Handbook of Fertility: Nutrition, Diet, Lifestyle and Reproductive Health

413 Pages·2015·24.52 MB·English

by  Ronald Ross Watson

HANDBOOK
OF FERTILITY
NUTRITION, DIET, LIFESTYLE
AND REPRODUCTIVE HEALTH
Edited by
Ronald Ross Watson
University of Arizona, Arizona Health Sciences Center, Tucson, AZ, USA
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List of Contributors
José-Alfonso Abecia, DVM, MSc, PhD Universidad de Aletta Dorothea Esterhuizen, PhD TUPS Stress,
Zaragoza, Zaragoza, Spain Medfem Fertility Clinic, Bryanston, Johannesburg,
Ashok Agarwal, PhD Center for Reproductive Medicine, South Africa
Cleveland Clinic, Cleveland, Ohio, USA Sandro C. Esteves, MD, PhD ANDROFERT, Referral Center
Diana Anderson, PhD University of Bradford, Medical for Male Reproduction, Campinas, SP, Brazil
Sciences, Bradford, West Yorkshire, UK Enrico Facchiano, MD Azienda Sanitaria di Firenze, Santa
Susana Astiz, MVD, PhD, Dip ECBHM INIA, Madrid, Maria Nuova Hospital, Florence, Italy
Spain Fabio Facchinetti, MD Policlinico Hospital – University of
Adolf Baumgartner, PhD University of Bradford, Medical Modena and Reggio-Emilia, Modena, Italy
Sciences, Bradford, West Yorkshire, UK Daniela Paes de Almeida Ferreira Braga, DVM, MSc
Fertility – Assisted Fertilization Centre; Sapientiae
Ranveer Singh Bedwal, MSc, PhD Cell Biology Laboratory,
Institute – Educational and Research Centre in Assisted
Department of Zoology, University of Rajasthan, Jaipur,
Reproduction, São Paulo, SP – Brazil
India
J. Gual Frau, MD Bs Urology Department, Corporació
Zulfiqar A. Bhutta, PhD, MBBS, FRCPCH, FAAP Robert
Sanitària Parc Taulí, Institut Universitari Parc Taulí,
Harding Chair in Global Child Health and Policy, Centre
Sabadell, Spain
for Global Child Health, Hospital for Sick Children,
Toronto, Canada Tod Fullston, BSc (Hons), PhD University of Adelaide,
South Australia, Australia
Edson Borges Jr., MD, PhD Fertility – Assisted Fertilization
Centre; Sapientiae Institute – Educational and Research C. Abad Gairín, MD Bs Urology Department, Corporació
Centre in Assisted Reproduction, São Paulo, SP – Brazil Sanitària Parc Taulí, Institut Universitari Parc Taulí,
Sabadell, Spain
Edolene Bosman, MSc TUPS Stress, Medfem Fertility
Clinic, Bryanston, Johannesburg, South Africaa Kathryn Gebhardt, PhD Repromed; University of Adelaide,
Adelaide, South Australia, Australia
Jean D. Brender, PhD, RN, FACE Texas A&M Health
Science Center, College Station, Texas, USA Antonio Gonzalez-Bulnes, MVD, PhD INIA, Madrid,
Spain
Cynthia H. Chuang, MD, MSc Penn State College of
Medicine, Hershey, Pennsylvania, USA Jaime Gosalvez, PhD Universidad Autonoma de Madrid,
Madrid, Spain
Frank H. Comhaire, MD, PhD Fertility-Belgium Centre,
Belgium N. Hannaoui Hadi, MD Bs Urology Department,
Corporació Sanitària Parc Taulí, Institut Universitari Parc
Giovanni Corona, MD, PhD University of Florence,
Taulí, Sabadell, Spain
Florence; Azienda Usl Bologna Maggiore-Bellaria Hospital,
Bologna, Italy Batool A. Haider, MD, MSc, ScD Harvard School of Public
Health, Boston, Massachusetts, USA
Giulia Dante, MD Policlinico Hospital – University of
Modena and Reggio-Emilia, Modena, Italy Roger Hart, MD School of Women’s and Infants’ Health,
