DETERMINANTS OF MALE AND FEMALE FECUNDITY AND FERTILITY-DATA COORDINATING CENTER

为了解决越来越多的人认识到许多试图怀孕的夫妇都不成功的问题，进行了一项预期怀孕研究，以确定男性和女性生育力和生育力的决定因素。以前涉及实验动物和野生动物种群的研究报告了与暴露于环境激素活性物质(HAAs)有关的一系列不利生殖和发育影响。尽管公众越来越关注化学品和环境污染物对人类生殖的影响，因此推动了这一研究，但几乎没有基于人口的流行病学研究解决这一问题。此外，还研究了几种据称会影响人类生殖的生活方式行为。这将是美国第一个使用基于夫妇的方法来研究生育和生育的决定因素的研究，特别是评估生活方式和哈斯之间的相互作用。由于目前只有患病率数据，它将是第一个估计不孕不育发病率的机构。这项研究的成功完成将有助于揭示人类生殖力和生育力受损的机制。 招募了501对希望怀孕的夫妇，并前瞻性地跟踪了12个高危月经周期，以确定HAAS和生活方式因素是否影响受孕、早孕丢失和不孕的概率。夫妇们完成了基线访谈，并提供了大约20毫升的血液，用于分析HAAs和香烟烟雾、咖啡因和膳食补充剂的代谢物。男性伴侣提供精液样本，以客观评估男性的繁殖力。情侣们使用日记记录日常香烟、酒精、咖啡因和膳食补充剂的使用情况，以及身体活动、生活压力源和性行为。指导妇女使用家庭生育监测仪和怀孕试剂盒来确定排卵(筛查雌二醇和黄体生成素)和hCG确认的怀孕。鉴于对夫妇的跟踪调查现已完成，数据目前正在分析中。 这是美国第一次使用基于夫妇的方法来研究生育力和生育力的决定因素，特别是评估生活方式和环境中的激素活性物质之间的相互作用。随后的数据将与负责对环境物质进行生殖和发育毒性分类的监管机构以及回应公众对环境化学品对怀孕结局和生殖健康影响的日益关注的公共卫生机构直接相关。这项研究还首次讨论了膳食补充剂对生殖和发育过程的影响，以及这种影响是由母亲、父亲还是父母中介的。这项研究直接回应了NICHD的战略框架，解决了先入为主、围产期和宫内对人类生殖和发育的影响。它响应了NICHD-S的几个目标(即，生殖健康的后遗症，增加良好生育结局的可能性，并帮助描绘健康差距的发展根源)。

To address growing recognition that many couples attempting pregnancy are unsuccessful, a prospective pregnancy study was conducted to identify determinants of male and female fecundity and fertility. Previous studies involving experimental animals and wildlife populations report a spectrum of adverse reproductive and developmental effects associated with exposure to environmental hormonally active agents (HAAs). Virtually no population based epidemiologic studies have addressed this issue, despite increasing public concern about the effect of chemicals and environmental contaminants on human reproduction and, thereby, serves as the impetus for study. In addition, several lifestyle behaviors alleged to affect human reproduction were studied as well. This will be the first study in the US to use a couple-based approach to study determinants of fecundity and fertility and, specifically, to assess the interplay between lifestyle and HAAs. It will be the first to estimate the incidence of infertility as only prevalence data currently exist. Successful completion of this study will help delineate mechanisms that underlie impaired human fecundity and fertility. A cohort of 501 couples desiring pregnancy were recruited and prospectively followed for 12 at- risk menstrual cycles to determine whether HAAs and lifestyle factors affect the probability of conception, early pregnancy loss, and infertility. Couples completed baseline interviews and provided approximately 20 ml of blood for the analysis of HAAs and metabolites of cigarette smoke, caffeine, and dietary supplements. Male partners provided semen samples for an objective assessment of male fecundity. Couples use journals to record daily use of cigarettes, alcohol, caffeine, and dietary supplements as well as physical activity, life stressors and intercourse. Women were instructed in the use of home fertility monitors and pregnancy kits to determine ovulation (screening for estradiol and LH) and hCG-confirmed pregnancies. The data are currently being analyzed, given that follow up of couples is now complete. This is the first study in the US to use a couple-based approach to study determinants of fecundity and fertility and, specifically, to assess the interplay between lifestyle and hormonally active agents in the environment. The ensuing data will be directly relevant to regulatory agencies charged with classifying environmental agents as to reproductive and developmental toxicity, and public health agencies that respond to growing public concern about the effects of environmental chemicals on pregnancy outcomes and reproductive health. This study is also the first to address the effect of dietary supplements on reproductive and developmental processes and whether the effect is maternally, paternally or parentally mediated. The study is directly responsive to the strategic framework of NICHD by addressing preconception, periconception and in utero influences on human reproduction and development. It is responsive to several of NICHD¿s goals (viz., sequelae of reproductive health, increasing the probability of good birth outcomes, and helping to delineate the developmental origins of health disparities).