It has been estimated that 7.4% of women and their husbands in the United States are infertile [1] and that the number of infertile people in the world may be as high as 15%, particularly in industrialized nations [2]. Decreasing the number of people affected by infertility has become a top priority for many health organizations, including Healthy People 2020 [3]. Lifestyle factors can be modified to enhance overall well-being and they are ultimately under one’s own control. They play a key role in determining reproductive health and can positively or negatively influence fertility.
The goal of this review is to demonstrate the potential effects of multiple lifestyles on reproductive health for both men and women. The review focuses primarily on modifiable lifestyles including the age when starting a family, nutrition, weight management, exercise, psychological stress, cigarette smoking, recreational drugs use, medications, alcohol use, caffeine consumption, environmental and occupation exposure, preventative care, clothing choices, hot water, and lubricants. While many aspects of life are not modifiable, lifestyles may be changed.
The age of a man or woman is a factor among others that can affect fertility. Due to pursuit of education and other factors, many couples are choosing to delay child-bearing. Fertility peaks and then decreases over time in both men and women, thus the reproductive timeline may be one aspect to consider when determining the ideal time to start a family. As men age, testosterone levels begin to decrease and hypogonadism results. However, if testosterone is used to treat hypogonadism, it can suppress spermatogenesis [4]. Semen parameters also begin a steady decline as early as age 35 [5]; semen volume and motility both decrease and morphology may become increasingly abnormal [4,6]. After the age of 40, men can have significantly more DNA damage in their sperm, as well as decline in both motility (40%) and viability (below 50%) (n = 504, p < 0.001) [7]. There may also be an increase in time to pregnancy with an increase in male age [8]. Hassan and Killick reported that when men were over the age of 45, their partner’s relative risk of an increase in time to pregnancy over one year increased to 4.6, and over two years increased to 12.5 (n = 1832, CI = 24.5-38.1) [9]. The authors also noted that the older population tended to consume more alcohol, have intercourse less often, had longer contraceptive usage, and smoked less cigarettes which could have been confounding factors. Another study found that there are also exponentially fewer infants born to fathers ≥35 to 39 years of age and older compared to younger age groups even when controlling for female age (n = 122,061) [10].
The reproductive timeline for women is complex. A woman is born with all the oocytes she will ever have, and only 400–500 are actually ovulated [6]. As the number of oocytes decline, a woman’s menstrual cycle shortens, infertility increases, and menstrual irregularity begins 6–7 years before menopause. Increasing age increases a woman’s time to pregnancy. When under the age of 30, a woman’s chances of conceiving may be as high 71%; when over 36, it may only be 41% [8]. The chances of becoming pregnant and being able to maintain a pregnancy are also affected. Matorras et al. reported that in a population of women, the number of infants born begins to exponentially decrease after the age bracket of 35–39 (n = 89,287) [10]. The odds of becoming pregnant and maintaining a pregnancy are believed to be connected to numerous factors, including euploidy. Euploidy has been found to be inversely correlated with female age (P < .01; n = 544) [11]. Another study reported that the rate of aneuploidy for women over 35 was 45.7% versus 34.8% for women under 35 (n = 352, p = .018) [12]. In comparison, Munné et al. reported the rates of euploidy decrease 50% for women under 35, decrease 40% for women between the ages of 35 and 40, and decrease 33.3% for women over 40 [13]. In addition, chromosomal abnormalities and aneuploidy may increase the risk of spontaneous abortion and implantation loss with increasing age [4,6]. Overall, women’s fertility is significantly lower in the 30s and 40s [6].