University of Western Australia, King Edward Memorial
Wim A.E. Decleer, MD Fertility-Belgium Centre, Belgium
Hospital, Perth, Western Australia, Australia; Fertility
Michael C. Dennedy, MD, PhD Galway Diabetes Research Specialists of Western Australia, Bethesda Hospital, Perth,
Centre; National University of Ireland, Galway, Ireland Western Australia, Australia
Sejal Doshi, MD Northeastern Ohio Medical University, Annemieke Hoek, MD, PhD Department of Obstetrics
Rootstown, Ohio, USA; Center for Reproductive Medicine, and Gynecology, University Medical Center Groningen,
Cleveland Clinic, Cleveland, Ohio, USA Groningen, The Netherlands
Damayanthi Durairajanayagam, PhD Department of Muhammad Sameem Javed, BSc, MSc University of
Physiology, Faculty of Medicine, MARA University of Agriculture, Faisalabad, Pakistan
Technology, Selangor, Malaysia
Ammar Ahmad Khan, BSc, MSc University of Agriculture,
Aoife M. Egan, MB, BCh, BAO Galway Diabetes Research Faisalabad, Pakistan
Centre, Galway, Ireland
Dariusz Kokoszyn´ski, PhD Department of Poultry
Omer Erdeve, MD Ankara University School of Medicine Breeding and Animal Products Evaluation, University of
Children’s Hospital, Ankara, Turkey Technology and Life Sciences, Bydgoszcz, Poland
xi
xii LIST OF CONTRIBUTORS
Jennifer L. Kraschnewski, MD, MPH Penn State College of Sayali Chintamani Ranade, PhD National Brain Research
Medicine, Hershey, Pennsylvania, USA Centre, Manesar, Haryana, India
Walter K. Kuchenbecker, MBChB Isala Fertility Center, Muhammad Atif Randhawa, BSc, MSc, PhD University of
Isala Clinics, Zwolle, The Netherlands Agriculture, Faisalabad, Pakistan
Deepa Kumari, MSc, PhD Cell Biology Laboratory, Leonardo Reis, MD, MSc, PhD University of Campinas;
Department of Zoology, University of Rajasthan, Jaipur, India Pontifical Catholic University of Campinas, Campinas SP,
Lesia O. Kurlak, PhD University of Nottingham, Brazil
Nottingham, UK Francisco Antonio Rodrigues, MBBCh TUPS Stress, Medfem
Abbie Laing, MBChB King Edward Memorial Hospital, Fertility Clinic, Bryanston, Johannesburg, South Africa
Perth, Western Australia, Australia Mandy J. Rodrigues, MA TUPS Stress, Medfem Fertility
Fiona Langdon, MBBS King Edward Memorial Hospital, Clinic, Bryanston, Johannesburg, South Africa
Perth, Western Australia, Australia Edmund S. Sabanegh, MD Glickman Urological and Kidney
J.L.M.R. Leroy, MSc, PhD-student Gamete Research Centre, Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA
Veterinary Physiology and Biochemistry, Department of Muhammad Wasim Sajid, BSc, MSc University of
Veterinary Sciences, University of Antwerp, Belgium Agriculture, Faisalabad, Pakistan
Marcello Lucchese, MD Azienda Sanitaria di Firenze, Santa Giulia Scaravelli, MD, PhD National Health Institute,
Maria Nuova Hospital, Florence, Italy Rome, Italy
Michaela Luconi, PhD University of Florence, Florence, Italy Thomas Ernst Schmid, PhD Klinikum rechts der Isar,
Mario Maggi, MD University of Florence, Florence, Italy Technische Universität München, Department of
Radiooncology, Germany
Ana Meikle, DVM, MSc, PhD Universidad de la República,
Montevideo, Uruguay Cecilia Sosa, DVM, MSc, PhD Universidad de Zaragoza,
