Why do hot water baths affect only males' fertility? Why not females'?

Why do hot water baths affect only males' fertility? Why not females'?

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Here is the link where urologists are warning men not to take hot water baths.

Why does it affect only males' fertility? Why not females also?

A mature human sperm has some mitochondria, a nucleus, an acrosome, and a flagellar apparatus. That's it. Because of the lack of other organelles in the sperm, they have to be kept in a kind of 'cold storage' so that they are viable for at least some time (usually a couple of days). The ideal temperature would be 1.8 °C to 2.5 °C below normal body temperature, i.e. 37.6 °C or 98 °F. If a man takes frequent hot water baths, his sperm count becomes low as the mature sperms get dessicated quickly.

The reason that women don't require this strict temperature regulation is that the mature ovum has the complete cellular machinery at its disposal- mitochondria, nucleus, golgi bodies, ER, the works. So it can remain viable for a much longer time (about seven days after ovulation) and has higher temperature tolerance than sperms.

Well, the answer by @An J has already explained the prima facie of your question which is: sperms need lower temperature for development. But I will be explaining in my answer: Why do the sperms actually need a lower temperature for their development?

This is a debatable subject, but there have been several models or hypothesis about this. I found this literature on it, and it summarises the thing excellently. Hope it helps:

Throughout the Cenozoic, the fitness benefits of the scrotum in placental mammals presumably outweighed the fitness costs through damage, yet a definitive hypothesis for its evolution remains elusive. Here, I present an hypothesis (Endothermic Pulses Hypothesis) which argues that the evolution of the scrotum was driven by Cenozoic pulses in endothermy, that is, increases in normothermic body temperature…

The model argues that stabilizing selection maintained an optimum temperature for spermatogenesis and sperm storage throughout the Cenozoic at the lower plesiomorphic levels of body temperature that prevailed in ancestral mammals for at least 163 million years. Evolutionary stasis may have been driven by reduced rates of germ‐cell mutations at lower body temperatures…

The fitness advantages of an optimum temperature of spermatogenesis outweighed the potential costs of testes externalization and paved the way for the evolution of the scrotum. The scrotum evolved within several hundred thousand years of the K‐Pg extinction, probably associated initially with the evolution of cursoriality, and arguably facilitated mid‐ and late Cenozoic metabolic adaptations to factors such as climate, flight in bats and sociality in primates.

About the function of the scrotum from the article

The scrotum is a sac‐like thermoregulatory structure that houses the testes at a temperature lower than the core body temperature (Tb; Moore, 1926; Wislocki, 1933; Ruibal, 1957; Setchell, 1998). The cremasteric muscles in the scrotum contract and relax to draw the testes closer to or allow them to dangle further away from the body in order to maintain the testes at an 'optimal' temperature for spermatogenesis (sensu Moore, 1926; Tsperm) and sperm storage of 34-35 °C (Setchell, 1998; Gallup et al., 2009; Mawyer et al., 2012). In humans, the scrotal temperature is maintained about 2.7 °C lower than the Tb (Momen et al., 2010). Notwithstanding the relative fitness benefits of a cooled epididymis vs. the cooled testis, four nonmutually exclusive hypotheses currently dominate explanations for the evolution of the scrotum: the Cool Spermatogenesis Hypothesis (Moore, 1926), the Galloping Hypothesis (Frey, 1991), the Mutation Hypothesis (Short, 1997) and the Activation Hypothesis (Gallup et al., 2009).

Cool Spermatogenesis Hypothesis

… argued that Tsperm and the maintenance of sperm viability during storage in the epididymis is about 34-35 °C (Moore, 1926; Appell et al., 1977). Scrotal temperatures that approach those of the core Tbcompromise fertility (Moore, 1926; Bedford, 1978b, 2004; Setchell, 1998), particularly if evaporative cooling of the scrotum is impaired (Momen et al., 2010).

The Galloping Hypothesis

… (Frey, 1991)proposes a trade‐off between testes vulnerability (fitness cost) and the avoidance of strong intra‐abdominal pressure fluctuations during galloping which impair spermatogenesis in abdominal testes (fitness benefit).

The Mutation Hypothesis

… maintains that the testis is a 'hot spot' for germ‐cell mutations and that the lower temperatures of the scrotum reduce the rates of mutation on the Y chromosome through mutagenic metabolites (Short, 1997).

