Environmental Epigenetics on Puberty

青春期的环境表观遗传学

• 批准号: 9048134
• 负责人: FRANK M BIRO
• 金额: $ 41.43万
• 依托单位: CINCINNATI CHILDRENS HOSP MED CTR
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-09-01 至 2017-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9048134
• 关键词: Adopted; Adult; Age; Age at Menarche; Behavior; Benchmarking; Biological Phenomena; Body Composition; Body fat; Breast; Community Outreach; Deposition; Development; Dietary intake; Dimensions; Endocrine Disruptors; Endocrine disruption; Energy Intake; Environmental Exposure; Environmental Risk Factor; Epidemiology; Epigenetic Process; Exposure to; Family Study; Fatty acid glycerol esters; Future; Genes; Genetic Polymorphism; Gonadal Steroid Hormones; Growth; Health; Height; Individual; Insulin Resistance; Knowledge; Life Style; Link; Mammary Gland Parenchyma; Mediating; Menarche; Minerals; Morbidity - disease rate; Obesity; Outcome; Participant; Pathway interactions; Physical activity; Phytoestrogens; Predisposition; Prevalence; Prevention strategy; Principal Investigator; Production; Protocols documentation; Puberty; Reporting; Risk; Series; Social Environment; Stress; Teenagers; Time; Toxic Environmental Substances; Visceral; Woman; Work; bone; chemical genetics; cohort; environmental chemical; evidence base; genetic variant; girls; high school; lipid metabolism; malignant breast neoplasm; mortality; obesity risk; outreach program; phthalates; toxicant; Adopted; Adult; Age; Age at Menarche; Behavior; Benchmarking; Biological Phenomena; Body Composition; Body fat; Breast; Community Outreach; Deposition; Development; Dietary intake; Dimensions; Endocrine Disruptors; Endocrine disruption; Energy Intake; Environmental Exposure; Environmental Risk Factor; Epidemiology; Epigenetic Process; Exposure to; Family Study; Fatty acid glycerol esters; Future; Genes; Genetic Polymorphism; Gonadal Steroid Hormones; Growth; Health; Height; Individual; Insulin Resistance; Knowledge; Life Style; Link; Mammary Gland Parenchyma; Mediating; Menarche; Minerals; Morbidity - disease rate; Obesity; Outcome; Participant; Pathway interactions; Physical activity; Phytoestrogens; Predisposition; Prevalence; Prevention strategy; Principal Investigator; Production; Protocols documentation; Puberty; Reporting; Risk; Series; Social Environment; Stress; Teenagers; Time; Toxic Environmental Substances; Visceral; Woman; Work; bone; chemical genetics; cohort; environmental chemical; evidence base; genetic variant; girls; high school; lipid metabolism; malignant breast neoplasm; mortality; obesity risk; outreach program; phthalates; toxicant

Puberty may serve as a window of susceptibility that impacts adult morbidity and mortality, and peripubertal breast tissue may be especially susceptible to environmental exposures. The majority of bone mineral is deposited during teen years, and insulin resistance rises during puberty. Visceral fat is an important factor that increases risk of obesity complications, but little is known about early factors that impact deposition of visceral fat Environmental exposures may impact body composition, as well as pubertal outcomes. Age at menarche is associated with risk of breast cancer, but pubertal growth velocity may be the underlying biologic phenomenon that impacts greater risk of breast cancer in taller women and those with earlier menarche. We will utilize a unique existing cohort of girls followed from ages 6 and 7 and who have had semiannual examinations over 3-5 years. Working closely with the other two BCERC epidemiology projects, and with the Cincinnati BCERC community outreach program, our study proposes to fill the gap towards understanding the relationships between timing of onset and pathway of puberty with menarche, interaction between endocrine disruptors and polymorphisms, and changes in body composition. We will complete the maturation assessment in this established cohort of girls, to include age at menarche, tempo of maturation, age/ value of peak height velocity, body composition and fat distribution, and bone mineral accrual during puberty, by pathway into puberty. We plan to assess dimensions of the physical/social environments including exposures to endocrine disrupting toxicants (EDCs), and how these factors contribute to impact onset of puberty and menarche. We will explore the relationships and interactions of EDCs and genetic polymorphisms, on benchmarks of pubertal maturation. The Cincinnati epidemiology and outreach programs will develop and disseminate materials for lay audiences about lifestyle choices and potential health risks of specific exposures in regard to breast cancer, and enhance protocols to report studyfindingsto study families. This proposal should allow us to understand better how changes during puberty can inform future prevention strategies to decrease the prevalence of breast cancer. RELEVANCE (See instructions): Puberty may serve as a window of susceptibility to adult morbidities and mortality, sucti as breast cancer. This protocol will continue to follow closely a group of girls recruited at ages 6 and 7, studying how the exposure to environmental factors interacts with genetic polymorphisms, and influence factors associated with breast cancer risk.

青春期可能是影响成人发病率和死亡率的敏感性窗口， 腹部乳房组织可能特别容易受到环境暴露的影响。大多数骨头 矿物质在青少年时期沉积，青春期期间胰岛素抵抗增长。内脏脂肪很重要 增加了肥胖并发症风险的因素，但对影响沉积的早期因素知之甚少 内脏脂肪环境暴露可能会影响人体成分以及青春期的结果。年龄 初潮与患乳腺癌的风险有关，但是青春期生长速度可能是基本的生物学 现象会影响较高的女性和初潮较早的女性的乳腺癌风险更大。 我们将利用一个独特的现有女孩，然后是6岁和7岁的女孩 考试超过3 - 5年。与其他两个BCERC流行病学项目紧密合作，并与 辛辛那提BCERC社区外展计划，我们的研究建议填补了解理解的空白 发病时机与青春期通路与初潮的相互作用之间的关系，内分泌之间的相互作用 破坏者和多态性以及身体成分的变化。 我们将完成这一既定女子队列的成熟评估，包括初潮的年龄 成熟的速度，峰高速度的年龄/价值，身体成分和脂肪分布以及骨矿物质 青春期期间的应计，途径进入青春期。我们计划评估身体/社会的维度 环境包括暴露于内分泌破坏毒物（EDC）的环境，以及这些因素如何促成 青春期和初潮的影响。我们将探索EDC和遗传的关系和相互作用 多态性，基于青春期成熟的基准。辛辛那提流行病学和外展计划 将开发和传播有关生活方式选择的材料，以及潜在的健康风险 关于乳腺癌的特定暴露，并增强了报告研究范围研究家庭的方案。 该建议应该使我们能够更好地了解青春期的变化如何能够告知未来 预防策略以降低乳腺癌的患病率。 相关性（请参阅说明）： 青春期可能是对成人病态和死亡率敏感的窗口，作为乳腺癌的sucti。 该协议将继续遵循一群在6岁和7岁时招募的女孩，研究如何 暴露于环境因素与遗传多态性相互作用，并影响相关的因素 乳腺癌风险。