Fels Institute for Cancer Research & Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Epigenomics. 2012 Aug;4(4):383-402. doi: 10.2217/epi.12.31.
Over the last decade, we have witnessed an explosion of information on genetic factors underlying common human diseases and disorders. This 'human genomics' information revolution has occurred as a backdrop to a rapid increase in the rates of many human disorders and diseases. For example, obesity, Type 2 diabetes, asthma, autism spectrum disorder and attention deficit hyperactivity disorder have increased at rates that cannot be due to changes in the genetic structure of the population, and are difficult to ascribe to changes in diagnostic criteria or ascertainment. A likely cause of the increased incidence of these disorders is increased exposure to environmental factors that modify gene function. Many environmental factors that have epidemiological association with common human disorders are likely to exert their effects through epigenetic alterations. This general mechanism of gene-environment interaction poses special challenges for individuals, educators, scientists and public policy makers in defining, monitoring and mitigating exposures.
在过去的十年中，我们见证了大量关于常见人类疾病和障碍遗传因素的信息的爆发。随着许多人类疾病和障碍的发生率迅速增加，这种“人类基因组学”信息革命发生了。例如，肥胖、2 型糖尿病、哮喘、自闭症谱系障碍和注意缺陷多动障碍的发病率增加的速度不能归因于人口遗传结构的变化，也很难归因于诊断标准或确定的变化。这些疾病发病率增加的一个可能原因是，人们接触到了更多可以改变基因功能的环境因素。许多与常见人类疾病有流行病学关联的环境因素可能通过表观遗传改变来发挥作用。这种基因-环境相互作用的一般机制给个体、教育工作者、科学家和公共政策制定者在定义、监测和减轻暴露方面带来了特殊挑战。