Aspects of a male’s diet may have an impact on his fertility. Consuming a diet rich in carbohydrates, fiber, folate, and lycopene [14] as well as consuming fruit (OR 2.3) and vegetables (OR 1.9) [15] correlates with improved semen quality. Consuming lower amounts of both proteins and fats were more beneficial for fertility [14]. Another potential benefit could be antioxidants, which play a pivotal role in the body by scavenging reactive oxygen species (ROS). Reactive oxygen species or ROS are a collection of free radicals and non-radical derivatives of oxygen such as superoxide anion (O2• -), hydrogen peroxide (H2O2), hydroxyl radical (OH•). This category also includes free radicals derived from nitrogen called reactive nitrogen species such as: nitric oxide (NO•), nitric dioxide (NO2•), peroxynitrite (ONOO-). Collectively they are termed as reactive oxygen species. These are by-products of cellular respiration that are necessary for certain cellular activity, including sperm capacitation; however, an overabundance of ROS may compromise sperm function, including sperm motility, altering DNA and decreasing membrane integrity [16]. Antioxidants are molecules such as albumin, ceruloplasmin, and ferritin; and an array of small molecules, including ascorbic acid, α-tocopherol, β-carotene, reduced glutathione, uric acid, and bilirubin or enzymes superoxide dismutase, catalase, and glutathione peroxidase. Antioxidants help remove the excess ROS in the seminal ejaculate and assist in the conversion of ROS to compounds that are less detrimental to cells. If there is more ROS than the local antioxidants can remove, it results in oxidative stress. Oxidative stress can result in sperm protein, lipid and DNA damage and sperm dysfunction [16]. However, there have been some disputes when it comes to research outcomes. Mendiola et al. demonstrated that vitamin C, but neither vitamin E nor selenium, had significant effects on semen quality (n = 61, p < 0.05) [14]. A high amount of antioxidants has been demonstrated to increase semen quality, compared to low or moderate amounts [17]. Another study reported that vitamin E and selenium decreased levels of malondialdehyde (MDA), a marker for damage done by reactive oxygen species, more so than did vitamin B [18]. Suleimen reported that Vitamin E decreased MDA levels, increased spermatozoa motility, and led to 21% couples conceiving over a 2.5 year period versus no conceptions in men who took a placebo (n = 52) [19]. An article reviewing previous studies on antioxidants concluded almost every study conducted pertaining to DNA damage and oxidative stress revealed that antioxidants caused significant improvement, particularly in asthenospermic patients [20]. A Cochrane review including 34 studies, determined that men who use oral antioxidants had a significant increase in live birth rate (OR 4.85; CI 1.92-12.24; P = 0.0008; n = 214) when compared to control [21]. Antioxidants were also associated with a significant increase in pregnancy rate when compared to control (OR 4.18; CI 2.65-6.59; P < 0.00001; n = 964) [21].
A woman’s diet may ultimately affect her fertility, particularly ovulation. Overall, replacing carbohydrates with animal protein was demonstrated to be detrimental to ovulatory fertility (OR 1.18) [22]. Adding just one serving of meat was correlated with a 32% higher chance of developing ovulatory infertility, particularly if the meat was chicken or turkey [22]. However, replacing carbohydrates with vegetable protein demonstrated a protective effect (OR 0.5) [22]. Choosing trans fats in the diet instead of monounsaturated fats has been demonstrated to drastically increase the risk of ovulatory infertility (RR 2.31) [23]. Consuming trans fats instead of carbohydrates correlated with a 73% increase in risk of ovulatory disorder (RR 1.73) [23]. The use of multivitamins and supplements also has an effect. Women who take multivitamins may be less likely to experience ovulatory infertility; women who take six or more tablets had the lowest relative risk for infertility (RR 0.59) followed by women who took three to five (RR 0.69), and two or less (RR 0.88) [24]. Chavarro et al. found that women with high “fertility diet” scores emphasized by a higher monounsaturated to trans-fat ratio, vegetable over animal protein, high-fat over low-fat dairy, a decreased glycemic load, and an increased intake of iron and multivitamins had lower rates of infertility due to ovulation disorders (p < 0.001) [25].
