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Epigenetics: an accessible mechanism through which to track and respond to an obesogenic environment

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Abstract

Obesity and its consequences impact everyone. Obesity occurs because of an interaction between an obesogenic environment and genetics. In order to confront obesity, we must understand the contribution of each of these components. Environmental influences on obesity include our extrinsic environment, such as food deserts, as well as our intrinsic environment, like perinatal exposures. Epigenetics provides a biological mechanism to reveal the accumulation of extrinsic and intrinsic environmental exposures from fetal life to adulthood. Human and animal studies demonstrate changes in epigenetic modifications which are associated with an obesogenic environment. Furthermore, evidence exists in humans and animal models that suggest environmental epigenetics may serve as a biomarker or a target for intervention. To successfully target obesity, we must intervene on an environmental as well as genetic level. Combating food deserts for example will help to change the extrinsic environment, while targeting epigenetic modification remains a goal for changing our biology.

Financial & competing interests disclosure

This work was supported by Medical College of Wisconsin, Children’s Hospital of Wisconsin. 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.

Key issues

  • An obesogenic environment contributes to the obesity pandemic through food deserts and the life course model.

  • The life course model states that health results from the interaction of genetics and accumulated risk factors including social, physical, cultural, behavioral and ancestral factors that may be manifested through environmental epigenetics.

  • Environmental epigenetics change and adapt to the environment. Human studies focused on DNA CpG methylation reveal associations between maternal obesity and methylation changes in imprinted genes, nonimprinted genes, as well as genome-wide studies in the offspring.

  • Animal models reveal that a maternal obesogenic environment can change epigenetic patterns in both the periphery and in the CNS throughout life and contribute to offspring phenotype.

  • Animal models may provide insight into the treatment of obesity by revealing genetic targets through transgenic animals, micronutrient supplementation and through taste preference programming.

  • Progress towards the resolution of the obesity pandemic depends on changing the obesogenic environment including food deserts and interpreting the meaning of epigenetic marks as they change with the environment.

  • You cannot change your genetics, but you can change your epigenetics.

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