Lifestyle factors and reproductive health: taking control of your fertility

Eating a healthy and varied diet may be a key part of maintaining good overall health. However, there are certain vitamins and food groups that could have a greater impact on reproductive health than others.

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.

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].

Air pollution is the release of pollutants such as sulfur dioxides, carbon monoxide, nitrogen dioxide, particulate matter, and ozone into the atmosphere from motor vehicle exhaust, industrial emissions, the burning of coal and wood, and other sources [132, 133]. While air pollution has received a tremendous amount of attention in the past few decades for many health reasons, its effects on fertility are less well-known.

There have been reports of air pollution and its impacts on male fertility. Several studies have been conducted in the Czech Republic regarding men living in two different locations, one more polluted than the other [134, 135]. Men who are exposed to higher levels of air pollution were more likely to experience abnormal sperm morphology, decreased motility, and an increased chance of DNA fragmentation (n = 48 or 408 respectively). There was also a significant negative correlation found between sperm concentration and the amount of ozone to which a man was exposed (n = 5134) [136].

Negative reproductive side effects of air pollution on women can include preterm delivery [132, 137], miscarriage, stillbirth, spontaneous abortion, and fetal loss [132]. Many times when fetal loss occurred, there were malformations within the fetal reproductive tract.

Heavy metals include metals such as lead, mercury, boron, aluminum, cadmium, arsenic, antimony, cobalt, and lithium. Only a few such heavy metals have been researched in connection to reproductive function. Lead, which is commonly found in batteries, metal products, paints, ceramics, and pipes, is one of the most prominent heavy metals. Lead interrupts the hypothalamic-pituitary axis and has been reported to alter hormone levels [132, 138], alter the onset of puberty, and decrease overall fertility [132]. Lead may alter sperm quality in men, and cause irregular menstruation, induce preterm delivery, and cause miscarriage, stillbirth, and spontaneous abortion in women [132]. Mercury is commonly found in thermometers, batteries, and industrial emissions. Mercury concentrations increase in the food chain, resulting in bioaccumulation that can negatively impact reproduction in humans who consume food, usually tainted seafood [132]. Ultimately, mercury can disrupt spermatogenesis and disrupt fetal development [138]. Boron is another heavy metal that is used in the manufacturing of glass, cement, soap, carpet, and leather; its effects on the hypothalamic-pituitary axis are comparable to lead [138]. While there is not much research on cadmium, it has been shown experimentally to cause testicular necrosis in mice, as well as marked changes in libido and infertility [139].

Many of the chemicals used world-wide in today’s society, including pesticides and endocrine disruptors, among others, may have various damaging effects on the reproductive health of both men and women. Mimicking natural hormones, impeding normal hormone activity, and varying regulation and function of the endocrine system are a few of the many ways that endocrine disruptors influence one’s body [138]. Numerous studies have reported negative effects of a variety of chemicals on reproductive health [132, 138, 140‐144] (Table 2).

Both men and women can be exposed to chemicals and other materials that may be detrimental to their reproductive health while on the job. Heavy metals and pesticides, as outlined in Table 2, have many negative side effects, particularly for those who work around them. Men working in agricultural regions and greenhouses which use pesticides have higher concentrations of common pesticides in their urine [145], overall reduced semen parameters [146], oligozoospermia [15], lower sperm counts [147], and sperm concentrations decreased by as much as 60% [148]. Organic solvents may also prove detrimental. Men who work with these substances often experience indirect consequences with their female partner having decreased implantation rates (n = 726) [149]. Welding is another possible source of occupational exposure, and plays a role in reduced reproductive health [15, 150]. There are also consequences for working in factories that manufacture chemicals and heavy metals. Factories that produce batteries where workers are exposed to lead may have negative impacts on reproductive capabilities, including asthenospermia and teratospermia (n = 150) [151]. Hobbies, while not often associated with excessive amounts of exposure, may be just as damaging as manufacturing. Gardeners may be in contact with pesticides [150]; crafters making jewelry, ceramics, and even stained glass may come in contact with lead [132]; painters may also come in contact with lead-based paints [150]. Whether it is manufacture or hobby, using any kind of heavy metal or pesticide likely will result in some exposure, and possibly reduce fertility.

Exposure to various kinds and amounts of radiation can have lasting effects in humans. Radiation that is in the form of x-rays and gamma rays can be devastating to the sensitive cells of the human body, including germ and Leydig cells. The damage done depends on the age of the patient and dose, and ultimately can result in permanent sterility [2, 152].

The incredible convenience of the cell phone has dramatically increased its usage in the last decade. However, it does not come without negative effects. There have been an increasing number of studies demonstrating negative effects of the radiofrequency electromagnetic waves (RFEMW) utilized by cell phones on fertility. Cell phone usage has been linked with decreases in progressive motility of sperm [153], decreases in sperm viability [153, 154], increases in ROS [154], increases in abnormal sperm morphology, and decreases in sperm counts [153]. One study evaluating 52 men demonstrated that men who carried a cell phone around the belt line or hip region were more likely to have decreased sperm motility (49.3 ± 8.2%) compared to men who carried their cell phones elsewhere or who did not carry one at all (55.4 ± 7.4%; P < .0001) [155]. Link between cell phones and fertilization capacity. Falzone et al. reported that when exposed to RFEMW, sperm head area significantly decreased from 18.8 ± 1.4 μm² to 9.2 ± .7 μm² and acrosomal area significantly decreases from 21.5 ± 4% to 35.5 ± 11.4% (P < .05) [156]. In addition, Falzone et al. found the mean number of sperm binding to the zona was significantly less in the exposed group (22.8 and 31.8 respectively) [156]. While amount of research demonstrating negative effects of cell phone usage and fertility grows, there can be no clear conclusion as no standard for analyzing cell phone effects is available and many studies have limitations [157, 158]. Another aspect to consider is the effect of text-messaging on the body, as it is becoming more prevalent in respect to making phone calls. While technology quickly advances, research lags behind [159], providing the opportunity for unforeseen damage to occur.

