ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Natural fertility and impact of lifestyle factors

Natural fertility and impact of lifestyle factors
Literature review current through: Jan 2024.
This topic last updated: Jul 08, 2022.

INTRODUCTION — Health care providers frequently receive questions about an individual's fertility potential and the possible impact of specific behaviors or environment on fertility. Patients may seek information on baseline fertility, optimal timing and frequency of coitus to achieve pregnancy, and behaviors to optimize or avoid to improve their fertility.

This topics will discuss natural fertility and the impact of lifestyle on fertility. The evaluation and treatment of individuals with infertility is discussed separately.

(See "Overview of infertility".)

(See "Female infertility: Evaluation".)

(See "Approach to the male with infertility".)

In this topic, when discussing study results, we will use the terms "woman/en", "man/en", or "patient(s)" as they are used in the studies presented. However, we encourage the reader to consider the specific counseling and treatment needs of transgender and gender diverse individuals.

TERMINOLOGY — Infertility is a "disease which generates disability as an impairment of function" [1]. It is defined as inability "to establish clinical pregnancy after 12 months of regular, unprotected sexual intercourse or due to an impairment of a person's capacity to reproduce either as an individual or with his/her partner" [2]. Fertility interventions may be started earlier than 12 months depending on the medical, sexual, and reproductive history; age; physical findings; and diagnostic testing. The terms "infertility" and "subfertility" are interchangeable.

Other terms used when discussing reproductive potential include [2]:

Fecundity is clinically defined as the capacity to have a live birth.

Fecundability is the probability of achieving a pregnancy in a single menstrual cycle with adequate sperm exposure and no contraception that results in a live birth.

Fertility is the ability to have a clinical pregnancy.

Sterility is a permanent state of infertility.

Time to pregnancy refers to the length of time, usually measured in months, that it takes a couple to conceive. This parameter is often used in epidemiological studies as a measure of subfecundity [3,4].

COMMON CLINICAL QUESTIONS

What is normal natural fertility? — Most pregnancies occur during the first six menstrual cycles of attempted conception [4-8]. Maximal fertility rates of approximately 30% per cycle have been reported in the first two cycles; fecundability decreases as the number of consecutive months without achieving pregnancy increases (figure 1) [5].

Six months – In the first six months of attempting pregnancy, approximately 80 percent of couples will conceive.

12 months – In the first 12 months, approximately 85 percent will conceive.

36 months – Over the next 36 months, approximately 50 percent of remaining couples will go on to conceive spontaneously [9].

48 months – The 5 to 7 percent of couples who have not conceived after 48 months of attempted conception will only occasionally go on to achieve a spontaneous conception.

Criteria for initiating an infertility evaluation vary depending on personal characteristics (eg, age) and are discussed separately.

(See "Female infertility: Evaluation".)

(See "Approach to the male with infertility".)

When is the fertile period of the menstrual cycle? — The fertile interval in each menstrual cycle is approximately six days (figure 2) and includes the five days prior to ovulation plus the day of ovulation (figure 3) [10]. The duration of the fertile period is not affected by age but can vary among women [11]. The highest probability of conception occurs when intercourse takes place one to two days prior to ovulation and on the day of ovulation [10,12-17]. (See "Normal menstrual cycle".)

How do I know if I am in my fertile period? — Multiple options exist for tracking the menstrual cycle and resultant physiologic changes to understand when ovulation is most likely to occur. Studies that establish the efficacy of these methods compared with no intervention or that directly compare these methods are generally lacking. Conversely, some individuals use the methods below to avoid having intercourse during their fertile interval and thus avoid conception. (See "Fertility awareness-based methods of pregnancy prevention".)

Low-resource interventions – These methods involve minimal cost and equipment. The time required for patient education can be a barrier to use.

Menstrual calendar – A menstrual calendar involves tracking the days of menses to help predict days of likely ovulation (figure 4). (See "Evaluation of the menstrual cycle and timing of ovulation", section on 'Menstrual cycle charting'.)

Tracking cervical mucous changes– Changes in cervical mucus can help predict ovulation; the highest probability of conception is on the day of peak production of slippery clear mucus. In a descriptive study of 22 women aged 18 to 39 years, 32 percent reported being "very to extremely" comfortable performing cervical mucous observation [18].

Basal body temperature measurements – Daily monitoring with a basal-body thermometer can detect the transient increase in body temperature that occurs after ovulation. (See "Evaluation of the menstrual cycle and timing of ovulation", section on 'Basal body temperature monitoring'.)

Commercially available methods – The interventions below are considered higher-resource because they involve more cost and/or equipment (ie, computer, smart phone) compared with the low-resource interventions above (table 1).

Luteinizing hormone (LH kits) – Women can attempt to predict the time of ovulation by using a kit to measure urinary luteinizing hormone (LH). Use of a home ovulation test kit may decrease the time to conception [19], particularly in women with irregular cycles or couples who have sexual intercourse infrequently. However, for most women, there is no substantial evidence that self-monitoring to predict ovulation increases cycle fecundability [20,21]. (See "Evaluation of the menstrual cycle and timing of ovulation", section on 'Measurement of LH surge and estradiol rise'.)

-Computer and phone applications (apps) – A novel approach to the issue of coital timing for reproduction involves the use of a mobile application (ie, app). A study of one proprietary app analyzed data from over 200,000 menstrual cycles and nearly 100,000 women to determine the probability of pregnancy in the periovulatory period [22]. The day-specific probability of pregnancy in relation to ovulation was 27, 33, 42, 20, and 8 percent for -3, -2, -1 days prior to ovulation, day of ovulation, and +1 days, respectively. The use of fertility apps to either time or avoid conception is presented in detail elsewhere. (See "Fertility awareness-based methods of pregnancy prevention", section on 'Computer and phone applications (apps)'.)

How often should I have sex? — The highest pregnancy rates occur in couples who have vaginal intercourse every one to two days (in the follicular phase (figure 2)) [12,23-25], but regular intercourse two to three times per week beginning soon after cessation of menses should ensure that intercourse falls within the fertile period and semen quality is optimal [26]. Most data indicate that optimum semen quality, measured in terms of motility, morphology, and total sperm count, occurs when there are two to three days of ejaculatory abstinence; longer intervals are associated with lower pregnancy rates [27].

Effect of lubricants — Some lubricants inhibit sperm motility in vitro (eg, KY jelly, Astroglide, Touch, Replens, olive oil, saliva, KY Sensitive, KY Warming, KY Tingling) [28-33]; however, a secondary analysis of couples in a prospective time-to-pregnancy study found no difference in fecundability between those who used and did not use lubricants (primarily Astroglide, KY Jelly, or Pre-seed) [34]. Although there are no compelling data to suggest that lubricant use impairs fertility, the use of lubricants that do not inhibit sperm motility, such as mineral oil, canola oil, mustard oil, or hydroxyethylcellulose-base (Pre-Seed), is prudent when lubricants are needed.

Coital factors that do not affect fertility — Coital position, presence or absence of female orgasm, and female position (eg, remaining supine) after male ejaculation do not appear to affect the likelihood of conception [20].

How does age affect fertility? — Delayed childbearing can decrease the probability of successful conception and should be taken into account in family and career planning. Women in their late 30s are approximately 40 percent less fertile than women in their early 20s. (See "Effects of advanced maternal age on pregnancy".)

The probability of conception is highly dependent upon maternal age, but paternal age also plays a minor role, especially after age 50 years [35]. In a large well-designed study, the probability of clinical pregnancy following intercourse on the most fertile day of the cycle in women of assumed fertility aged 19 to 26 years, 27 to 34 years, and 35 to 39 years was approximately 50, 40, and 30 percent, respectively, if the male partner was the same age, but 45, 40, and 15 percent, respectively, if he was five years older [36].