An individual’s weight is often associated with his or her eating habits and amount of activity. Body mass index (BMI) is reported as a number. If it is below 18.5 it is considered underweight, between 18.5 and 24.9 is normal, above 25 is overweight, and over 30 is considered obese [26]. Body weight can have significant effects on health, including cardiovascular disease, diabetes, and infertility [27].
The obesity epidemic has recently become is a serious issue, particularly in industrialized nations. The goal set by Healthy People 2010 of reducing obesity in the United States to 15% was not met [28]. In fact, adult obesity increased to 35.7% in 2010 [29]. The rising number of obese individuals may be due in part to an energy-rich diet as well as insufficient physical exercise [30]. In addition to other potential health risks, obesity can have a significant impact on male and female fertility.
The proportion of men over 20 years of age in the U.S. that are obese has risen to 35.5% [29]. BMI may be a significant factor in fertility, as an increase in BMI in the male by as little as three units can be associated with infertility (OR 1.12) [31]. Obese men are three times more likely to exhibit a reduction in semen quality than men of a normal weight [32]. Several studies have demonstrated that an increase in BMI is correlated with a decrease in sperm concentration [33,34], and a decrease in motility [35]. Overweight men have also been found to have increased DNA damage in sperm [36,37].
A relationship also exists between obesity and erectile dysfunction (ED). Corona et al. reported that 96.5% of men with metabolic syndrome presented with ED (n = 236) [38]. ED may be the consequence of the conversion of androgens to estradiol. The enzyme aromatase is responsible for this conversion, and is found primarily in adipose tissue [39]. As the amount of adipose tissue increases, there is more aromatase available to convert androgens, and serum estradiol levels increase [36,39]. Other hormones including inhibin B and leptin, may also be affected by obesity. Inhibin B levels have been reported to decrease with increasing weight, which results in decreased Sertoli cells and sperm production [40]. Leptin is a hormone associated with numerous effects including appetite control, inflammation, and decreased insulin secretion [41]. A study conducted in mice demonstrated that leptin was nearly five times higher in obese mice than lean mice, and that the higher leptin levels corresponded to five times lower fertility in the obese mice [41]. It was also noted that there was a down regulation of the leptin receptors located on the testes, possibly indicating that leptin resistance could play a role in male infertility [41].
In 2010, 35.8% of women in the U.S. over the age of 20 were considered obese [29]. Women with a BMI over 30 have longer time to pregnancy than women who have a BMI between 20 and 25, although this trend was not significant, and the study was conducted via a questionaire (n = 2,472) [8]. In a systematic review, Boots & Stephenson reported a miscarriage rate of 10.7% in women with a normal BMI, which was significantly lower than that of 13.6% in obese women (OR: 1.31; 95% CI 1.18-1.46) [42]. Furthermore, obese women had a higher rate of recurrent, early miscarriage compared to non-obese women. There is evidence that miscarriage in obese women may not necessarily be due to the karyotype of the developing fetus. Overweight and obese women under the age of 35 were found to have lower rates of aneuploidy, suggesting that miscarriage may be due to other influences such as endometrium receptiveness [12,43]. Additionally, Bellver et al. found a negative correlation between increasing BMI and implantation (r2 = .03, P = .008) [44]. A decreased ongoing pregnancy rate of 38.3% per cycle was also found in women who were overweight in comparison to the 45.5% in non-overweight women (n = 2656) [44]. There is speculation that these negative outcomes may be related to follicular environment, which differs in women who are obese compared to normal weight women. Some of the differences may include an increase in follicular fluid levels of insulin, lactate, triglycerides, and C-reactive protein; there may also be decreases in SHBG [45]. The negative effects of obesity on fertility in women may be reversible. Clark et al. found that after losing an average of 10.2 kg, 90% of obese previously anovulatory women began ovulating [46].
Obesity is not the only way in which weight can impact fertility. Men who are underweight are also at risk of infertility. Men who are underweight tend to have lower sperm concentrations than those who are at a normal BMI [36]. As the majority of the available literature focuses on the impact of obesity, more research is needed into the effects that being underweight may have on male fertility.