The Activation Hypothesis

… storage of sperm at a lowered temperature ensures that they undergo 'thermal shock' during ejaculation into the higher temperatures of the female, which increases their motility and hence the probability of a successful insemination (Gallup et al., 2009).

To keep sperm viable in natural body conditions, they are kept at a relative lower temperature than the body temperature, and this can achieved by the scrotum. As sperm is produced in testis, and testis are situated in the scrotum outside the main part of the body, a pouch like structure. This arrangement is going to help to achieve a slightly lower temperature relative to the body temperature. Definitely, frequent hot water bath will lower the sperm count by hampering spermatogenesis as it disturbs the normal physiological conditions inside the testis by increasing temperature.

Another side, in females, the body temperature is not going to affect the oogenesis (ovum formation process). Instead of that you will see an increase in basal body temperature (about 0.5 °C) during ovulation (release of ovum). That means a hot water bath isn't an issue for female fertility.

9 Surprising Things Every Woman Needs to Know About Semen

The male body holds many mysteries. Why are guys always scratching their balls? What exactly is a foreskin supposed to do? Why doਏlaccid penises look so ridiculous?

But the most pressing questions we have concern semen𠅊lso known as ejaculate, spunk, and by a host of less printable nicknames. Sure we know it contains sperm, but what else is in there? Why does it lookਊnd smell਍ifferent sometimes, and is it just a myth that it&aposs great for your skin? To answer these and other questions, we talked to a men&aposs health specialist, who shared some seriously fascinating facts.

There's more to semen than sperm

Semen and sperm are not the same thing. Sperm are tadpole-shaped, microscopic cells that are part of semen. Their job is to fertilize an egg inside your body, and to get there, they&aposre carried along by fluid that&aposs produced by different male sex organs.

“The prostate fluid contains chemicals that make semen more liquid-y so the sperm can swim more freely,” Michael Reitano, MD, physician in residence for the men’s health service Roman, tells Health. “The seminal vesicles [two tubes in the pelvis] provide fructose, a sugar that gives spermatozoa the energy it needs to swim all the way to the female egg.” All together, these components make up semen.

It has actual nutrients

Dr. Reitano says that sperm contains vitamin C, B12, ascorbic acid, calcium, citric acid, fructose, lactic acid, magnesium, zinc, potassium, sodium, fat, and hundreds of different proteins. But don’t quit your daily vitamin just yet. “The quantity of actual nutritional components is tiny,” he says, and most of it is simply water. What about the calorie count? "If the actual nutritional elements are added—meaning all the fats, proteins, and carbohydrates—then a ¾ teaspoonful of semen may provide little more than a few calories of nutrition.”

A lot less comes out than you might think

The average amount of semen released during਎jaculation averages between two and five ml, the equivalent of about one teaspoon. But this stuff pack a punch—there are nearly 15 million to 200 million sperm in an average milliliter of semen.

Semen quality changes with age

True, men can produce sperm throughout their entire lives. But it isn’t always viable. Dr. Reitano says that according to one study, sperm produced by men over age 52 were more likely to be abnormal than the sperm of younger men. Young guys also produce more sperm per ejaculation. “Semen production is highest in men in their 20s or so, but can decrease slowly starting at any point from that age onward,” he says.

Pre-ejaculate is a different fluid

Precum, or the pre-ejaculate fluid that comes out of a man&aposs penis when he&aposs turned on, contains barely any viable sperm. “Most of the evidence leans toward pre-ejaculate containing no sperm, or only very tiny amounts of sperm,” Dr. Reitano says. “What sperm is found [in precum] tends to be poorly formed and immobile. Men are considered infertile if they have too little sperm, so the tiny amounts that may be found in pre-ejaculate are extremely unlikely to result in pregnancy.” (Good to know, but it&aposs probably wise to make sure the stuff doesn&apost get inside you if you really don&apost want to get pregnant.)

So what&aposs the point of precum? It&aposs nature&aposs lube, in part. "Pre-ejaculate is a slightly basic secretion released from glands called Cowper glands," Dr. Reitano says. "The clear secretion protects sperm from the acid environment of the urethra and the vagina, as well as lubrication to some degree."

It's not supposed to smell bad (or turn yellow)

Stinky semen could be indicative of a larger issue. 𠇏oul-smelling semen can be a sign of an infection, possibly a sexually transmitted infection. STIs may also be at work if the semen takes on a yellow or green color,” says Dr. Reitano. “On occasion, a broken blood vessel in the urethra or prostate can make semen appear brown or reddish.”