(See "Effect of advanced paternal age on fertility and pregnancy".)

(See "Effect of advanced paternal age on fertility and pregnancy".)

Environmental factors — Environmental pollutants and toxicants, such as dry cleaning solvents, heavy metals, pesticides, and possibly bisphenol A (BPA) can have adverse effects on fertility and pregnancy. (See "Overview of occupational and environmental risks to reproduction in females".)

A review of studies on sauna bathing concluded that this activity does not influence fertility in women or men [37]. Although hormonal changes occur during sauna bathing, the changes are transient.

EFFECT OF SPECIFIC FACTORS ON FERTILITY

There are no large-scale, randomized, clinical trials examining the effect of lifestyle issues such as cigarette smoking, body mass index (BMI), stress, or alcohol and caffeine consumption on fertility. Most studies are observational and subject to many potential biases. As an example, numerous investigators have reported that primary tubal infertility is increased in women who report a history of many sexual partners, an earlier age at first intercourse, and cigarette smoking. However, women with more sexual partners and an earlier age at first intercourse may also be more likely to smoke cigarettes; thus, it is often difficult to definitively determine if cigarette smoking is an independent contributor to infertility or whether cigarette smoking is largely associated with infertility through other exposures, such as sexually transmitted infections [38,39]. In addition, women who smoke cigarettes tend to consume more alcohol and caffeine than women who do not smoke. This raises the possibility that the relationship between cigarette smoking and reduced fertility may influence observations of an association between alcohol and caffeine consumption and diminished fertility.

In many of the studies discussed below, attempts were made to control for some of the potential confounding interactions through the use of logistic regression and multivariate analyses. However, the absence of data from randomized trials is a major weakness of the evidence in this area. An additional limitation is that there is no biomarker that can be measured to indicate the potential for human conception [40].

Overweight and obesity — Both overweight (25.0 to 29.9 kg/m2) and obese (≥30 kg/m2) body mass indexes (BMIs) have been associated with decreased fertility as well as other adverse effects on health [41]. The effect of BMI on male fertility is unclear. A BMI of 18.5 to 25 kg/m2 is associated with little or no increased health risks and, for this reason, is desirable for both females and males irrespective of fertility issues. (See "Overweight and obesity in adults: Health consequences".)

Effect on fertility

Female partner

Elevated body mass index (BMI) Both overweight (25.0 to 29.9 kg/m2) and obese (≥30 kg/m2) BMIs have been associated with decreased fertility [41].

Time to pregnancy and pregnancy rates – Obesity in childhood contributes to menstrual cycle abnormalities and infertility [42]. A cross-sectional study in the United States reported that adolescents who self-reported being obese (BMI >30 kg/m2) were more than twice as likely to remain childless than normal-weight adolescents after adjusting for confounding variables such as adult BMI, nongestational amenorrhea, marital status, ethnicity, geographical location, and socioeconomic status [43]. Even in regularly ovulating women, increasing obesity appears to be associated with decreasing spontaneous pregnancy rates and increased time to pregnancy [44-46]. In addition to absolute body weight, weight gain in adulthood may also increase the amount of time needed to conceive, irrespective of baseline weight or menstrual cyclicity. As an example, a prospective cohort study of nearly 2000 women reported that every 5 kg body weight increase (from the patient's baseline weight at age 18) was associated with a 5 percent increase in the mean duration of time needed for attempted conception (95% CI 3-7 percent) [47]. Of note, approximately 90 percent of the women in this study had regular menstrual cycles which suggests that altered ovulation was not the mechanism. Therefore, women who wish to conceive are counseled about the importance of achieving and maintaining a normal weight.

Ovulatory dysfunction – Most studies in adults report a BMI greater than 27 kg/m2 or a BMI less than 17 kg/m2 is associated with increased ovulatory dysfunction and resultant infertility [48-50].

Metabolic changes – For women with an elevated BMI, subfertility appears to be related to insulin resistance leading to insulin excess [51]. Hyperinsulinemia may lead to androgen excess by reducing sex-hormone-binding globulin synthesis, thereby increasing free testosterone, and by stimulating ovarian androgen production rates. Excess androgen, in turn, is a major factor leading to altered hypothalamic-pituitary and ovarian physiology and anovulation. Obesity-associated hyperleptinemia may be an additional factor in anovulation, not only through the induction of insulin resistance, but also through direct impairment of ovarian function. Factors other than anovulation also likely play a role in obesity-related subfertility [52]. (See "Diagnosis of polycystic ovary syndrome in adults".)

Weight loss – Prior observational studies have reported both nonsurgical [53-55] and surgical [56-62] weight loss increased the frequency of ovulation and natural conception. However, weight reduction does not appear to be associated with increased fecundability or live birth rate [63-65]. A large, multicenter trial of obese (BMI ≥29 kg/m2) and infertile women reported no difference in birth rates of term singletons or overall live birth rates among women who received a six-month structured weight-loss intervention prior to infertility treatment and control women who went directly to infertility treatment [64]. There were also no differences in the obstetric outcomes of gestational diabetes or hypertensive disorders of pregnancy between intervention and control groups. In the trial, women in the intervention group were more likely to conceive spontaneously (26 versus 16 percent) and underwent fewer fertility treatment cycles (679 versus 1067 treatment cycles) compared with the control women. Study limitations include that target weight loss was reached by only 38 percent of women in the intervention group and the intervention discontinuation rate was 22 percent. It is not known if greater weight reduction per person, increased proportion of women reaching target weight loss, or increased patient continuation rates would increase fecundability.

We continue to advise weight loss for infertile women with an elevated BMI because weight reduction aids in spontaneous conception in some studies and reduces the need for fertility treatment, in addition to providing long-term benefits for overall health [53,55]. In a study of 67 women who had an average weight loss of 10 kg over six months, spontaneous ovulatory cycles resumed in nearly 90 percent (60 of 67), with 52 women becoming pregnant and 45 having a live birth. None of the control patients, consisting of study drop-outs, resumed ovulatory cycles or conceived. One lifestyle modification to achieve weight loss includes increased moderate physical activity, such as walking 150 minutes weekly [66,67]. Dietary intake should be decreased by 500 to 1000 cal/day, which will result in a 1 to 2 pound weekly weight loss. Consuming a low-calorie diet of 1000 to 2000 kcal/day should result in a 10 percent decrease in BMI over six months [68]. Maintaining a 10 percent weight loss with lifestyle modification is uncommon and only achieved by 20 percent after one year [69]. Those participating in a lifestyle moderation program may have an improved chance of maintaining weight reduction as compared with those not in a structural program [70]. (See "Obesity in adults: Overview of management".)

Male partner — The impact of the male partner's BMI on fertility has not been examined extensively. Some observational and animal data suggest an association between increasing male BMI and lower pregnancy rates [71-73]. There is consistent evidence that obesity affects reproductive hormone levels, but studies have reported conflicting results on the effect of obesity on semen parameters [74-77]. An observational study of nearly 4000 sperm donors in China, with an average of eight repeated semen measures per donor, reported that being underweight (BMI <18.5 kg/m2) was associated with lower sperm concentration, total sperm number, and total motile sperm count while being overweight (BMI 25.0 to 29.9 kg/m2) was associated with lower semen volume, total sperm number, and total motile sperm count [78]. The study controlled for age, ethnicity, education, smoking status, marital status, abstinence period, and season. Only 1 percent (n = 38) of the study population were obese (BMI ≥30 kg/m2), which limited the study's ability to identify statistical significance at this weight level. While weight reduction can correct the hormonal imbalance, the effect of weight loss on semen parameters and pregnancy rate has not been studied.