Zaragoza, Spain
Hiten D. Mistry, PhD University of Bern, Berne,
Switzerland Roberta Spoletini, PhD National Health Institute, Rome,
Italy
Ricardo Miyaoka, MD, PhD University of Campinas,
Lakshana Sreenivasan, BSc The University of Arizona,
Campinas SP; ANDROFERT, Referral Center for Male
Arizona, USA
Reproduction, Campinas SP; Sumaré State Hospital,
Sumaré SP, Brazil Helena J. Teede, MBBS, PhD, FRACP Monash University;
Diabetes and Vascular Medicine, Monash Health, Victoria,
Lisa J. Moran, BSc (Hons), BND, PhD University of Adelaide,
Australia
South Australia; Monash University, Victoria, Australia
Gülcan Türker, MD Kocaeli University, Kocaeli, Turkey
Aditi Mulgund, MD Northeastern Ohio Medical
University, Rootstown; Center for Reproductive Medicine, Eva Tvrda, PhD Center for Reproductive Medicine,
Cleveland Clinic, Cleveland, Ohio, USA Cleveland Clinic, Cleveland, Ohio, USA; Department of
Animal Physiology, Slovak University of Agriculture, Nitra,
Neena Nair, MSc, PhD Cell Biology Laboratory, Department
Slovakia
of Zoology, University of Rajasthan, Jaipur, India
S.D.M. Valckx, PhD Gamete Research Centre, Veterinary
Isabella Neri, MD Policlinico Hospital – University of
Physiology and Biochemistry, Department of Veterinary
Modena and Reggio-Emilia, Modena, Italy
Sciences, University of Antwerp, Belgium
Mehmet Yekta Oncel, MD Zekai Tahir Burak Maternity
Carolina Viñoles, DVM, MSc, PhD Instituto Nacional de
Teaching Hospital, Ankara, Turkey
Investigación Agropecuaria, Tacuarembó, Uruguay
A. García Peiró, PhD Centro de Infertilidad Masculina y
Anna Wilkanowska, MSc Department of Agricultural,
Análisis de Barcelona (CIMAB), Edifici Eureka, Bellaterra,
Environmental and Food Sciences, University of Molise,
Spain
Campobasso, Italy
Karen P. Phillips, PhD Interdisciplinary School of Health
Linda Wu, BPharmSc, PhD University of Adelaide, South
Sciences, University of Ottawa, Ottawa, Ontario, Canada
Australia, Australia
Alan Scott Polackwich Jr., MD Glickman Urological and
Deirdre Zander-Fox, PhD Repromed; University of
Kidney Institute, Cleveland Clinic Foundation, Cleveland,
Adelaide, Adelaide, South Australia, Australia
Ohio, USA
Preface
Many factors affect fertility, positively and negatively. written by Michaela Luconi, Giovanni Corona, Enrico
Toxins and contaminants are important in cell functions Facchiano, Marcello Lucchese, and Mario Maggi shows
and the growth of eggs. that surgery to reduce weight has a positive effect in
male fertility via improvements in hormone levels. Tod
Fullston, Linda Wu, Helena J. Teede, and Lisa J. Moran
SECTION A: OVERVIEW ON FERTILITY
broadly review the role of obesity in men as well as women
in reproductive dysfunction. Michael Conall Dennedy re-
Karen P. Phillips describes the public’s perception of views obesity per se and gestational outcomes.
environmental risks, especially those that affect the ability
to conceive and carry to birth. Diana Anderson, Thomas
Ernst Schmid, and Adolf Baumgartner focus on the well- SECTION C: EXERCISE AND LIFESTYLE
known role of mothers who use tobacco. This leads to IN FERTILITY
transgenerational damage in the offspring. Mehmet Y.