For women, being underweight and having extremely low amounts of body fat are associated with ovarian dysfunction and infertility [47]. Additionally, the risk of ovulatory infertility increases in women with a BMI below 17 (RR 1.6) [48]. A meta-analysis of 78 studies, which included 1,025,794 women, found that underweight women had an increased risk of pre-term birth (RR 1.29) [49]. Eating disorders such as anorexia nervosa are also associated with extremely low BMI. The lifetime prevalence of anorexia nervosa in women is 0.9%, with the average age of onset being 19 years old [50]. Although relatively uncommon, eating disorders can negatively affect menstruation, fertility, and maternal and fetal well-being [51]. It was found that among infertile women suffering from amenorrhea or oligomenorrhea due to eating disorders, 58% had menstrual irregularities (n = 66) [51]. Freizinger et al. reported 20.7% of infertile women seeking intra uterine insemination (IUI) had been diagnosed with an eating disorder, suggesting that women with history of eating disorders may be at a higher risk for infertility [52].
A healthy amount of exercise in men can be beneficial. Physically active men who exercised at least three times a week for one hour typically scored higher in almost all sperm parameters in comparison to men who participated in more frequent and rigorous exercise (n = 45) [53]. Moderately physically active men had significantly better sperm morphology (15.2%), the only ones to be ranked above Kruger’s strict criteria in comparison to the men who played in a competitive sport (9.7%) or were elite athletes (4.7%) (P < .001). Other parameters including total sperm number, concentration, and velocity also showed a similar trend but were not nearly as marked [53]. Bicycling more than five hours per week has been demonstrated to have a negative correlation with both total motile sperm counts (OR 2.05) and sperm concentration (OR 1.92) [54]. Diet combined with exercise in obese male rats has been shown to increase both sperm motility (1.2 times) and sperm morphology (1.1 times), and to decrease both sperm DNA damage (1.5 times) and reactive oxygen species (1.1 times) (n = 40; P < .05) [55].
Physical activity has been shown to confer a protective effect on fertility when coupled with weight loss in obese women [46]. However, excessive exercise can negatively alter energy balance in the body and affect the reproductive system [56]. When energy demand exceeds dietary energy intake, a negative energy balance may occur and may result in hypothalamic dysfunction and alterations in gonadotropin-releasing hormone (GnRH) pulsality, leading to menstrual abnormalities, particularly among female athletes [57]. Increased frequency, intensity, and duration of exercise were found to be significantly correlated with decreased fertility in women, including an OR of 3.5 for infertility in women who exercised every day (n = 24,837) [58]. A study examining 2,232 women undergoing in vitro fertilization (IVF) found that women who engaged in cardiovascular exercise for 4 hours or more per week for as little as one year prior to the treatment had a 40% decrease in live birth rate (OR .6; 95% CI .4-.8), as well as higher risks of cycle cancellation (OR 2.8; 95% CI 1.5-5.3) and implantation failure (OR 2.0; 95% CI 1.4-3.1) [59]. Wise et al. also found a significant positive dose–response relationship between vigorous activity and time to pregnancy [60]. However, moderate physical activity was determined to be weakly correlated with increases in fecundity, independent of BMI.
Stress is a prominent part of any society, whether it is physical, social, or psychological. Infertility itself is stressful, due to the societal pressures, testing, diagnosis, treatments, failures, unfulfilled desires, and even fiscal costs with which it is associated [61].