Effect of obesity on fertility therapy — Some studies report poorer outcomes of infertility treatment in obese females (eg, insufficient follicular development, lower oocyte counts, lower fertilization rates) [79-83], while others report outcomes are comparable to nonobese females, but higher doses of ovulation inducing agents need to be used [84-87]. The risk of unsuccessful IVF increases with increasing BMI and may be related to poor oocyte quality, ovarian function, endometrial quality, or a combination of these factors. In a systematic review and meta-analysis including 33 studies and almost 48,000 IVF/ICSI treatment cycles, women who were overweight or obese (BMI ≥25 kg/m2) had a statistically significant small reduction in clinical pregnancy rate (RR 0.90) and live birth rate (RR 0.84) and a significantly higher miscarriage rate (RR 1.31) than normal weight women (BMI <25 kg/m2) [88].

(See "In vitro fertilization: Overview of clinical issues and questions", section on 'Minimal or unclear effect'.)

Spontaneous abortion — Most studies report an increased spontaneous abortion (SAB) rate in obese women undergoing ART [87-95]. A meta-analysis of 33 studies reported a slightly higher SAB rate (RR 1.31) in women with a BMI >25 kg/m2 compared with those with a BMI <25 kg/m2 (90 g). An increased risk for pregnancy loss was also noted in those with a BMI >25 kg/m2 following single fresh (OR 2.7, 95% CI 1.5-4.9) or frozen blastocyst transfer [94].

Healthy lifestyle

Diet — In healthy couples, there is no strong evidence that dietary variations such as vegetarian diets, low-fat diets, and vitamin or antioxidant-enriched diets improve fertility [20,96]. However, undiagnosed/untreated celiac disease may cause female or male subfertility, which resolves by adopting a gluten-free diet. (See "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults".)

Female partner – Data on the relationship between diet and fertility in women are from observational studies. One of the largest of these studies was a prospective cohort study of over 18,000 married, premenopausal women without a history of infertility who attempted pregnancy or became pregnant [97-102]. Based on their own data and that from other studies, the authors considered the following dietary habits components of a "fertility diet": higher monounsaturated to trans-fat ratio, high percentage of protein from vegetable rather than animal sources, low glycemic index carbohydrates, high fat dairy foods, and use of iron and multivitamin supplements. Healthy women whose diet reflected this composition had a significantly reduced risk of ovulatory disorder infertility. They hypothesized that this diet was favorable to glucose homeostasis and insulin sensitivity, factors that play a role in ovulatory function. The results were based on dietary recall, and thus were subject to recall bias. Other smaller observational studies have supported the beneficial effects of a Mediterranean diet, reduced trans-fat intake, and increased omega-3 fatty acid intake on achieving natural or assisted conception [103-106]. There is no harm to such diets, but no strong data at this time to recommend dietary changes solely for enhancement of fertility.

Male partner – Observational studies in men have reported improved semen parameters among men with healthy dietary habits; pregnancy rates were not evaluated [107-109].

Caffeine — Female fertility does not appear to be affected by caffeine intake less than 200 mg per day, even for women undergoing IVF therapy [110,111]. A cohort study of over 1700 couples undergoing fertility treatment reported a higher chance of a live birth among women consuming 1 to 5 cups of coffee per day compared with a relevant non-coffee drinking cohort (adjusted relative risk 1.53, 95% CI 1.06-2.21) [112]. Therefore, women contemplating pregnancy probably can have one or two 6 to 8 ounce cups of coffee per day without negatively impacting their ability to conceive (table 2). The impact of caffeine consumption on fertility and reproductive outcomes is presented in detail elsewhere. (See "Caffeine: Effects on reproductive outcomes in females".)

There is no strong evidence to support limiting caffeine intake in the male partner.

Exercise — Female fertility can be adversely affected by increased intensity and duration of exercise. For this reason, we suggest women with BMI <25 kg/m2 who are attempting to conceive limit vigorous exercise to fewer than five hours per week. Male fertility does not appear to be affected by exercise.

Female partner — The intensity and duration of exercise can affect female fertility, but the specific type of exercise does not appear to be a factor. In some epidemiological studies, vigorous/intense physical activity was associated with ovulatory infertility [113,114], while others have not observed a significant association [100]. Baseline patient characteristics appear to play a role. In a well-designed study of Danish women, vigorous physical activity (running, fast cycling, aerobics, swimming, gymnastics) was associated with a reduction in fecundity; however, the effect was confined to women with a BMI <25 kg/m2; there was a slightly positive effect of all levels of exercise among overweight and obese women [115]. In women undergoing IVF, another study noted that ≥4 hours of strenuous exercise weekly over a period of years was associated with poorer outcomes [116].

The effects of strenuous exercise on fertility could be related to (1) reduced progesterone production during the luteal phase of the menstrual cycle in ovulatory women (ie, luteal phase defect), (2) alterations in GnRH production, LH and FSH secretion, and estradiol production and metabolism, resulting in anovulation, or (3) changes in leptin levels [117-119]. Other factors may include decreased body fat and changes in diet, such as an increase in fiber and a decrease in fat intake, in women who exercise strenuously. (See "Functional hypothalamic amenorrhea: Pathophysiology and clinical manifestations".)

However, from a population perspective, inadequate levels of exercise associated with obesity may be a more common cause of anovulation and subsequent infertility than exercise-associated anovulation [120,121]. (See 'Overweight and obesity' above.)

Male partner — The relationship between fertility and exercise in the male has not been well characterized. One large retrospective study examined the association between regular physical exercise and semen quality in 2261 men whose partners were undergoing IVF [122]. Overall, none of the semen parameters studied was affected by exercise; however, men who bicycled ≥5 hours/week demonstrated lower sperm concentrations and lower numbers of total motile sperm than their non-exercising counterparts; pregnancy rates were not evaluated. Results were not influenced by age, BMI or a history of male infertility.

Stress and stress reduction — Many observational studies have suggested that stress is associated with infertility and, in turn, the diagnosis and treatment of infertility clearly can be stressful. No clinical trial has demonstrated definitively that reducing stress prior to infertility treatment improves pregnancy rates. (See "Psychological stress and infertility".)

Impact of stress on assisted reproductive outcomes – In a 2011 meta-analysis that pooled 31 prospective trials examining the association between stress, distress in female patients, and assisted reproductive technology (ART) outcomes, small but statistically significant negative correlations were observed between ART outcomes and stress and anxiety [123]. Importantly, however, the association with anxiety disappeared when live birth rates were examined, and too few trials using stress were included to allow statistical analysis.

Impact of stress reduction – A 2021 meta-analysis of 15 trials evaluating the impact of psychosocial interventions for individuals undergoing assisted reproductive technology reported a small but significant increase in live birth rate with psychosocial interventions, particularly long-term and mind-body interventions (risk ratio 1.21, 95% CI 1.04-1.43 and risk ratio 1.25, 95% CI 1.00-1.55, respectively) [124]

Substance use

Tobacco — Use of tobacco by the female partner, and possibly by the male partner, has been associated with subfertility, and may account for as much as 13 percent of cases [125]. Observational studies suggest that much of the subfertility associated with smoking can be reversed within a year of cessation [126-129].

Given the multiple health risks associated with cigarette smoking, cessation should be encouraged irrespective of fertility and pregnancy issues. (See "Benefits and consequences of smoking cessation" and "Overview of smoking cessation management in adults".)