Oncel and Omer Erdeve review the role of tobacco smok- Ashok Agarwal and Damayanthi Durairajanayagam
ing on after conception and its damage on fetal health, and review lifestyle factors and reproductive health. Anna
they describe a key mechanism – serum folate levels. S. D. Wilkanowska and Dariusz Kokoszyński use animal mod-
M. Valckx and J. L. M. R. Leroy approach this issue in an- els wherein animals are not purposely exercised. They
other way by evaluating the effects of maternal metabolic review the normal activity of farm animals on their health
health. Then they evaluate the effects of maternal health and reproductive performance. Jennifer L. Kraschnewski
as well as diet on follicular fluid composition. Finally, they describes the data and mechanism of the effects of physi-
review the consequences on the embryo as well as the oo- cal activity on gestational weight gain. Clearly, exercise
cyte. Gülcan Türker reviews heavy metals, such as mercu- can change the growth and body mass. Walter K. Kuchen-
ry, which are well known major toxins. He describes their becker and Annemieke Hoek review lifestyles to modu-
actions on preterm mortality and morbidity. Jean D. Bren- late ovulation. Lifestyle intervention was able to increase
der reviews common materials on foods, like bacon, and ovulation in anovulatory women, especially those with
known to cause cancer. They review nitrate and nitrite, obesity or infertility. Finally, A. Gonzalez-Bulnes reviews
which are metabolites of foods that mothers consume, and reproduction learned from animal models.
nitrosable drugs for their effects on congenital malforma-
tions. Giulia Scaravelli and Roberta Spoletini describe the
SECTION D: NUTRITION
application of reproductive techniques on worldwide epi-
AND REPRODUCTION
demiology phenomenon and treatment outcomes. Frank
H. Comhaire and W. A. E. Decleer discuss the effect of en-
vironmental hormone disrupters on infertility. Then the In chapter “Green Leafy Vegetables: A Health Promot-
authors review strategies to reverse the effects of agents ing Source” written by Muhammad Atif Randhawa, A.
affecting hormones. Finally, Carolina Viñoles, Cecilia Khan, Muhammad Sameem Javed, and Wasim Sajid be-
Sosa, Ana Meikle, and José-Alfonso Abecia review animal gin the reviews of food, metabolism, and nutrition on
models where experimental studies can be done. They fertility. They found that green leafy vegetables, as with
review damage to embryos during nutritional supple- most health situations, are very helpful for the promotion
mentation in animal models. Finally, they review human of infants’ health. Leonardo Reis and Ricardo Miyaoka
embryo losses and nutrition and nutritional deficiencies. found nutrition lifestyle and obesity in urology. Batool
A. Haider and Zulfiqar A. Bhutta describe the role of
multiple micronutrients in perinatal health and mortal-
SECTION B: BARIATRIC SURGERY, ity reduction. Similarly, Lakshana Sreenivasan and Ron-
OBESITY, AND FERTILITY ald R. Watson found that nutrition and hormones have
a role in male infertility. S. C. Ranade found that nutri-
Humans are more frequently obese, which affects male tion had effects on the development and programming
and female fertility. In chapter “Fertility and Testosterone of neurological systems. Fabio Facchinetti, Giulia Dante,
Improvement in Male Patients After Bariatric Surgery” and Isabella Neri review herbs and their components in
xiii
xiv Preface
dietary supplements that affect delivery and conception. outcomes. They emphasize hyperinsulinemia on male
Nutrition supplements also affect pregnancy. Hiten D. regulation of in vitro fertilization.