What is semen supposed to smell like? "Semen can typically have a slight ammonia or bleach-like odor," he adds. "Anecdotally, semen can have a slight change in odor or taste with changes in food, meaning eating asparagus may result in a similar change in the odor of semen as noted with urine."

Semen helps sperm live longer

Sperm can live up to five days inside a woman&aposs reproductive tract, just waiting for that egg to appear so they can fertilize it and do what nature intends them to do. But outside of the body, semen can’t survive very long. “If ejaculation occurs in a hot tub with chemicals, the sperm can live no more than a few seconds. If it is deposited into a bath of warm water that is approximately 98 degrees, [they] may live for a few minutes,” Dr. Reitano says. “If it is deposited into the air and onto a hard surface, it will live until the semen is dry. The sperm dies when that occurs.”

Semen facials are an actual thing

For whatever reason, semen seems to be the latest trend in skincare. But Dr. Reitano says that while it&aposs likely safe, it&aposs probably not going to benefit your skin in any way. "Semen doesn’t have any inherent components that are bad by nature," says Dr. Reitano. Stick to acne products to clear up those breakouts instead.

You really can be allergic to it

Remember the woman who went into anaphylactic shock after her partner ejaculated in her mouth? Yeah, so do we. Unfortunately, semen allergies are possible. Says Dr. Reitano: "

This is a rare condition but it exists. The allergic reaction is usually localized and causes redness or swelling at the point of contact—usually the vagina." To be precise, it&aposs the proteins in semen that trigger the allergic reaction.

"Another way a partner can be allergic to their partner&aposs semen is if she has an allergy to a particular food or antibiotic, as examples, and the male partner has eaten the food or is taking the antibiotic to which she is allergic," adds Dr. Reitano. "The allergen accumulates in the male&aposs semen, and when it is placed in the vagina, the allergen is absorbed into the bloodstream. The female partner may develop widespread hives or worse." Yikes!

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The fetal testis develops in the abdomen, but eventually moves into the scrotum, where it is normally located at birth. Scrotal temperature is about 2 degrees Fahrenheit lower than in the rest of the body. This temperature in required for the process of sperm development, or spermatogenesis, to proceed normally.

The testicular blood supply is also specialized to help maintain a lower scrotal temperature. Although blood in the testicular artery is at normal body temperature when it enters the scrotum, a complex system of veins that carries cooler blood back from the testis to the heart surrounds this artery. This venous system, called the pampiniform plexus, cools the arterial blood before it reaches the testis, helping ensure the organ stays at the proper temperature. Several problems can arise that may raise the scrotal temperature and interfere with a man's fertility.

Weed Is Whack

istockphoto The stuff in marijuana that makes you feel high - tetrahydrocannabinol, or THC - can lay low your sperm.

Seems THC is mimics testosterone, so smoking dope exposes sperm to a hormonal imbalance that can cause sperm counts to fall, according to Dr. Niederberger.

And pot isn't the only drug that can affect male hormones. Heavy use of narcotics like the morphine derivative hydromorphone ( Dilaudid) can cause testosterone levels to plummet. When that happens, a guy's sperm production - and sex drive - goes along for the ride.


Polycystic Ovary Syndrome is a common endocrine system disorder amongst women of child-bearing age. Women diagnosed with the condition may have enlarged ovaries which contain follicles, or small collections of fluid, located in each ovary. The exact cause of the condition is not known.

As a result of PCOS, explains Declan Keane, ovulation can be delayed or simply does not happen. "There can be a metabolic effect that can cause a woman to be overweight or underweight, which can affect her ovarian function and thus her menstrual cycle," he says, adding that when fertility experts discover that a woman has PCOS, the priority is to regulate the cycle in order to ensure good quality eggs.

"PCOS is a potential factor in infertility but it is not always the cause," he says, adding however, that the condition can lead to diminished ovarian reserve, which in turn means egg numbers can be low and this will further affect fertility. However, PCOS doesn't have to be the end of the world, reassures Dr John Waterstone, medical director of the Cork Fertility Centre.

"PCOS is a common condition where women can have too many eggs in their ovaries," he says, adding that a scan may show that although a woman has more eggs than normal, she is not releasing them every month as normal.

"However, PCOS is not the worst thing in the world to have - we would prefer a woman to have too many eggs than too few," he says, adding that women can become very concerned on hearing that they have PCOS: "It is very common and often simpler treatments will work," he says.


Infections can also cause infertility in men and women.

