Although this book and most other work on obesity and reproductive health focuses on women, there is a growing body of literature demonstrating adverse effects of obesity on male reproductive function [6]. Obese men have decreased testosterone and gonadotropin levels, and increased circulating estrogen levels [6]. The increase in estrogen is likely secondary to peripheral aromatization of androgens. As estrogen negatively feedbacks onto the hypothalamus, a hypogonadotropic hypogonad state is created leading to lower sperm counts, poorer sperm quality, and increased rates of erectile dysfunction [6–9]. Increase in local heat secondary to obesity also impairs spermatogenesis [10]. Ultimately sperm from obese men can contribute to poor embryo quality [11]. Due to a paucity of data on the topic, we do not formally address male obesity and reproductive function in this book, but we look forward to seeing future research in this area.

It is generally accepted that obesity adversely affects female reproductive function [12–14]. However, the mechanisms are not fully understood and are a popular area of research. Obesity likely affects reproductive health through a cumulative process starting with abnormalities in the hypothalamic–pituitary–ovarian (HPO) axis. Abnormal signalling through the hypothalamus and pituitary may affect follicular recruitment and influence subsequent oocyte quality thus contributing to overall subfertility in obese women. Studies of women undergoing assisted reproductive technologies (ART) provide a unique opportunity for direct visualization of reproductive tissues in obese women and have demonstrated that obesity also has direct effects on oocytes, embryos and on the endometrium. Several retrospective studies have associated obesity with increased risk for miscarriage in spontaneous conceptions [15], as well as in obese women receiving donor oocytes after IVF [16, 17]. The pathophysiology underlying this association is complex and likely multifactorial, involving the oocyte, embryonic development, and the endometrium.

Ultimately, obese women who conceive spontaneously or with ART are at increased risk for adverse pregnancy outcomes, including preeclampsia, gestational diabetes, fetal growth abnormalities, stillbirth, congenital abnormalities, and the need for cesarean delivery [10, 18]. Patients and their physicians must be aware of the additional risks obesity confers in pregnancy and outline a plan of care including counseling preconceptionally, antepartum, intrapartum and post-partum in order to decrease morbidity. Ensuring obese women are using the most effective methods of contraception until they are ready to conceive is also important to reduce unintended pregnancy and subsequently obesity-related morbidities.

Aside from fertility and pregnancy concerns, evidence demonstrates that obesity may influence the timing of puberty, the transition to menstrual cyclicity, and ovarian aging. The mechanisms by which obesity influences these transitions are not fully understood, but we have recruited experts in reproductive biology and reproductive specialists involved in the clinical care of obese women to summarize the current understanding of obesity’s impact on female reproductive health.

Perhaps the most concerning information presented in the chapters that follow is that highlighting the fact that obesity’s adverse effects are likely transgenerational (see Chap. 5). Children born to obese mothers are at increased risk for obesity, diabetes and cardiovascular disease later in life [19]. This is possibly secondary to epigenetic modifications of the embryonic genome in response to the alterations of the in utero environment caused by obesity.