Mistry and Lesia O. Kurlak review a key nutrient with
the potential to provide toxicity with too much consump-
tion. They found that selenium affects reproduction and SECTION F: NUTRITION, LIFESTYLE,
fertility. It may function in part by antioxidant activity. AND MALE FERTILITY
Finally, Aditi Mulgund, Sejal Doshi, and Ashok Agarwal
found a role for antioxidant stress in endometriosis, Clearly, the needs of males for fertility are differ-
while Ashok Agarwal, Eva Tvrda, and Aditi Mulgund ent from females. Deepa Kumari, Neena Nair, and R.S.
found that oxidative stress promotes preeclampsia. Bedwal found that zinc deficiency changed testicular
apoptosis. Inadequate cell division is a serious inhibition
to sperm growth. Edson Borges Jr. and Daniela Braga
SECTION E: NUTRITION AND LIFESTYLE found that environmental factors, food intake, and so-
IN IN VITRO FERTILIZATION cial habits modify male patients and their relationship
to intracytoplasmic sperm injection outcomes. Alan Po-
In vitro fertilization has been shown to be affected by lackwich and Edmund S. Sabanegh Jr. review the role of
nutrition and lifestyle. Mandy J. Rodrigues and Francisco over-the-counter supplements in male infertility as diet
Antonio Rodrigues review the regulation and manage- and medicines do not have to be new pharmaceutical
ment of the psychological effects of infertility. Kathryn drugs. Sandro C. Esteves and Ricardo Miyaoka review
Gebhardt and Deidre L. Zander-Fox found that the role of sperm physiology and assessment of spermatogenesis ki-
body mass index or obesity is associated with the success netics in vivo, which is critical for understanding the role
or failure on assisted reproductive treatment outcome. of lifestyle and food in cell growth for male fertility. Car-
Fiona Langdon, Abbie Laing, and Roger Hart review los Abad, N. Hannaoui Hadi, and A García Peiró discuss
the health outcomes of children conceived through as- antioxidant treatment and prevention of human sperm
sisted reproductive technology. Edolene Bosman, Aletta DNA fragmentation, specifically its role in health and
Dorothea Esterhuizen, and Francisco Antonio Rodrigues fertility. Finally, Eva Tvrda, Jaime Gosalvez, and Ashok
review chronic diseases and their influences on in vitro Agarwal review epigenetics and its role in male infertility.
Acknowledgments
The work of Dr. Watson’s editorial assistant, was graciously provided by the Natural Health
Bethany L. Stevens, in communicating with authors Research Institute (www.naturalhealthresearch.org),
and working on the manuscripts was critical to the a nonprofit health promotion institute. Finally, the
successful completion of the book. It is very much work of the librarian at the Arizona Health Science
appreciated. The encouragement, advice, and support Library, Mari Stoddard, was vital and very helpful
of Jeffrey Rossetti in Elsevier book preparation were in identifying the key researchers who participated in
very helpful. Support for Ms. Stevens and Dr. Watson the book.
xv
C H A P T E R
1
Perceptions of environmental
risks to Fertility
Karen P. Phillips, PhD
Interdisciplinary School of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada
INTRODUCTION pollution, and heavy metals are identified as risk fac-
tors to fertility [4–6] (Box 1.1). Environmental exposures
Environmental risks, including lifestyle habits, infec- and lifestyle habits represent sex-specific risks to fertil-
tious disease, and occupational exposures, are increas- ity based on differences in reproductive physiology and
ingly examined as modifiable infertility risk factors. This urogenital anatomy. Common lifestyle and environmen-
chapter will provide an overview of infertility risk fac- tal determinants of fertility and reproductive health are
tors and explain how risk perception is formed. Percep- summarized next.