Female partner — Studies of the impact of smoking on fertility have typically analyzed the effects of "cigarettes smoked per day" on fecundability. Most series report that fecundability is decreased if the female partner smokes more than 10 cigarettes per day. In a 1998 meta-analysis including data from almost 11,000 smoking women and over 19,000 nonsmokers, cigarette smoking by the female partner was associated with a statistically significant increase in infertility compared with nonsmokers (odds ratio [OR] 1.60, 95% CI 1.34-1.91) [130]. Although only observational studies were included, the evidence was compelling because of the consistency of the effect across different study designs, sample sizes, and types of outcome. Others have reported that the time to achieve pregnancy increases with the number of cigarettes smoked per day (figure 5) [131].

An additional concern is that subfertility in smokers cannot necessarily be overcome by assisted reproductive technology (ART). The same 1998 meta-analysis found that the odds of pregnancy per number of in vitro fertilization (IVF) cycles was significantly lower in smokers compared with nonsmokers (OR 0.66, 95% CI 0.49-0.88) [130].

Possible mechanisms for subfertility in smokers include adverse tubal and/or cervical changes, damage to gametes, and increase in spontaneous abortion and ectopic pregnancies [39,132]. Numerous studies linking smoking to early menopause suggest that cigarette smoking causes premature depletion of the ovarian pool of oocytes and premature aging of the ovary by one to four years [133,134]; this decrease in ovarian reserve can account for the subfertility observed in smokers.

Components of cigarette smoke may cause oxidative stress and DNA damage to the ovarian follicle [135,136]. For this reason, smoking by a pregnant woman may be harmful to the ovaries of her fetus [137]. In a study of the effect of in-utero exposure to cigarette smoke on the fertility of the female partner, fecundability was reduced among women exposed to cigarette smoke in-utero (fecundability ratio 0.5, 95% CI 0.4-0.8) [138]. This association was present after adjusting for age of the female partner, frequency of intercourse, current smoking status, age at menarche, childhood exposure to cigarette smoke, body mass of the female partner, alcohol and caffeine consumption, educational level, and reproductive history. There may also be adverse reproductive effects of maternal smoking on male fetuses. An epidemiologic study reported that adult male offspring of mothers who smoked more than 10 cigarettes/day during pregnancy had lower sperm counts than the sons of nonsmokers [139].

Male partner — Dose-dependent decreases in semen quality have been observed in men who smoke, but available evidence does not prove that smoking decreases male fertility. An analysis of 27 epidemiologic studies addressing the effect of smoking on sperm concentration, motility, and morphology in fertile and infertile men found a modest reduction in semen quality and altered hormone levels among smokers compared with nonsmokers, but did not find a reduction in male fertility associated with paternal smoking [140]. Fertile male smokers had a 23 percent decrease in sperm concentration and a 13 percent decrease in sperm motility compared with fertile male nonsmokers.

A deleterious effect on male fertility or a secondary deleterious effect on female fertility cannot be definitively excluded, especially among men with marginal semen quality. Studies in subfertile populations that evaluated the effect of smoking by the male partner on the success rate of IVF and intracytoplasmic sperm injection (ICSI) have reported a significant decrease in the number of pregnancies achieved [141,142].

Alcohol intake — Moderate alcohol consumption <2 drinks/day (1 drink = 10 g of ethanol) probably has no or minimal adverse effects on fertility, but higher levels of alcohol consumption should probably be avoided when attempting pregnancy [20,143-146]. Abstinence at conception and during pregnancy is generally recommended because a safe level of prenatal alcohol consumption has not been established. In both men and women, the dose-response relationship between alcohol intake and fertility requires additional study.

Female partner — Most observational studies have reported moderate and heavy female drinkers tend to take longer to achieve a pregnancy and are at higher risk of undergoing an infertility evaluation [144,145,147-149]. Others have not noted an adverse effect of moderate alcohol intake on fertility [150,151] nor a difference in risk of ovulatory dysfunction between women with high versus low alcohol intake [152]. Heavy alcohol intake is typically defined as ≥14 drinks per week, and moderate intake is usually defined as 3 to 13 drinks per week, but these definitions are arbitrary and vary in different studies. However, alcohol consumption can impact the developing fetus. (See "Alcohol intake and pregnancy".)

Moderate alcohol use may affect success rates of women undergoing IVF, but the supporting data are mixed. A retrospective study on alcohol consumption reported that women who drank at least four drinks per week were at 16 percent less odds of a live birth after IVF compared with women who had fewer drinks (OR 0.84, CI 0.71-0.99) [153]. By contrast, a prospective study of 300 women undergoing IVF failed to find an association between alcohol conception and live birth. The authors divided their subjects corresponding to <0.5 glass of alcohol/day, 0.5 to 1 glass/day, 1 to 2 glasses/day, and >2 glasses per day. No difference in live births was observed [110]. A Danish cohort study involving over 1700 women and their partners who underwent intrauterine insemination, IVF, or ICSI treatment failed to demonstrate an effect of alcohol consumption on any of the three treatment modalities for 1 to 2, 3 to 7, and >7 drinks per week. For the IVF/ICSI groups, the adjusted relative risk of achieving live birth was 1.00 (95% CI 0.83-1.21), 0.95 (95% CI 0.75-1.20), and 0.89 (95% CI 0.53-1.51) for 1 to 2, 3 to 7, and >7 drinks per week, respectively, compared with a nondrinking cohort [154].

Male partner — Heavy alcohol use by the male partner is related to abnormalities in gonadal function, including reduced testosterone production, impotence, and decreased spermatogenesis [155-157]. In the IVF study cited above [153], in couples in which both partners consumed at least four drinks per week, the odds of a live birth were diminished by 21 percent compared with couples in which both partners drank less than four or more drinks per week. For patients with a live birth, a meta-analysis of 55 studies reported paternal alcohol use prior to conception was associated with an increased risk of total congenital heart defects in the offspring (OR 1.44, 95% CI 1.19-1.74) [158].

Other drugs — There are minimal data on the effects of recreational drug use on fertility [159]. A study of self-reported marijuana use by individuals undergoing fertility treatment reported a higher risk of pregnancy loss in marijuana smokers compared with past or never-users (n = 308, 379 cycles, adjusted probability 54 versus 26 percent) [160]. Unexpectedly, a higher pregnancy rate was reported for couples undergoing IVF when the male partner smoked marijuana while the female partner did not. These drugs should be avoided because of their general health risks.

(See "Substance use during pregnancy: Screening and prenatal care".)

(See "Substance use during pregnancy: Overview of selected drugs".)

LIFESTYLE EFFECTS ON ESTABLISHED PREGNANCY — Cigarette smoking, obesity, alcohol and caffeine consumption, and recreational drug use can have a significant adverse impact on pregnancy and fetal outcomes. The combined impact of these exposures on both fertility and pregnancy outcome emphasizes the importance of lifestyle interventions for the couple planning a pregnancy. (See "The preconception office visit".)

(See "Obesity in pregnancy: Complications and maternal management".)

(See "Caffeine: Effects on reproductive outcomes in females".)

(See "Cigarette and tobacco products in pregnancy: Impact on pregnancy and the neonate".)

(See "Alcohol intake and pregnancy" and "Prenatal substance exposure and neonatal abstinence syndrome (NAS): Clinical features and diagnosis".)

(See "Substance use during pregnancy: Screening and prenatal care".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Female infertility".)

SUMMARY AND RECOMMENDATIONS — Lifestyle factors can affect the duration of time before achieving pregnancy and modifying these factors may enhance fertility. The recommendations below are based upon data from observational studies; no randomized trials have been performed.