Untreated gonorrhea and chlamydia in women can lead to pelvic inflammatory disease, which might cause scarring that blocks the fallopian tubes. Untreated syphilis increases the risk for a pregnant woman to have a stillbirth. More information about infections that may affect fertility can be found on the sexually transmitted infections (STIs) health topic page.

Chronic infections in the cervix and surgical treatment of cervical lesions associated with human papillomavirus (HPV) infection can also reduce the amount or quality of cervical mucus. Problems with this sticky or slippery substance that collects on the cervix and in the vagina can make it difficult for women to get pregnant. 1

The Centers for Disease Control and Prevention recommends that all boys and girls age 11 or 12 be vaccinated against HPV. Men and women who weren't vaccinated as preteens can also get the vaccine into their early to mid-20s. 2

What do the experts say about children in hot tubs?

Both the American Association of Pediatrics and the Mayo Clinic do not ban children from using hot tubs within limits, but they do not recommend children in diapers to use a hot tub. Hot tubs are not advised for infants and toddlers, and older children are suggested to not exceed 20 minutes at a time. Infants must never be in a spa with a temperature of over 100ºF (38ºC). You should, of course, always follow the recommendations of your doctor.


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 reproductive timeline

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 =�, p <𠂐.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 =�, CI =�.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 � to 39 years of age and older compared to younger age groups even when controlling for female age (n =�,061) [10].

The reproductive timeline for women is complex. A woman is born with all the oocytes she will ever have, and only 400� are actually ovulated [6]. As the number of oocytes decline, a woman’s menstrual cycle shortens, infertility increases, and menstrual irregularity begins 6𠄷 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� (n =�,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 =�) [11]. Another study reported that the rate of aneuploidy for women over 35 was 45.7% versus 34.8% for women under 35 (n =�, 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].

Impacts of diet and exercise


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 =�, p <𠂐.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 =�) [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 =𠂐.0008 n =�) 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 <𠂐.00001 n =�) [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 �rtility 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 <𠂐.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 =�) [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 =𠂒,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 (r 2  = .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 =�) [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].

Eating disorders and being underweight

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 =�) [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 =�) [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 =� 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 =�,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.

Psychological effects

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 = 𢄠.25 CI 𢄠.38 to 𢄠.11), total sperm counts (log scale, β = 𢄠.30 CI 𢄠.45 to 𢄠.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.

Receiving 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].

Recreational and prescription substances

Cigarette smoking

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� 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.


Illicit drugs

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].

Prescription drugs

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 =�) [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].

Table 1

Medications and their respective effects on both male and female reproductive function

MedicationEffect on reproductive function
Anabolic SteroidsImpairment of spermatogenesis (up to one year recovery) may cause hypogonadism through pituitary–gonadal axis
Antiandrogens:Impairment of spermatogenesis erectile dysfunction
Cyproterone acetate, danazol, finasteride, ketoconazole, spironolactone Reversible
Antibiotics:Impairment of spermatogenesis
Ampicillin, cephalotin, cotrimoxazole, gentamycin, neomycin, nitrofurantoin, Penicillin G, spiramycin Reversible
Antibiotics:Impairment of sperm motility
Cotrimoxazole, dicloxacillin, erythromycin, lincomycin, neomycin, nitrofurantoin, quinolones, tetracycline, tylosin
Antiepiletics:Impairment of sperm motility
Phenytoin Reversible
Antihypertensives:Fertilization failure
Calcium channel blockers (nifedipine)
Antihypertensives:Erectile dysfunction
Alpha agonists (clonidine), alpha blockers (prazocin), beta blockers, hydralazine, methyldopa, thiazide diuretics
Anti-inflammatory 5-ASA and derivatives:Impairment of spermatogenesis and sperm motility
Mesalazine, sulfasalazine Reversible
Antimalarials:Impairment of sperm motility
Quinine and its derivatives Reversible
Antimetabolites ⁄ Antimitotics:Arrest of spermatogenesis azoospermia
Colchicines, cyclophosphamide
Anti-oestrogensImpairment of endometrial development
Clomiphene citrate reversible
Anti-progestins:Impairment of both implantation and tubal function
Emergency contraceptive pills, progesterone-only pills
Antipsychotics:Increase prolactin concentrations that can lead to sexual dysfunction
Alpha blockers, phenothiazine, antidepressants (particularly SSRIs)
Antipsychotics:Impairment of spermatogenesis and sperm motility
Butyrophenones Reversible
Antischistozomal:Impairment of spermatogenesis and sperm motility
Niridazole Reversible
CorticosteroidsImpairment of sperm concentration and motility
Exogenous testosterone, GnRH analoguesImpairment of spermatogenesis
H2 blockers:Increase prolactin concentrations that can lead to impairment of luteal function, loss of libido, and erectile dysfunction
Cimetidine, ranitidine
Local anaesthetics, halothaneImpair sperm motility
MetoclopramideErectile dysfunction
MethadoneSuppress spermatogenesis and sperm motility
Non-steroidal anti-inflammatory drugs, Cox-2 inhibitorsImpairment of follicle rupture, ovulation, and tubal function