Males who experienced more than two stressful life events before undergoing infertility treatment were more likely to be classified below WHO standards for sperm concentration, motility, and morphology [62]. In a study including 950 men conducted by Gollenberg et al., stress such as a job, life events, and even social strain were seen to have a significant impact on sperm density (log scale, β = −0.25; CI −0.38 to −0.11), total sperm counts (log scale, β = −0.30; CI −0.45 to −0.15), forward motility (OR 1.54; 95% CI 1.04-2.29), and morphology (OR 1.93; 95% CI 1.02-3.66) [63]. Semen parameters may potentially be linked to stress. Stress and depression are thought to reduce testosterone and luteinizing hormone (LH) pulsing [62,64], disrupt gonadal function [64], and ultimately reduce spermatogenesis and sperm parameters. It has yet to be determined if depression causes low testosterone, or if low testosterone can cause depression [65]. Although there appears to be a relationship between stress and infertility, it is uncertain which is the cause and which is the effect. The perceived stress of providing a semen sample was reported to be negatively linked to overall semen quality with a 39% decrease in sperm concentration, 48% decrease in motility, and worse overall semen parameters on the day of oocyte retrieval, although there was no change in either volume or morphology [66,67].
Stress can increase after diagnosis of infertility, follow-up appointments, and failed IVF treatments [65]. When men present to fertility clinics, 10% met the criteria for having an anxiety disorder or depression, the latter being more common [66]. Coping with various life styles also affect fertility. It was reported that actively coping with stress, such as being assertive or confrontational, may negatively impact fertility [69,70], by increasing adrenergic activation, leading to more vasoconstriction in the testes. This vasoconstriction results in lower testosterone levels and decreased spermatogenesis. While men are not often thought to report their anxiety or sexual stress, the link between anxiety and sexual stress was surprisingly strong [70]. Decreased stress levels have been associated with improvements in fertility. In one study, higher ranks in the WHO (five) Well-Being Index correlated with higher sperm concentrations [71] for each successive gain in rank, an increase in concentration of 7.3% was observed.
Physical stress has been implicated in influencing female fertility. Women who had a job and worked more than 32 hours a week experienced a longer time to conception compared to women who worked 16 to 32 hours a week [8]. Psychological stress, such as anxiety disorder or depression, affects 30% of women who attend infertility clinics, possibly due in part to infertility diagnosis and treatments [68,72]. However, this rate is not any higher than women who attend a gynecologist, but it is significantly higher than women in their second trimester of pregnancy. Only one fifth of women participating in this study were actively seeking counseling.
Dr Eliran MorReceiving instruction on how to deal effectively or merely receiving support made a significant difference for women undergoing fertility treatment. There was a higher conception rate for women who were part of a cognitive behavioral intervention group (55%) or a support group (54%) than for those women who were not receiving any intervention (20%) [73]. Women who receive support and counseling may reduce their anxiety and depression levels, and increase their chances of becoming pregnant [74]. Positive moods correlated with increased chances of delivering a live baby while higher levels of anxiety increased chances of stillbirth [75]. Fertilization of oocytes also decreased when stress increased. A possible explanation for these associations may lie in stress hormone levels. One study reported that alpha amylase, but neither cortisol nor adrenalin, negatively correlated with fertility, and that the chances of conceiving in the short time period surrounding ovulation decreased [76]. Althoughthe mechanisms by which alpha amylase may decrease fertility are unknown, it is hypothesized that catecholamine receptors could alter the blood flow in the fallopian tubes [76].
