84:1470–4.PubMed

36.

Johannes CB, et al. Incidence of erectile dysfunction in men 40 to 69 years old: longitudinal results from the Massachusetts male aging study. J Urol. 2000;163:460–3.CrossRefPubMed

37.

Rosety-Rodriguez M, et al. Home-based treadmill training improved seminal quality in adults with type 2 diabetes. Actas Urol Esp. 2014;38:589–93.CrossRefPubMed

38.

Maleki BH, Tartibian B, Vaamonde D. The effects of 16 weeks of intensive cycling training on seminal oxidants and antioxidants in male road cyclists. Clin J Sport Med. 2014;24:302–7.CrossRefPubMed

39.

Khoo J, et al. Comparing effects of low- and high-volume moderate-intensity exercise on sexual function and testosterone in obese men. J Sex Med. 2013;10:1823–32.CrossRefPubMed

40.

Bunn Jr PA. Worldwide overview of the current status of lung cancer diagnosis and treatment. Arch Pathol Lab Med. 2012;136:1478–81.CrossRefPubMed

41.

Practice Committee of American Society for Reproductive Medicine. Smoking and infertility. Fertil Steril. 2008;90:S254–9.

42.

Hull MG, North K, Taylor H, Farrow A, Ford WC. Delayed conception and active and passive smoking. The Avon Longitudinal Study of Pregnancy and Childhood Study Team. Fertil Steril. 2000;74:725–33.CrossRefPubMed

43.

Hughes EG, Brennan BG. Does cigarette smoking impair natural or assisted fecundity? Fertil Steril. 1996;66:679–89.CrossRefPubMed

44.

U.S. Department of Health and Human Services. Women and smoking: a report of the surgeon general. Atlanta, GA: U.S. Department of Health and Human Services; 2001 http://​www.​cdc.​gov/​tobacco/​data_​statistics/​sgr/​2001/​complete_​report/​index.​htm.

45.

Pasqualotto FF, Sobreiro BP, Hallak J, Pasqualotto EB, Lucon AM. Cigarette smoking is related to a decrease in semen volume in a population of fertile men. BJU Int. 2006;97:324–6.CrossRefPubMed

46.

Kunzle R, et al. Semen quality of male smokers and nonsmokers in infertile couples. Fertil Steril. 2003;79:287–91.CrossRefPubMed

47.

Stewart TM, Liu DY, Garrett C, Brown EH, Baker HW. Recruitment bias in studies of semen and other factors affecting pregnancy rates in fertile men. Hum Reprod. 2009;24:2401–8.CrossRefPubMed

48.

Ghaffari MA, Rostami M. Lipid peroxidation and nitric oxide levels in male smokers’ spermatozoa and their relation with sperm motility. J Reprod Infertil. 2012;13:81–7.PubMedPubMedCentral

49.

He J, et al. Cigarette smoking and erectile dysfunction among Chinese men without clinical vascular disease. Am J Epidemiol. 2007;166:803–9.CrossRefPubMed

50.

McVary KT, Carrier S, Wessells H, Subcommittee on Smoking and Erectile Dysfunction Socioeconomic Committee, Sexual Medicine Society of North America. Smoking and erectile dysfunction: evidence based analysis. J Urol. 2001;166:1624–32.CrossRefPubMed

51.

Mannino DM, Klevens RM, Flanders WD. Cigarette smoking: an independent risk factor for impotence? Am J Epidemiol. 1994;140:1003–8.PubMed

52.

Grodstein F, Goldman MB, Cramer DW. Infertility in women and moderate alcohol use. Am J Public Health. 1994;84:1429–32.CrossRefPubMedPubMedCentral

53.

Rosen R. Alcohol and drug effects on sexual response: human experimental and clinical studies. Annu Rev Sex Res. 1991;2:119–49.

54.

Abel EL. A review of alcohol’s effects on sex and reproduction. Drug Alcohol Depend. 1980;5:321–32.CrossRefPubMed

55.

Miller NS, Gold MS. The human sexual response and alcohol and drugs. J Subst Abus Treat. 1988;5:171–7.CrossRef

56.

Taniguchi N, Kaneko S. [Alcoholic effect on male sexual function]. Nihon Rinsho. 1997;55:3040–4.PubMed

57.

Kim JH, et al. Suppression by ethanol of male reproductive activity. Brain Res. 2003;989:91–8.CrossRefPubMed

58.

Vaillant GE. Is alcoholism more often the cause or the result of depression? Harv Rev Psychiatry. 1993;1:94–9.CrossRefPubMed

59.

Seftel AD, Sun P, Swindle R. The prevalence of hypertension, hyperlipidemia, diabetes mellitus and depression in men with erectile dysfunction. J Urol. 2004;171:2341–5.CrossRefPubMed

60.

La Vignera S, Condorelli RA, Balercia G, Vicari E, Calogero AE. Does alcohol have any effect on male reproductive function? A review of literature. Asian J Androl. 2013;15:221–5.CrossRefPubMed

61.