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 (I 2 ) 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 =� P = .0009) [84]. In addition, oligozoospermia was another common classification for heavy drinkers (64%) in this study (P =𠂐.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 =𠂑.59, CI 1.09 𠄲.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 =𠂗,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 consumed does matter. While it is clear alcohol can have an impact, the amount it takes to negatively influence reproductive function is not clear as there is no standard 𠇍rink”. Amounts of alcohol ranging from one drink a week to 5 units a day can have various effects including increasing the time to pregnancy (P = .04 95% CI .85-1.10) [8], decreasing probability of conception rate by over 50% [118] and decreasing implantation rate, increasing both the risk of spontaneous abortion (OR 4.84) [119] and of fetal death [120], and causing anovulation, luteal phase dysfunction, and abnormal blastocyst development [121]. Researchers believe that these effects may be due to hormonal fluctuations including increases in estrogen levels, which reduce FSH and suppress both folliculogenesis and ovulation [116,121], but many mechanisms are still unknown.


Caffeine has become an integral part of society with consumption varying from 50 mg in a 16 oz. bottle of Pepsi to 330 mg in a 16 oz. cup of Pikes Place Roast from Starbucks [122,123]. However, caffeine has been reported to have negative effects on female fertility. Caffeine has been associated with an increase in the time to pregnancy of over 9.5 months, particularly if the amount is over 500 mg per day (OR 1.45 95% CI1.03-2.04) [124]. The negative effects that are emphasized in recent research are miscarriage, spontaneous abortion, fetal death and still birth. Women who consumed more than 100 mg of caffeine a day were more likely to experience a miscarriage (151 mg-300 mg: OR 3.045 95% CI: 1.237𠄷.287, p =𠂐.012 over 300 mg OR 16.106 95% CI 6.547�.619, p <𠂐.00 n =�) [125] or spontaneous abortion [126,127]. The karyotypes of those spontaneously aborted fetuses in women who consumed more than 500 mg of caffeine a day were also more likely to be normal (n =𠂑,515 OR 1.4 95% CI .5-3.7) [126], indicating that spontaneous abortions may not be due to genetic defects, but perhaps an unknown mechanism triggered by caffeine. Greenwood et al. demonstrated that caffeine consumption during the first trimester is related to both miscarriage and still birth (n =𠂒,643) [128]. The women who miscarried or had a still birth in their study had an average of 145 mg of caffeine per day (95% CI 85�) and women who had live births consumed an average of 103 mg per day (95% CI 98�), indicating that there may be a narrow window for caffeine to impact fertility. Women who consumed more than 375 mg of caffeine a day had an odds ratio for spontaneous abortion higher than women who had fewer than 200 mg a day (330 subjects, 1168 controls OR 2.21 CI 2.53-3.18) [119]. In 2003, Wisborg et al. found that after adjusting for smoking and drinking, women who drank four to seven cups of coffee had nearly an 80% increase in chance of still birth, and those who consumed more than 8 cups of coffee a day had nearly a 300% increase (OR 3.0 95% CI 1.5-5.9 n =�.478) [129]. Another study including over 88,000 women demonstrated that if over 8 cups of coffee were consumed, the risk for fetal death increased [130].

Environmental and occupational exposures

Many potential threats to reproductive health are encountered in every-day life through biological (viruses), physical (radiation), and toxic (chemicals) sources [131]. While the human body has defenses to protect itself, these threats can still influence one’s health through inhalation, ocular and dermal contact, ingestion, and vertical and horizontal transfer [132]. These hazards may also have negative ramifications for fertility.

Air Pollution

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 =� 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 =�) [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

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].

Pesticides, endocrine disruptors, and other chemicals

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 ).