Couples should be informed that delayed childbearing, especially after age 30 years, can decrease the probability of successful conception, and they should take this into account in family and career planning. (See 'How does age affect fertility?' above.)

We suggest sexual intercourse two to three times per week from soon after cessation of menses through the day of ovulation to ensure that intercourse falls within the most fertile period (up to two days before ovulation) and semen quality is optimal (Grade 2C). (See 'When is the fertile period of the menstrual cycle?' above.)

We recommend smoking cessation for couples who smoke based on the overall health benefits of smoking cessation (Grade 1A). Use of tobacco by the female partner, and possibly the male partner, appears to be associated with subfertility. For couples planning pregnancy, observational studies suggest fertility is enhanced when use of tobacco products is terminated. (See 'Tobacco' above.)

A body mass index (BMI) greater than 27 kg/m2 or less than 17 kg/m2 is associated with an increased risk of anovulatory infertility. The former is often related to polycystic ovary syndrome and the latter is often related to amenorrhea caused by excessive exercise or poor caloric intake (eg, eating disorders). We suggest couples try to achieve a BMI of 18.5 to 25 kg/m2 (Grade 2C). Women in this weight range are less likely to have ovulatory dysfunction than women at either extreme of BMI. This range is associated with little or no increased health risks and, for this reason, is desirable for both women and men. There is little information on the relationship between male fertility and BMI. (See 'Overweight and obesity' above.)

Moderate and heavy female drinkers tend to take longer to achieve a pregnancy and are at higher risk of undergoing an infertility evaluation. We suggest that women who are attempting to conceive avoid all alcohol, given a safe level of prenatal alcohol consumption with respect to the fetus has not been determined (Grade 2C). Moderate alcohol intake by the male partner does not appear to be associated with decreased fertility. (See 'Alcohol intake' above.)

It is unclear whether high caffeine consumption affects female fertility; it does not appear to affect male fertility. We suggest women contemplating pregnancy limit caffeine intake to no more than one or two cups of coffee per day (total of 200 mg caffeine) (Grade 2C). (See 'Caffeine' above.)

