Epigenetics and the Burden of Noncommunicable Disease: A Paucity of Research in Africa

Abstract

Epidemiological evidence suggests that an adverse in utero environment is associated with an increased risk for developing adult onset diseases. The molecular mechanisms for susceptibility to chronic noncommunicable diseases are not fully understood, although recent research has proposed that epigenetic modifications play an important role in fetal programming. Genetic and environmental factors contribute to interindividual and spatiotemporal tissue-specific methylation patterns. Although the diverse environments and high genetic diversity of African populations provide unparalleled potential to investigate the effects of environmental change on the epigenetic profile in humans, only a small percentage of genomic and epigenetic studies have focused on populations from this continent. This emphasizes the need to build capacity in Africa for research that leads to an understanding of the association between genetic, epigenetic and environmental risk factors for noncommunicable diseases on the continent.

Keywords::

• Africa
• DNA methylation
• epigenetics
• epigenome-wide association studies

Disclaimer

M Ramsey is a South African Research Chair in Genomics and Bioinformatics of African Populations hosted by the University of the Witwatersrand, funded by the Department of Science and Technology and administered by the National Research Foundation of South Africa (NRF). AH is supported by an NIH Fogarty Training Fellowship. The content of the review is solely the responsibility of the authors and does not necessarily represent the official views of the Fogarty International Centre, the NIH or the NRF.

Financial & competing interests disclosure

The authors wish to acknowledge support from the National Health Laboratory Service and the Sydney Brenner Institute of Molecular Bioscience, as well as a training grant from the Fogarty International Centre (1D43TW008330) (NIH) which supported A Hobbs. 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

The authors wish to acknowledge support from the National Health Laboratory Service and the Sydney Brenner Institute of Molecular Bioscience, as well as a training grant from the Fogarty International Centre (1D43TW008330) (NIH) which supported A Hobbs. 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.