The Epigenetic Lorax: Gene–Environment Interactions in Human Health

Abstract

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.

KEYWORDS::

• aging
• behavior
• DNA methylation
• endocrine disruptors
• maternal diet
• windows of sensitivity

Financial&competing interests disclosure

Research in the authors‘ laboratories is supported in part by grants from the NIH National Institute of Child Health and Development (HD43092; KE Latham), the NIH Office of the Director, Comparative Medicine Branch, Office of Research Infrastructure Program, R24OD012221-12 (KE Latham), U54HD068157 (C Sapienza), and RO1GM093066 and K22CA140361-3 (N Engel). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Research in the authors‘ laboratories is supported in part by grants from the NIH National Institute of Child Health and Development (HD43092; KE Latham), the NIH Office of the Director, Comparative Medicine Branch, Office of Research Infrastructure Program, R24OD012221-12 (KE Latham), U54HD068157 (C Sapienza), and RO1GM093066 and K22CA140361-3 (N Engel). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.