  1. Practice Committee of the American Society for Reproductive Medicine. Electronic address: [email protected]. Definitions of infertility and recurrent pregnancy loss: a committee opinion. Fertil Steril 2020; 113:533.
  2. Zegers-Hochschild F, Adamson GD, Dyer S, et al. The International Glossary on Infertility and Fertility Care, 2017. Fertil Steril 2017; 108:393.
  3. Joffe M, Key J, Best N, et al. Studying time to pregnancy by use of a retrospective design. Am J Epidemiol 2005; 162:115.
  4. Gnoth C, Godehardt D, Godehardt E, et al. Time to pregnancy: results of the German prospective study and impact on the management of infertility. Hum Reprod 2003; 18:1959.
  5. Zinaman MJ, Clegg ED, Brown CC, et al. Estimates of human fertility and pregnancy loss. Fertil Steril 1996; 65:503.
  6. GUTTMACHER AF. Factors affecting normal expectancy of conception. J Am Med Assoc 1956; 161:855.
  7. Wang X, Chen C, Wang L, et al. Conception, early pregnancy loss, and time to clinical pregnancy: a population-based prospective study. Fertil Steril 2003; 79:577.
  8. Slama R, Hansen OK, Ducot B, et al. Estimation of the frequency of involuntary infertility on a nation-wide basis. Hum Reprod 2012; 27:1489.
  9. Gnoth C, Godehardt E, Frank-Herrmann P, et al. Definition and prevalence of subfertility and infertility. Hum Reprod 2005; 20:1144.
  10. Dunson DB, Baird DD, Wilcox AJ, Weinberg CR. Day-specific probabilities of clinical pregnancy based on two studies with imperfect measures of ovulation. Hum Reprod 1999; 14:1835.
  11. Keulers MJ, Hamilton CJ, Franx A, et al. The length of the fertile window is associated with the chance of spontaneously conceiving an ongoing pregnancy in subfertile couples. Hum Reprod 2007; 22:1652.
  12. Wilcox AJ, Weinberg CR, Baird DD. Timing of sexual intercourse in relation to ovulation. Effects on the probability of conception, survival of the pregnancy, and sex of the baby. N Engl J Med 1995; 333:1517.
  13. Trussell J, Rodríguez G, Ellertson C. New estimates of the effectiveness of the Yuzpe regimen of emergency contraception. Contraception 1998; 57:363.
  14. Weinberg CR, Gladen BC, Wilcox AJ. Models relating the timing of intercourse to the probability of conception and the sex of the baby. Biometrics 1994; 50:358.
  15. Masarotto G, Romualdi C. Probability of conception on different days of the menstrual cycle: an ongoing exercise. Adv Contracept 1997; 13:105.
  16. Bilian X, Heng Z, Shang-chun W, et al. Conception probabilities at different days of menstrual cycle in Chinese women. Fertil Steril 2010; 94:1208.
  17. Practice Committee of the American Society for Reproductive Medicine in collaboration with the Society for Reproductive Endocrinology and Infertility. Electronic address: [email protected], Practice Committee of the American Society for Reproductive Medicine in collaboration with the Society for Reproductive Endocrinology and Infertility. Optimizing natural fertility: a committee opinion. Fertil Steril 2017; 107:52.
  18. Ayoola AB, Slager D, Feenstra C, Zandee GL. A Feasibility Study of Women's Confidence and Comfort in Use of a Kit to Monitor Ovulation. J Midwifery Womens Health 2015; 60:604.
  19. Tiplady S, Jones G, Campbell M, et al. Home ovulation tests and stress in women trying to conceive: a randomized controlled trial. Hum Reprod 2013; 28:138.
  20. Practice Committee of American Society for Reproductive Medicine in collaboration with Society for Reproductive Endocrinology and Infertility. Optimizing natural fertility: a committee opinion. Fertil Steril 2013; 100:631.
  21. Manders M, McLindon L, Schulze B, et al. Timed intercourse for couples trying to conceive. Cochrane Database Syst Rev 2015; :CD011345.
  22. Faust L, Bradley D, Landau E, et al. Findings from a mobile application-based cohort are consistent with established knowledge of the menstrual cycle, fertile window, and conception. Fertil Steril 2019; 112:450.
  23. Elzanaty S, Malm J, Giwercman A. Duration of sexual abstinence: epididymal and accessory sex gland secretions and their relationship to sperm motility. Hum Reprod 2005; 20:221.
  24. Levitas E, Lunenfeld E, Weiss N, et al. Relationship between the duration of sexual abstinence and semen quality: analysis of 9,489 semen samples. Fertil Steril 2005; 83:1680.
  25. Check JH, Epstein R, Long R. Effect of time interval between ejaculations on semen parameters. Arch Androl 1991; 27:93.
  26. Stanford JB, Dunson DB. Effects of sexual intercourse patterns in time to pregnancy studies. Am J Epidemiol 2007; 165:1088.
  27. Jurema MW, Vieira AD, Bankowski B, et al. Effect of ejaculatory abstinence period on the pregnancy rate after intrauterine insemination. Fertil Steril 2005; 84:678.
  28. Agarwal A, Deepinder F, Cocuzza M, et al. Effect of vaginal lubricants on sperm motility and chromatin integrity: a prospective comparative study. Fertil Steril 2008; 89:375.
  29. Frishman GN, Luciano AA, Maier DB. Evaluation of Astroglide, a new vaginal lubricant: effects of length of exposure and concentration on sperm motility. Fertil Steril 1992; 58:630.
  30. Anderson L, Lewis SE, McClure N. The effects of coital lubricants on sperm motility in vitro. Hum Reprod 1998; 13:3351.
  31. Goldenberg RL, White R. The effect of vaginal lubricants on sperm motility in vitro. Fertil Steril 1975; 26:872.
  32. Kutteh WH, Chao CH, Ritter JO, Byrd W. Vaginal lubricants for the infertile couple: effect on sperm activity. Int J Fertil Menopausal Stud 1996; 41:400.
  33. Sandhu RS, Wong TH, Kling CA, Chohan KR. In vitro effects of coital lubricants and synthetic and natural oils on sperm motility. Fertil Steril 2014; 101:941.
  34. Steiner AZ, Long DL, Tanner C, Herring AH. Effect of vaginal lubricants on natural fertility. Obstet Gynecol 2012; 120:44.
  35. Dunson DB, Baird DD, Colombo B. Increased infertility with age in men and women. Obstet Gynecol 2004; 103:51.
  36. Dunson DB, Colombo B, Baird DD. Changes with age in the level and duration of fertility in the menstrual cycle. Hum Reprod 2002; 17:1399.
  37. Hannuksela ML, Ellahham S. Benefits and risks of sauna bathing. Am J Med 2001; 110:118.
  38. Cramer DW, Goldman MB, Schiff I, et al. The relationship of tubal infertility to barrier method and oral contraceptive use. JAMA 1987; 257:2446.
  39. Phipps WR, Cramer DW, Schiff I, et al. The association between smoking and female infertility as influenced by cause of the infertility. Fertil Steril 1987; 48:377.
  40. Louis GM, Cooney MA, Lynch CD, Handal A. Periconception window: advising the pregnancy-planning couple. Fertil Steril 2008; 89:e119.
  41. Tang J, Zhu X, Chen Y, et al. Association of maternal pre-pregnancy low or increased body mass index with adverse pregnancy outcomes. Sci Rep 2021; 11:3831.
  42. Lake JK, Power C, Cole TJ. Women's reproductive health: the role of body mass index in early and adult life. Int J Obes Relat Metab Disord 1997; 21:432.
  43. Polotsky AJ, Hailpern SM, Skurnick JH, et al. Association of adolescent obesity and lifetime nulliparity--the Study of Women's Health Across the Nation (SWAN). Fertil Steril 2010; 93:2004.
  44. van der Steeg JW, Steures P, Eijkemans MJ, et al. Obesity affects spontaneous pregnancy chances in subfertile, ovulatory women. Hum Reprod 2008; 23:324.
  45. Gesink Law DC, Maclehose RF, Longnecker MP. Obesity and time to pregnancy. Hum Reprod 2007; 22:414.
  46. Ramlau-Hansen CH, Thulstrup AM, Nohr EA, et al. Subfecundity in overweight and obese couples. Hum Reprod 2007; 22:1634.
  47. Gaskins AJ, Rich-Edwards JW, Missmer SA, et al. Association of Fecundity With Changes in Adult Female Weight. Obstet Gynecol 2015; 126:850.
  48. Grodstein F, Goldman MB, Cramer DW. Body mass index and ovulatory infertility. Epidemiology 1994; 5:247.
  49. Rich-Edwards JW, Goldman MB, Willett WC, et al. Adolescent body mass index and infertility caused by ovulatory disorder. Am J Obstet Gynecol 1994; 171:171.
  50. McKinnon CJ, Hatch EE, Rothman KJ, et al. Body mass index, physical activity and fecundability in a North American preconception cohort study. Fertil Steril 2016; 106:451.
  51. Pasquali R, Gambineri A. Metabolic effects of obesity on reproduction. Reprod Biomed Online 2006; 12:542.
  52. Luke B, Brown MB, Missmer SA, et al. The effect of increasing obesity on the response to and outcome of assisted reproductive technology: a national study. Fertil Steril 2011; 96:820.
  53. Clark AM, Ledger W, Galletly C, et al. Weight loss results in significant improvement in pregnancy and ovulation rates in anovulatory obese women. Hum Reprod 1995; 10:2705.