While it is well documented that cigarette smoke contains over 4,000 chemicals [77] and is associated with a number of potential health complications such as cardiovascular disease, more research is needed to establish a link to infertility. It is estimated that 35% of reproductive-aged males smoke [78]. Men who smoke before or during attempts to conceive risk decreasing their fertility (OR 1.6) in comparison to non-smokers [79]. Men who smoke tend to have a decrease in total sperm count, density [63], motility [80,81], normal morphology [63,81], semen volume [63], and fertilizing capacity [82]. One study, using a procedure involving hyaluronan (HA)-coated slides, found that sperm that were of a normal motility and morphology were positively correlated with high HA binding; the study determined that men who smoked had decreased HA binding, indicating that the sperm characteristics were below normal [83]. Calogero et al. concluded from their study that smoking could reduce the mitochondrial activity in spermatozoa, and lead to a decreased fertilization capacity [80]. Guar et al. reported that only 6% of 100 smokers participating in their study were classified as normozoospermic while 39% of light smokers, 19.2% of moderate smokers, and no heavy smokers experienced isolated asthenozoospermia [84]. Both moderate and heavy smokers in this study experienced astheno-, oligo-, and teratozoospermia simultaneously. Smoking also can impact DNA integrity of the sperm, with several studies noting an increase in DNA damage [80,85-88]. Saleh et al. attributed the increase in DNA damage to increased amounts of seminal leukocytes, which may have increased ROS generation to 107% [87,89]. The exact mechanism by which leukocytes and ROS affect fertility remains uncler, though it is hypothesized to be linked with the inflammatory response induced by the metabolites of cigarette smoking [87]. In addition, total antioxidant capacity (TAC) was not reduced in smokers in this study [87], contrary to other reports [90,91]. Endocrine function may also be affected by smoking, as increases in serum levels of both FSH and LH and decreases in testosterone have been reported [74].
Among women who are of reproductive age, 30% are smokers [78]. Augood et al. determined that women who smoked had a significantly higher odds ratio of infertility (OR 1.60; 95% CI 1.34-1.91), in comparison to non-smokers [79]. The reductions in fertility among female smokers may be due to decreases in ovarian function and a reduced ovarian reserve. Sharara et al. found that the incidence of reduced ovarian reserve was significantly higher in women who smoked than in age-matched non-smokers (12.31% and 4.83%, respectively), and that these women had similar fertilization and pregnancy rates [92]. This suggests that ovarian reserve may be the primary mechanism by which smoking affects fertility in women [92]. Disruption of hormone levels may also be a possible mechanism. Women who smoked 10 or more cigarettes per day were found to have a 30-35% increase in urinary FSH levels at the time of cycle transition; and women who smoked 20 or more cigarettes per day had lower luteal-phase levels of progesterone [93]. These disruptions in endocrine function could contribute to the menstrual dysfunction and infertility observed in female smokers. The uterine tube and uterus may also be targets of cigarette smoke. Chemicals in cigarette smoke may impair oocyte pick-up and the transport of fertilized embryos within the oviduct, leading to an increased incidence of ectopic pregnancies, longer times to conception, and infertility among women who smoke [94]. While using donor oocytes, Soares et al. found that women who smoked 0–10 cigarettes per day had a significantly higher pregnancy rate (52.2%) than women who smoked 10 or more cigarettes each day (34.1%), suggesting that a compromised uterine environment due to cigarette smoke was responsible for the lower pregnancy rate observed in smokers [95]. Alterations in ovarian, uterine tube, and uterine functioning, as well as disruptions in hormone levels likely contribute to the infertility observed in women who smoke.
Studies of the effects of illegal drugs on human fertility have been scarce due to ethical considerations, as well as subject to under-reporting and bias due to the characteristics of the population being studied, such as low socioeconomic status or improper prenatal care [61]. Use of illicit drugs appear to have a negative impact on fertility, though more in-depth research in this area is required to make a clear link.
Marijuana is one of the most commonly used drugs around the world [96], and it acts both centrally and peripherally to cause abnormal reproductive function. Marijuana contains cannabinoids which bind to receptors located on reproductive structures such as the uterus or the ductus deferens. In males, cannabinoids have been reported to reduce testosterone released from Leydig cells, modulate apoptosis of Sertoli cells, decrease spermatogenesis, decrease sperm motility, decrease sperm capacitation and decrease acrosome reaction [96]. Females who use marijuana are at an increased risk of primary infertility in comparison to non-users (RR 1.7; 95% CI 1.0-3.0) [97]. In women, use of marijuana can negatively impact hormonal regulation; over short periods of time, marijuana may cause a drop in the levels of luteinizing hormone, but over long periods of time, the hormone levels may remain constant due to developed tolerance [98]. Marijuana and its cannabinoids have been reported to negatively impact movement through the oviducts, placental and fetal development, and may even cause stillbirth [96-99].