While contraceptives are often associated with preventing pregnancy, several studies have demonstrated that both condom usage and oral contraceptives can preserve fertility in women [8, 160]. In 2010, Revonta et al. concluded that infertile women used less oral contraception [117]; women who considered themselves infertile might be less inclined to use contraceptives [8]. Contraceptives are believed to reduce the chances of contracting a sexually transmitted infection, thus reducing infertility. Contraceptives also may decrease time to conception. In one study, condom users had shorter time to conception compared to oral contraceptive users; oral contraceptive users in turn had shorter time to conception than those women not using any contraceptives [117]. In addition, oral contraceptives were demonstrated to have positive effects on the prevention and management of endometriosis and pelvic inflammatory disease [117]. This evidence suggests that contraceptives may increase a woman’s fertility, lending to the overall fertility of the couple.

Scheduling regular doctor appointments may be beneficial for fertility. Males tend to not seek medical treatment for sexual dysfunctions or infections. It was reported that when men experience sexual problems, only 10.5% seek help (n = 11,161) [157]. When the problems become on-going, 20.5% of men turn to health care professionals [161]. Mercer et al. concluded that the low amount of males seeking treatment is most likely due to lack of awareness of treatment and guidance [161].

For women, visiting the gynecologist to receive an annual pap smear has been associated with being protective of fertility (n = 10,847) [160]. Kelly-Weeder and Cox also concluded from their study that when a woman reports her health status as good, she is more likely to be fertile. Both pap smears and self-reported health status may be related to better screening for disease, STI detection, more available information, and overall better access to care.

The type of clothing a man chooses to wear, may have effects on reproductive health. Many studies have been conducted hoping to find an answer to the question of what type of clothing is best for fertility. The view that elevation of scrotal temperature negatively impacts spermatogenesis and sperm parameters is universally acknowledged [162]. But the question of whether tight-fitting underwear actually has an effect on scrotal temperature and therefore semen quality has long been debated. There have been studies that have found significantly higher temperatures with tight-fitting clothing versus loose-fitting or no clothing [163, 164]. Increases in scrotal temperatures could be due to an increase in temperature of about 3.5°C of the air between the clothing and the skin in comparison the ambient air [164].

One study followed 20 participants who wore tight-fitting underwear for 6 months then switched to loose-fitting underwear for 6 months [165]. Semen samples were taken every 2 weeks for the duration of the study. While half of the participants dropped out, there was a significant 50% decrease in sperm parameters in the tight-fitting versus loose-fitting underwear, demonstrating that the effects of tight-fitting underwear reversible. In another study, men who wore tight-fitting underwear and pants had a relative risk of 2.5 of having impaired semen quality [166]. They also noted that only wearing one or the other caused an insignificant decrease in semen quality. While there are studies that conclude that the type of underwear influences scrotal temperature, there are also some that did not find significant temperature differences [167, 168].

Literature providing evidence that wet heat is tied to infertility is scarce. Many fertility authorities rely on the data provided from research of the effects of temperature on sperm function and then apply the idea to hot baths, jacuzzis, or saunas. One study conducted by Shefi et al. actually studied the effects of wet heat on 11 male subjects who were exposed to wet heat for greater than 30 minutes every week for at least 3 months prior to any experimentation [169]. These 11 men were then told to avoid wet heat exposure for 3 months. Three different semen samples were assessed: one from the onset of the study representing the exposed, one before 3 months into the experiment, and another at 3 to 6 months. Nearly half of the participants saw an increase in semen quality. Sperm motility saw a significant 22% increase for responders, and the improvement appeared to continue longer than 3 months (P = .02). When reviewing the non-responders, Shefi et al. found that other lifestyle factors could have accounted for the lack of semen quality increase, such as tobacco use.

Many sexually active couples choose to utilize vaginal lubricants to treat vaginal dryness and pain during intercourse [170]. While attempting to conceive, nearly 75% of participating couples reported to an internet study that they used lubricants to ease the female partner’s vaginal dryness, and 26% had claimed that they almost always used a lubricant [171]. Some non-commercial products used as lubricants include olive oil, vegetable oil, and saliva, and they have been demonstrated to negatively impact sperm function. Several products available to the public have been researched for possible effects on sperm function. A study conducted by Agarwal et al. compared Replens, Astroglide, FemGlide, K-Y Jelly, and Pre ~ Seed against a control medium [170]. In relation to the control, Astroglide, FemGlide, and Replens all significantly decreased sperm motility after 30 minutes of contact with semen (P < .01). Astroglide and Replens had a greater impact on motility in comparison to FemGlide’s. They also found that FemGlide and K-Y Jelly significantly increased sperm chromatin damage in comparison to the control medium (P < .05). While Pre ~ Seed caused an increase in chromatin damage, it was not significant.