  54. Norman RJ, Noakes M, Wu R, et al. Improving reproductive performance in overweight/obese women with effective weight management. Hum Reprod Update 2004; 10:267.
  55. Clark AM, Thornley B, Tomlinson L, et al. Weight loss in obese infertile women results in improvement in reproductive outcome for all forms of fertility treatment. Hum Reprod 1998; 13:1502.
  56. Dixon JB, Dixon ME, O'Brien PE. Pregnancy after Lap-Band surgery: management of the band to achieve healthy weight outcomes. Obes Surg 2001; 11:59.
  57. Nelson SM, Fleming R. Obesity and reproduction: impact and interventions. Curr Opin Obstet Gynecol 2007; 19:384.
  58. Marceau P, Kaufman D, Biron S, et al. Outcome of pregnancies after biliopancreatic diversion. Obes Surg 2004; 14:318.
  59. Martin LF, Finigan KM, Nolan TE. Pregnancy after adjustable gastric banding. Obstet Gynecol 2000; 95:927.
  60. Weiner R, Blanco-Engert R, Weiner S, et al. Outcome after laparoscopic adjustable gastric banding - 8 years experience. Obes Surg 2003; 13:427.
  61. Eid GM, Cottam DR, Velcu LM, et al. Effective treatment of polycystic ovarian syndrome with Roux-en-Y gastric bypass. Surg Obes Relat Dis 2005; 1:77.
  62. Teitelman M, Grotegut CA, Williams NN, Lewis JD. The impact of bariatric surgery on menstrual patterns. Obes Surg 2006; 16:1457.
  63. Taghavi SA, van Wely M, Jahanfar S, Bazarganipour F. Pharmacological and non-pharmacological strategies for obese women with subfertility. Cochrane Database Syst Rev 2021; 3:CD012650.
  64. Mutsaerts MA, van Oers AM, Groen H, et al. Randomized Trial of a Lifestyle Program in Obese Infertile Women. N Engl J Med 2016; 374:1942.
  65. Legro RS, Hansen KR, Diamond MP, et al. Effects of preconception lifestyle intervention in infertile women with obesity: The FIT-PLESE randomized controlled trial. PLoS Med 2022; 19:e1003883.
  66. American Diabetes Association. Standards of medical care in diabetes--2013. Diabetes Care 2013; 36 Suppl 1:S11.
  67. Wyatt HR. Update on treatment strategies for obesity. J Clin Endocrinol Metab 2013; 98:1299.
  68. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2:51S.
  69. Wing RR, Hill JO. Successful weight loss maintenance. Annu Rev Nutr 2001; 21:323.
  70. Wadden TA, Foster GD. Behavioral treatment of obesity. Med Clin North Am 2000; 84:441.
  71. Sallmén M, Sandler DP, Hoppin JA, et al. Reduced fertility among overweight and obese men. Epidemiology 2006; 17:520.
  72. Nguyen RH, Wilcox AJ, Skjaerven R, Baird DD. Men's body mass index and infertility. Hum Reprod 2007; 22:2488.
  73. Mitchell M, Bakos HW, Lane M. Paternal diet-induced obesity impairs embryo development and implantation in the mouse. Fertil Steril 2011; 95:1349.
  74. Hofny ER, Ali ME, Abdel-Hafez HZ, et al. Semen parameters and hormonal profile in obese fertile and infertile males. Fertil Steril 2010; 94:581.
  75. Duits FH, van Wely M, van der Veen F, Gianotten J. Healthy overweight male partners of subfertile couples should not worry about their semen quality. Fertil Steril 2010; 94:1356.
  76. Hammiche F, Laven JS, Twigt JM, et al. Body mass index and central adiposity are associated with sperm quality in men of subfertile couples. Hum Reprod 2012; 27:2365.
  77. Belloc S, Cohen-Bacrie M, Amar E, et al. High body mass index has a deleterious effect on semen parameters except morphology: results from a large cohort study. Fertil Steril 2014; 102:1268.
  78. Ma J, Wu L, Zhou Y, et al. Association between BMI and semen quality: an observational study of 3966 sperm donors. Hum Reprod 2019; 34:155.
  79. Wang JX, Davies M, Norman RJ. Body mass and probability of pregnancy during assisted reproduction treatment: retrospective study. BMJ 2000; 321:1320.
  80. Crosignani PG, Ragni G, Parazzini F, et al. Anthropometric indicators and response to gonadotrophin for ovulation induction. Hum Reprod 1994; 9:420.
  81. Petersen GL, Schmidt L, Pinborg A, Kamper-Jørgensen M. The influence of female and male body mass index on live births after assisted reproductive technology treatment: a nationwide register-based cohort study. Fertil Steril 2013; 99:1654.
  82. Sermondade N, Huberlant S, Bourhis-Lefebvre V, et al. Female obesity is negatively associated with live birth rate following IVF: a systematic review and meta-analysis. Hum Reprod Update 2019; 25:439.
  83. Vural F, Vural B, Çakıroğlu Y. The Role of Overweight and Obesity in In Vitro Fertilization Outcomes of Poor Ovarian Responders. Biomed Res Int 2015; 2015:781543.
  84. Maheshwari A, Stofberg L, Bhattacharya S. Effect of overweight and obesity on assisted reproductive technology--a systematic review. Hum Reprod Update 2007; 13:433.
  85. Balen AH, Platteau P, Andersen AN, et al. The influence of body weight on response to ovulation induction with gonadotrophins in 335 women with World Health Organization group II anovulatory infertility. BJOG 2006; 113:1195.
  86. Al-Azemi M, Omu FE, Omu AE. The effect of obesity on the outcome of infertility management in women with polycystic ovary syndrome. Arch Gynecol Obstet 2004; 270:205.
  87. Souter I, Baltagi LM, Kuleta D, et al. Women, weight, and fertility: the effect of body mass index on the outcome of superovulation/intrauterine insemination cycles. Fertil Steril 2011; 95:1042.
  88. Rittenberg V, Seshadri S, Sunkara SK, et al. Effect of body mass index on IVF treatment outcome: an updated systematic review and meta-analysis. Reprod Biomed Online 2011; 23:421.
  89. Zhang D, Zhu Y, Gao H, et al. Overweight and obesity negatively affect the outcomes of ovarian stimulation and in vitro fertilisation: a cohort study of 2628 Chinese women. Gynecol Endocrinol 2010; 26:325.
  90. Fedorcsák P, Dale PO, Storeng R, et al. Impact of overweight and underweight on assisted reproduction treatment. Hum Reprod 2004; 19:2523.
  91. Mulders AG, Laven JS, Eijkemans MJ, et al. Patient predictors for outcome of gonadotrophin ovulation induction in women with normogonadotrophic anovulatory infertility: a meta-analysis. Hum Reprod Update 2003; 9:429.
  92. Moragianni VA, Jones SM, Ryley DA. The effect of body mass index on the outcomes of first assisted reproductive technology cycles. Fertil Steril 2012; 98:102.
  93. Zaadstra BM, Seidell JC, Van Noord PA, et al. Fat and female fecundity: prospective study of effect of body fat distribution on conception rates. BMJ 1993; 306:484.
  94. Rittenberg V, Sobaleva S, Ahmad A, et al. Influence of BMI on risk of miscarriage after single blastocyst transfer. Hum Reprod 2011; 26:2642.
  95. Wang JX, Davies MJ, Norman RJ. Obesity increases the risk of spontaneous abortion during infertility treatment. Obes Res 2002; 10:551.
  96. Showell MG, Brown J, Clarke J, Hart RJ. Antioxidants for female subfertility. Cochrane Database Syst Rev 2013; :CD007807.
  97. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Dietary fatty acid intakes and the risk of ovulatory infertility. Am J Clin Nutr 2007; 85:231.
  98. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Iron intake and risk of ovulatory infertility. Obstet Gynecol 2006; 108:1145.
  99. Chavarro JE, Rich-Edwards JW, Rosner B, Willett WC. A prospective study of dairy foods intake and anovulatory infertility. Hum Reprod 2007; 22:1340.
  100. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Diet and lifestyle in the prevention of ovulatory disorder infertility. Obstet Gynecol 2007; 110:1050.
  101. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Protein intake and ovulatory infertility. Am J Obstet Gynecol 2008; 198:210.e1.
  102. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Use of multivitamins, intake of B vitamins, and risk of ovulatory infertility. Fertil Steril 2008; 89:668.
  103. Toledo E, Lopez-del Burgo C, Ruiz-Zambrana A, et al. Dietary patterns and difficulty conceiving: a nested case-control study. Fertil Steril 2011; 96:1149.
  104. Vujkovic M, de Vries JH, Lindemans J, et al. The preconception Mediterranean dietary pattern in couples undergoing in vitro fertilization/intracytoplasmic sperm injection treatment increases the chance of pregnancy. Fertil Steril 2010; 94:2096.
  105. Wise LA, Wesselink AK, Tucker KL, et al. Dietary Fat Intake and Fecundability in 2 Preconception Cohort Studies. Am J Epidemiol 2018; 187:60.
  106. Nassan FL, Chiu YH, Vanegas JC, et al. Intake of protein-rich foods in relation to outcomes of infertility treatment with assisted reproductive technologies. Am J Clin Nutr 2018; 108:1104.