Another commonly used recreational drug is cocaine, a stimulant for both peripheral and central nervous systems which causes vasoconstriction and anesthetic effects. It is thought to prevent the reuptake of neurotransmitters [100], possibly affecting behavior and mood. Long term users of cocaine claim that it can decrease sexual stimulation; men found it harder to achieve and maintain erection and to ejaculate [101]. Cocaine has been demonstrated to adversely affect spermatogenesis, which may be due to serum increases in prolactin, as well as serum decreases in total and free testosterone [102,103]. Peugh and Belenko suggest that the effects of cocaine in men depend on dosage, duration of usage, and interactions with other drugs [104]. While less is known about cocaine’s effects on females, impaired ovarian responsiveness to gonadotropins and placental abruption have both been reported [105-107].
Opiates comprise another large group of illicit drugs. Opiates, such as methadone and heroin, are depressants that cause both sedation and decreased pain perception by influencing neurotransmitters [104]. In men taking heroin, sexual function became abnormal and remained so even after cessation [108]. Sperm parameters, most noticeably motility, also decrease with the use of heroin and methadone [103,109]. In women, placental abruption with the use of heroin may also be a cause of infertility [61].
In general, there are more studies reviewing the effects of medication on male than female fertility. It is necessary to first determine which medications cause fertility issues, and to then determine if these effects are permanent. A study headed by Hayashi, Miyata, and Yamada investigated the effects of antibiotics, antidepressants, antiepileptics, β stimulators, H1 and H2 receptor antagonists, mast cell blockers, and sulfonylurea compounds (n = 201) [110]. Male participants were divided so one group had medication switched or stopped and the other served as the control. The intervention group improved 93% in semen quality and 85% of the group conceived in 12.5 months ± .64 months; and the control group improved 12% in semen quality and only 10% conceived. The authors suggested that this study may link certain tested medications with impaired semen qualities [110]. Additional medications and their effects on both males and females are represented in Table 1[61].
Many studies have been conducted on the effects of alcohol and aspects of health, including fertility. While there are studies that demonstrate the link between alcohol and infertility, it is not entirely clear what amount relates to an increased risk.
In men, alcohol consumption has been linked with many negative side effects such as testicular atrophy, decreased libido, and decreased sperm count [111-113]. One meta-analysis including 57 studies and 29,914 subjects found a significant association between alcohol and semen volume (P = .0007; I squared statistics (I2) n = 35) [63]. A link between alcohol and sperm morphology has also been found. Very few men who are classified as alcoholics were normozoospermic with only 12% of men in one study being designated as such; most alcoholics were found to be teratozoospermic, with 73% of heavy drinkers and 63% moderate drinkers falling in this category (n = 100; P = .0009) [84]. In addition, oligozoospermia was another common classification for heavy drinkers (64%) in this study (P = 0.0312). Alcohol seems to have a large impact on both sperm morphology and sperm motility [84]. While alcohol may have effects on sperm morphology, there is little conclusive evidence linking alcohol with oxidative stress, and infertility. Oxidative stress has been found to systemically increase with alcohol consumption [114,115], but there is not yet a clear link between sperm oxidative stress and alcohol [91].
Women who drink large amounts of alcohol have a higher chance of experiencing an infertility examination than moderate drinkers (RR = 1.59, CI 1.09 –2.31) in comparison to those who consumed low amounts, who had a decreased chance of experiencing an infertility examination (RR 0.64; CI 0.46-0.90) (n = 7,393) [116]. A common result of drinking is a hangover. Women who experienced hangovers were more likely to be infertile than women who did not experience hangovers [117], suggesting that the amount of alcohol