tions of fertility risks within specific populations will
Lifestyle and Infertility
also be examined. Finally, a public health framework is
proposed to enhance fertility-specific health promotion Body Weight
and enable mitigation of modifiable risks to fertility. Obesity (body mass index (BMI) ≥ 30 kg/m2) is in-
creasingly described as a global phenomenon, contribut-
ing significantly to morbidity and mortality (cardiovas-
Infertility – Definitions, Manifestations,
cular disease, diabetes, mobility issues, etc.). For both
and Risk Factors
men and women, obesity contributes to hypogonadism
Infertility is generally defined as the absence of con- and other perturbations of the endocrine system that
ception after 1 year of regular, unprotected intercourse. may contribute to infertility [7–10]. Obese women have
Prevalence of current infertility in North America generally poor outcomes with assisted reproductive
ranges from 11.5% to 15.7% in Canada [1] and 15.5% technologies (ART) [11,12] including fewer metaphase
among US women [2]. The pathophysiology of infertil- II oocytes retrieved, oocyte spindle defects [13], more
ity may include genetic/chromosomal anomalies, con- canceled cycles [14], decreased fertilization [15] and de-
genital or infectious malformations of the reproductive creased live birth rates [12, 16–18]. Similarly, obesity in
tract, and endocrine disorders (hypogonadism, anovu- the male partner may be associated with decreased clini-
lation) in both men and women. Additionally, female cal pregnancy [19,20] and live birth rates [10,20]. Obese
infertility is caused by advanced age, endometriosis, women also face increased risks during pregnancy, such
polycystic ovarian syndrome, and diminished ovarian as gestational diabetes, hypertension, spontaneous abor-
reserve [3]. Infertility manifests as ovulatory dysfunc- tion, large fetuses for gestational age, and concomitant
tion, amenorrhea, implantation failure/spontaneous delivery complications [21,22]. Poor ART outcomes,
abortion, and diminished semen parameters [3]. For coupled with concerns of increased pregnancy compli-
about 10–15% of infertile couples, infertility is unex- cations in the obese mother, have prompted suggestions
plained, with minimal abnormal findings upon medi- that ART be denied to women with BMI ≥ 30–35 kg/m2
cal investigation [3]. [22]. Critics of such policies argue that greater empha-
Most modifiable risk factors can be categorized under sis should be placed on weight–hip ratio as a predictor
“environment.” Diet, lifestyle habits (cigarette smok- of reproductive risk, BMI limits are discriminatory and
ing, alcohol use), history of sexually transmitted infec- stigmatizing, and sustained weight loss is difficult to
tions (STI), pharmaceutical/medical treatments, as well achieve for many individuals [22]. Over half of American
as environmental exposures to chemicals, radiation, air men and women surveyed supported BMI limits for
Handbook of Fertility. http://dx.doi.org/10.1016/B978-0-12-800872-0.00001-9
Copyright © 2015 Elsevier Inc. All rights reserved.
3
4 1. PercePtiOns OF envirOnmental risks tO Fertility
BOX 1.1
MODIFIABLE RISKS TO INFERTILITY
• BMI > 30 mg/kg2 less evidence for
• BMI< 18 mg/kg2
• Environmental contaminants (ambient exposure
• Alcohol
levels)
• Cigarette smoke
• Caffeine
• Recurrent sexually transmitted infections
ART, citing risks of pregnancy complications in obese metabolite cotinine, and polycyclic aromatic hydro-
patients and possibility of health complications includ- carbons, such as benzo[a]pyrene (B[a]P), are examples
ing obesity in offspring [23]. BMI ART treatment limits of some of the toxic compounds contained in cigarette
have not been proposed for obese male patients. As life- smoke and have also been detected in follicular fluid
style modifications are difficult to achieve and sustain, [29,38,39]. Accumulation of toxicants in the follicular
support for weight management should be a component compartment has the potential to perturb oocyte growth,
of preconception care [11,24]. induce follicular atresia, and dysregulate necessary hor-
Underweight individuals also face fertility challenges monal support for the initiation of meiotic resumption
and may be less responsive to ART [11,21]. women with and ovulation [38,40,41].