Table 2

Chemicals and their respective effects on both male and female reproductive function

ChemicalPossible reproductive effectsSources included
BPAInhibits binding to androgen receptor, decreased semen quality, erectile dysfunction, chromosomal abnormalities in oocyte, recurrent miscarriage, [132,140,144]
Disinfection by-products   
Organochemicals and Pesticides e.g. DDT, DDE, Methoxyclor Change in hormone levels, irregular menstruation, decreased fertility, decreased semen quality, chromosomal abnormalities in sperm, altered histology of testes, decreased libido, fetal loss, miscarriage [132,138,142-144]
DioxinsChanges in hormone levels, altered puberty, altered start of menarche, endometriosis, decreased fertility, fetal loss [132,143]
PhthalatesDecreased semen quality, oligozoospermia, earlier menarche, altered menstrual cycle, infertility [132,144]
SolventsChange in hormone levels, decreased semen quality, irregular menstruation, decreased fertility, miscarriage, fetal loss[132]

Occupation and hobbies

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 =�) [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 =�) [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 ±𠂘.2%) compared to men who carried their cell phones elsewhere or who did not carry one at all (55.4 ±𠂗.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 ±𠂑.4 μm 2 to 9.2 ± .7 μm 2 and acrosomal area significantly decreases from 21.5 ±𠂔% to 35.5 ±�.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.

Preventative care

Contraceptive use

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.

Doctor visits

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 =�,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 =�,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.

Other factors


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 3.5ଌ 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].

Hot water

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.


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Steinberger, E, and WJ Dixon (1959) “Some observations on the effect of heat on the testicular germinal epithelium.” Fertility and Sterility 10(6): 578-95.

Thonneau, P, L Bujan, L Multigner and R Mieusset (1998) “Occupational heat exposure and male fertility: a review.” Human Reproduction 13(8): 2122–5.

Vogeli, M (1954) “Data on the thermic method for temporary male sterilization.” Unpublished. Smith College Archives.
Vogeli, M (1956) “Contraception through temporary male sterilization.” Unpublished. Smith College Archives.

Mieusset, R, and L Bujan (1994) “The potential of mild testicular heating as a safe, effective and reversible contraceptive method for men.” International Journal of Andrology 17: 186-191.

Mieusset, R, L Bujan, A Mansat, H Grandjean and F Pontonnier (1991) “Heat induced inhibition of spermatogenesis in man.” In Zorgniotti (ed.) Temperature and Environmental Effects on the Testes. Plenum Press, NY.

Mieusset, R, L Bujan, A Mansat, F Pontonnier and H Grandjean (1987) “Hyperthermia and human spermatogenesis: enhancement of the inhibitory effect obtained by ‘artificial cryptorchidism’.” International Journal of Andrology 10: 571-80.

Articles to Check Out

Here are a few tips to help you maximize your fertility by keeping your boys cool and your troops happy.

Take Breaks : Brief exposures to heat are ok as long as you get up, move around, and let the boys cool off. If you are watching TV curled up under a warm blanket, typing with a laptop on your lap, or taking a dip in a hot tub, make sure to have a cool-off break. If you work in a hot environment, try to take extra trips to the water cooler. (You should be getting hydration anyways). Chef Ramsey discovered that all the time around hot ovens had impacted his fertility, and began a campaign to improve fertility safety for chefs (Read more).

Watch what you wear: This starts with your underwear. Make sure its loose enough to let your boys breath. This applies to your jeans too. Again if you have occupational exposure to heat, investigate options for clothing that deflects heat.

Stay cool in the summer: Studies have shown that there is a natural decline in sperm count during the summer due to increased temperatures. Dips in the pool, time in air conditioning, or even a solid breeze can do a lot to keep your fertility up.

Ice your balls: Sounds awful but could be an effective way to reduce heat in cases of fever or even varicoceles before treatment. We first heard about this idea from the guys behind snowballs. More research is needed to see if this is an effective approach, but it doesn’t hurt to try.

Lose weight: Never would have guessed it, but it is actually possible to gain a layer of fat in the scrotum which acts as a nice cozy blanket over the testicle, raising the temperature ever so slightly. Often enough to mess with sperm quality. Fortunately, when people lose weight, they most frequently lose it in out of the way places like fingers, wrists, and feet (I’m going to guess that balls make this list) before taking off the spare tire. So you might not need to lose a ton of pounds to notice a difference in your fertility.

Visit a urologist: Get evaluated to find out if you have a varicocele or other physiological abnormality that contributes to over-heating your testicles. Corrective surgeries are often out-patient procedures and have a high success rate.