Pajarinen J, Savolainen V, Perola M, Penttila A, Karhunen PJ. Polymorphism in the cytochrome P450 2E1 gene and alcohol-induced disorders of human spermatogenesis. Int J Androl. 1996;19:314–22.CrossRefPubMed

62.

Mueller BA, Daling JR, Weiss NS, Moore DE. Recreational drug use and the risk of primary infertility. Epidemiology. 1990;1:195–200.CrossRefPubMed

63.

Palha AP, Esteves M. Drugs of abuse and sexual functioning. Adv Psychosom Med. 2008;29:131–49.CrossRefPubMed

64.

Rajagopal A, Vassilopoulou-Sellin R, Palmer JL, Kaur G, Bruera E. Hypogonadism and sexual dysfunction in male cancer survivors receiving chronic opioid therapy. J Pain Symptom Manag. 2003;26:1055–61.CrossRef

65.

Deyo RA, et al. Prescription opioids for back pain and use of medications for erectile dysfunction. Spine. 2013;38:909–15.CrossRefPubMedPubMedCentral

66.

Room R. Legalizing a market for cannabis for pleasure: Colorado, Washington, Uruguay and beyond. Addiction. 2014;109:345–51.CrossRefPubMed

67.

Whan LB, West MC, McClure N, Lewis SE. Effects of delta-9-tetrahydrocannabinol, the primary psychoactive cannabinoid in marijuana, on human sperm function in vitro. Fertil Steril. 2006;85:653–60.CrossRefPubMed

68.

Vescovi PP, et al. Chronic effects of marihuana smoking on luteinizing hormone, follicle-stimulating hormone and prolactin levels in human males. Drug Alcohol Depend. 1992;30:59–63.CrossRefPubMed

69.

Kolodny RC, Masters WH, Kolodner RM, Toro G. Depression of plasma testosterone levels after chronic intensive marihuana use. N Engl J Med. 1974;290:872–4.CrossRefPubMed

70.

Smith AM, et al. Cannabis use and sexual health. J Sex Med. 2010;7:787–93.CrossRefPubMed

71.

Bracken MB, et al. Association of cocaine use with sperm concentration, motility, and morphology. Fertil Steril. 1990;53:315–22.CrossRefPubMed

72.

Ragni G, De Lauretis L, Bestetti O, Sghedoni D, Gambaro V. Gonadal function in male heroin and methadone addicts. Int J Androl. 1988;11:93–100.CrossRefPubMed

73.

World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia and oligozoospermia in normal men. Fertil Steril. 1996;65:821–9.CrossRef

74.

Ko EY, Siddiqi K, Brannigan RE, Sabanegh Jr ES. Empirical medical therapy for idiopathic male infertility: a survey of the American Urological Association. J Urol. 2012;187:973–8.CrossRefPubMed

75.

Jung A, Schuppe HC. Influence of genital heat stress on semen quality in humans. Andrologia. 2007;39:203–15.CrossRefPubMed

76.

Sergerie M, Mieusset R, Croute F, Daudin M, Bujan L. High risk of temporary alteration of semen parameters after recent acute febrile illness. Fertil Steril. 2007;88(970):e971–7.

77.

Saikhun J, Kitiyanant Y, Vanadurongwan V, Pavasuthipaisit K. Effects of sauna on sperm movement characteristics of normal men measured by computer-assisted sperm analysis. Int J Androl. 1998;21:358–63.CrossRefPubMed

78.

Levine RJ, et al. Differences in the quality of semen in outdoor workers during summer and winter. N Engl J Med. 1990;323:12–6.CrossRefPubMed

79.

Shafik A, Olfat S. Scrotal lipomatosis. Br J Urol. 1981;53:50–4.CrossRefPubMed

80.

Thonneau P, Ducot B, Bujan L, Mieusset R, Spira A. Effect of male occupational heat exposure on time to pregnancy. Int J Androl. 1997;20:274–8.CrossRefPubMed

81.

Munkelwitz R, Gilbert BR. Are boxer shorts really better? A critical analysis of the role of underwear type in male subfertility. J Urol. 1998;160:1329–33.CrossRefPubMed

82.

Wdowiak A, Wdowiak L, Wiktor H. Evaluation of the effect of using mobile phones on male fertility. Ann Agric Environ Med. 2007;14:169–72.PubMed

83.

Rago R, et al. The semen quality of the mobile phone users. J Endocrinol Investig. 2013;36:970–4.

84.

Agarwal A, et al. Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human ejaculated semen: an in vitro pilot study. Fertil Steril. 2009;92:1318–25.CrossRefPubMed

85.

Matthews TJ, Hamilton BE. Delayed childbearing: more women are having their first child later in life. NCHS Data Brief. 2009;21:1–8.PubMed

86.

Mathews TJ, Hamilton BE. Mean age of mother, 1970–2000. Nat Vital Stat Rep. 2002;51:1–13.

87.

Practice Committee of the American Society for Reproductive Medicine. Aging and infertility in women: a committee opinion. Fertil Steril. 2002;78:215–19.CrossRef

88.

Satcher D, Okafor M, Dill LJ. Impact of the built environment on mental and sexual health: policy implications and recommendations. ISRN Public Health. 2012;2012:7.CrossRef



If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!