a BMI <18 mg/kg2 are at increased risk for ovulatory Side-stream or second-hand smoke exposure is also
dysfunction and pregnancy complications, such as pre- detrimental to fertility. women exposed to side-stream
term labor. General recommendations for fertility plan- smoke or mainstream smoke face compromised ART
ning include maintenance of healthy body weight, nutri- outcomes including reductions in implantation and
tious diet, and moderate exercise [11,21,25]. pregnancy rates [39]. As described, obese women tend
to respond poorly to ART; however, obese smokers may
Tobacco
face even greater reproductive challenges [18]. Given
Tobacco smoking is a leading cause of adverse health the significant health risks posed by tobacco smok-
effects, including cancer, cardiovascular, and respiratory ing, it is clearly evident that smoking cessation should
disease. Although cigarette smoking is declining, 18.1% be recommended prior to commencement of natural
of American adults [26] and 16% of Canadian adults [27] conception or ART for both men and women [42]. En-
were smokers in 2012. Globally, tobacco use is increas- couragingly, the effects of smoking on oocyte/embryo
ing rapidly among young girls aged 13–15 years. Despite developmental potential may be transient, as former
health promotion efforts, continued use of tobacco by smokers have an increased pregnancy rate compared
these young girls may herald future increases in global with smokers [36].
rates of smoking among adult women [28]. Cigarette
Alcohol
smoke represents a well-established mixture of repro-
ductive toxicants for both men and women [29,30]. Re- Heavy alcohol consumption is generally associated
productive pathology may result from vasoconstriction, with poor fertility outcomes in both men and wom-
generation of reactive oxygen species and concomitant en, along with significant pregnancy complications
oxidative stress, and alterations in endocrine signal- and adverse fetal development [21,35]. Both moder-
ing. Male smoking is associated with decreased sperm ate (7–8 drinks/week) and low alcohol consumption
count, motility, seminal volume, and reduced ART out- (1 drink/week) may be associated with impaired fertil-
comes [31,32] – manifested at a cellular level as sperm ity [21]. Alcohol’s reproductive toxicity may be due to
DNA damage (e.g., DNA fragmentation, formation of impaired hypothalamic–pituitary–testicular signaling
DNA adduct) and pathological changes to the acrosomal manifesting as decreased semen quality [35]. Female
membrane and tail [25,33,34]. fertility may also be reduced by alcohol consumption
For women, smoking is associated with earlier age at with possible effects on the hypothalamus resulting in
menopause, premature ovarian failure, infertility, and decreased luteinizing hormone secretion and anovula-
spontaneous abortion [35]. Female smokers respond tion [35]. Alcohol’s teratogenic effects on the developing
poorly to ART gonadotropin stimulation, producing embryo and fetus have prompted general advisements
fewer oocytes with low developmental potential, and for women attempting to conceive to abstain from alco-
decreased live birth rates [18,36,37]. Cadmium, nicotine- hol [21,35].
A. OvERvIEw ON FERTIlITy
intrOductiOn 5
Caffeine urethritis, or less commonly, prostatitis or epididymitis
The literature examining effects of caffeine intake on [49,55]. Men with chlamydial infections tend to exhibit
fertility is limited by methodological issues (retrospec- diminished semen quality along with sperm DNA dam-
tive studies – recall bias of caffeine intake) and lack of age; however, it is unclear whether these deficits sig-
consensus [11,21,25,35]. The effects of caffeine consump- nificantly impair fertility [56,57]. Further study is war-
tion on prolonged time-to-pregnancy may be confound- ranted regarding the history of recurrent STI and male
ed by other negative lifestyle habits such as smoking infertility.