  107. Mendiola J, Torres-Cantero AM, Moreno-Grau JM, et al. Food intake and its relationship with semen quality: a case-control study. Fertil Steril 2009; 91:812.
  108. Zampieri N, Zamboni C, Ottolenghi A, Camoglio FS. The role of lifestyle changing to improve the semen quality in patients with varicocele. Minerva Urol Nefrol 2008; 60:199.
  109. Afeiche MC, Bridges ND, Williams PL, et al. Dairy intake and semen quality among men attending a fertility clinic. Fertil Steril 2014; 101:1280.
  110. Abadia L, Chiu YH, Williams PL, et al. The association between pre-treatment maternal alcohol and caffeine intake and outcomes of assisted reproduction in a prospectively followed cohort. Hum Reprod 2017; 32:1846.
  111. Machtinger R, Gaskins AJ, Mansur A, et al. Association between preconception maternal beverage intake and in vitro fertilization outcomes. Fertil Steril 2017; 108:1026.
  112. Lyngsø J, Kesmodel US, Bay B, et al. Impact of female daily coffee consumption on successful fertility treatment: a Danish cohort study. Fertil Steril 2019; 112:120.
  113. Green BB, Daling JR, Weiss NS, et al. Exercise as a risk factor for infertility with ovulatory dysfunction. Am J Public Health 1986; 76:1432.
  114. Gudmundsdottir SL, Flanders WD, Augestad LB. Physical activity and fertility in women: the North-Trøndelag Health Study. Hum Reprod 2009; 24:3196.
  115. Wise LA, Rothman KJ, Mikkelsen EM, et al. A prospective cohort study of physical activity and time to pregnancy. Fertil Steril 2012; 97:1136.
  116. Morris SN, Missmer SA, Cramer DW, et al. Effects of lifetime exercise on the outcome of in vitro fertilization. Obstet Gynecol 2006; 108:938.
  117. Bullen BA, Skrinar GS, Beitins IZ, et al. Induction of menstrual disorders by strenuous exercise in untrained women. N Engl J Med 1985; 312:1349.
  118. Ellison PT. Salivary steroids and natural variation in human ovarian function. Ann N Y Acad Sci 1994; 709:287.
  119. Puder JJ, Monaco SE, Sen Gupta S, et al. Estrogen and exercise may be related to body fat distribution and leptin in young women. Fertil Steril 2006; 86:694.
  120. Prentice AM, Jebb SA. Obesity in Britain: gluttony or sloth? BMJ 1995; 311:437.
  121. Rich-Edwards JW, Spiegelman D, Garland M, et al. Physical activity, body mass index, and ovulatory disorder infertility. Epidemiology 2002; 13:184.
  122. Wise LA, Cramer DW, Hornstein MD, et al. Physical activity and semen quality among men attending an infertility clinic. Fertil Steril 2011; 95:1025.
  123. Matthiesen SM, Frederiksen Y, Ingerslev HJ, Zachariae R. Stress, distress and outcome of assisted reproductive technology (ART): a meta-analysis. Hum Reprod 2011; 26:2763.
  124. Katyal N, Poulsen CM, Knudsen UB, Frederiksen Y. The association between psychosocial interventions and fertility treatment outcome: A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol 2021; 259:125.
  125. Practice Committee of the American Society for Reproductive Medicine. Smoking and infertility: a committee opinion. Fertil Steril 2012; 98:1400.
  126. Howe G, Westhoff C, Vessey M, Yeates D. Effects of age, cigarette smoking, and other factors on fertility: findings in a large prospective study. Br Med J (Clin Res Ed) 1985; 290:1697.
  127. Hughes EG, Lamont DA, Beecroft ML, et al. Randomized trial of a "stage-of-change" oriented smoking cessation intervention in infertile and pregnant women. Fertil Steril 2000; 74:498.
  128. Hughes EG, Brennan BG. Does cigarette smoking impair natural or assisted fecundity? Fertil Steril 1996; 66:679.
  129. Curtis KM, Savitz DA, Arbuckle TE. Effects of cigarette smoking, caffeine consumption, and alcohol intake on fecundability. Am J Epidemiol 1997; 146:32.
  130. Augood C, Duckitt K, Templeton AA. Smoking and female infertility: a systematic review and meta-analysis. Hum Reprod 1998; 13:1532.
  131. Bolumar F, Olsen J, Boldsen J. Smoking reduces fecundity: a European multicenter study on infertility and subfecundity. The European Study Group on Infertility and Subfecundity. Am J Epidemiol 1996; 143:578.
  132. Bouyer J, Coste J, Fernandez H, Job-Spira N. [Tobacco and ectopic pregnancy. Arguments in favor of a causal relation]. Rev Epidemiol Sante Publique 1998; 46:93.
  133. Cramer DW, Barbieri RL, Xu H, Reichardt JK. Determinants of basal follicle-stimulating hormone levels in premenopausal women. J Clin Endocrinol Metab 1994; 79:1105.
  134. Adena MA, Gallagher HG. Cigarette smoking and the age at menopause. Ann Hum Biol 1982; 9:121.
  135. Paszkowski T, Clarke RN, Hornstein MD. Smoking induces oxidative stress inside the Graafian follicle. Hum Reprod 2002; 17:921.
  136. Sinkó I, Mórocz M, Zádori J, et al. Effect of cigarette smoking on DNA damage of human cumulus cells analyzed by comet assay. Reprod Toxicol 2005; 20:65.
  137. Sharpe RM, Franks S. Environment, lifestyle and infertility--an inter-generational issue. Nat Cell Biol 2002; 4 Suppl:s33.
  138. Weinberg CR, Wilcox AJ, Baird DD. Reduced fecundability in women with prenatal exposure to cigarette smoking. Am J Epidemiol 1989; 129:1072.
  139. Storgaard L, Bonde JP, Ernst E, et al. Does smoking during pregnancy affect sons' sperm counts? Epidemiology 2003; 14:278.
  140. Vine MF. Smoking and male reproduction: a review. Int J Androl 1996; 19:323.
  141. Zitzmann M, Rolf C, Nordhoff V, et al. Male smokers have a decreased success rate for in vitro fertilization and intracytoplasmic sperm injection. Fertil Steril 2003; 79 Suppl 3:1550.
  142. Nizard J. [What are the epidemiological data on maternal and paternal smoking?]. J Gynecol Obstet Biol Reprod (Paris) 2005; 34 Spec No 1:3S347.
  143. Hassan MA, Killick SR. Negative lifestyle is associated with a significant reduction in fecundity. Fertil Steril 2004; 81:384.
  144. Jensen TK, Hjollund NH, Henriksen TB, et al. Does moderate alcohol consumption affect fertility? Follow up study among couples planning first pregnancy. BMJ 1998; 317:505.
  145. Eggert J, Theobald H, Engfeldt P. Effects of alcohol consumption on female fertility during an 18-year period. Fertil Steril 2004; 81:379.
  146. Hakim RB, Gray RH, Zacur H. Alcohol and caffeine consumption and decreased fertility. Fertil Steril 1998; 70:632.
  147. Olsen J, Bolumar F, Boldsen J, Bisanti L. Does moderate alcohol intake reduce fecundability? A European multicenter study on infertility and subfecundity. European Study Group on Infertility and Subfecundity. Alcohol Clin Exp Res 1997; 21:206.
  148. Juhl M, Nyboe Andersen AM, Grønbaek M, Olsen J. Moderate alcohol consumption and waiting time to pregnancy. Hum Reprod 2001; 16:2705.
  149. Rostad B, Schei B, Sundby J. Fertility in Norwegian women: results from a population-based health survey. Scand J Public Health 2006; 34:5.
  150. Tolstrup JS, Kjaer SK, Holst C, et al. Alcohol use as predictor for infertility in a representative population of Danish women. Acta Obstet Gynecol Scand 2003; 82:744.
  151. Parazzini F, Chatenoud L, Di Cintio E, et al. Alcohol consumption is not related to fertility in Italian women. BMJ 1999; 318:397.
  152. Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Caffeinated and alcoholic beverage intake in relation to ovulatory disorder infertility. Epidemiology 2009; 20:374.
  153. Rossi BV, Berry KF, Hornstein MD, et al. Effect of alcohol consumption on in vitro fertilization. Obstet Gynecol 2011; 117:136.
  154. Lyngsø J, Ramlau-Hansen CH, Bay B, et al. Low-to-moderate alcohol consumption and success in fertility treatment: a Danish cohort study. Hum Reprod 2019; 34:1334.
  155. Nagy F, Pendergrass PB, Bowen DC, Yeager JC. A comparative study of cytological and physiological parameters of semen obtained from alcoholics and non-alcoholics. Alcohol Alcohol 1986; 21:17.
  156. Gomathi C, Balasubramanian K, Bhanu NV, et al. Effect of chronic alcoholism on semen--studies on lipid profiles. Int J Androl 1993; 16:175.
  157. Emanuele MA, Emanuele NV. Alcohol's effects on male reproduction. Alcohol Health Res World 1998; 22:195.
  158. Zhang S, Wang L, Yang T, et al. Parental alcohol consumption and the risk of congenital heart diseases in offspring: An updated systematic review and meta-analysis. Eur J Prev Cardiol 2020; 27:410.
  159. Mueller BA, Daling JR, Weiss NS, Moore DE. Recreational drug use and the risk of primary infertility. Epidemiology 1990; 1:195.
  160. Nassan FL, Arvizu M, Mínguez-Alarcón L, et al. Marijuana smoking and outcomes of infertility treatment with assisted reproductive technologies. Hum Reprod 2019; 34:1818.
Topic 5411 Version 54.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