[11]. It is accepted that caffeine intake of <200–300 mg
Summary
per day is unlikely to cause detrimental reproductive
outcomes such as spontaneous abortion or fetal devel- In addition to the described lifestyle risks (obesity, be-
opment [21]. women who are trying to conceive or are ing underweight, alcohol, smoking, and STI), stress and
pregnant are advised to limit caffeine intake to 100– anxiety prior to ART have also been proposed as infertil-
200 mg per day [21]. ity risk factors [30,58]. Men and women planning to con-
ceive should optimize fertility by maintaining a healthy
Sexually Transmitted Infections
body weight, abstaining from excessive alcohol or caf-
STI risk is particularly high in adolescents and feine intake, and be supported to quit smoking. Sexual
young adults. Despite mandatory sexual health educa- health promotion strategies (education, screening, con-
tion in public schools in Canada [43], increased rates of dom distribution) enable early detection and treatment
infection with Chlamydia trachomatis and Neisseria gon- of STI, thereby preventing later fertility issues.
orrhoeae have been reported [44]. In the United States,
public school sexual health education varies by state Environmental Disruption of Reproductive Health
[45] with regional, ethnic, and race disparities evident Reproductive and developmental health are adversely
in STI prevalence [46]. Rates of chlamydial infections affected by ionizing radiation, heavy metals, lead, indus-
have continued to rise in many European countries de- trial chemicals/solvents, temperature, and contaminated
spite implementation of screening programs [47]. Re- food and water (biological/chemical) [4,6] (Fig. 1.1). It is
current STI within high-risk groups, safe sex fatigue, also biologically plausible, though there is less evidence,
high-risk sexual encounters facilitated by social media, that exposures to air pollution [6,59,60], electromagnetic
and lack of awareness of long-term consequences of or radiofrequency fields (wiFi [61], cell phones [62,63]),
STI, such as cancer and infertility, may explain these along with social environmental factors, particularly dis-
trends [48]. parities in socioeconomic status (SES) and social stress
STI are caused by viruses, bacteria, and other patho- [64–66], impair human reproduction and development.
gens. Although viral infections may pose risks for repro- Endocrine disrupters are perhaps the most widely stud-
ductive health, most studies have emphasized bacterial ied environmental modulators of fertility and reproduc-
STI as risks to fertility. Although isolated infections of tive health, with effects demonstrated in wildlife, labora-
C. trachomatis or N. gonorrhoeae pose little risk to fertil- tory animals, and humans [67,68]. Endocrine disrupters
ity or perinatal outcomes if promptly treated, for many encompass a wide range of chemical species, mixtures,
men and women, STI may be asymptomatic, which may and compounds including phytoestrogens, pesticides,
preclude medical interventions [47,49]. women with a industrial chemicals, and by-products [67,69]. Endocrine
history of bacterial STI may experience inflammatory disrupters have been linked to adverse health effects
obstructions of the reproductive tract (pelvic inflamma- including infertility, abnormal prenatal and childhood
tory disease – PID), including scarring of the fallopian development (spontaneous abortion, male reproductive
tubes – a major cause of female infertility and risk factor tract abnormalities and other birth defects, sex ratios,
for ectopic pregnancy [50]. PID had been strongly associ- precocious puberty), and reproductive cancers (prostate,
ated with chlamydial and gonorrheal infections; howev- breast, ovarian, endometrial, and testicular) [67,71]. It is
er, rates of PID seem to be decreasing along with related hypothesized that global declines in men’s reproductive
complications such as tubal factor infertility and ectopic health characterized by poor semen quality, urogenital
pregnancy [47,51–53]. A history of recurrent chlamydial birth defects (cryptorchidism, hypospadias), and testicu-
or gonorrheal infections remains a significant risk fac- lar cancer, collectively called “testicular dysgenesis syn-
tor for these reproductive tract pathologies [47,50]; how- drome,” are caused by exposures to endocrine disrupt-
ever, improved screening and prompt treatment may be ers [67,70,71].
responsible for reducing the rates of these complications Endocrine disruption represents one of the most plau-
even in high-risk groups [52]. sible mechanisms by which environmental chemical
The relationship between bacterial STI and male in- exposures may adversely affect reproductive capacity
fertility is less clear [54]. Bacterial STI gain entry to the [67,69,71]. Molecular mechanisms of these contaminants
reproductive tract via urogenital passages, producing may include endocrine receptor agonists, antagonists,
A. OvERvIEw ON FERTIlITy