Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease

Area of Science:

• Environmental epigenetics
• Developmental origins of health and disease (DOHaD)

Background:

• Early life environment quality is linked to noncommunicable disease (NCD) risk in humans.
• Animal models reveal epigenetic mechanisms, including DNA methylation and histone modifications, underlie stable, gene-specific phenotypic changes in offspring.
• These epigenetic alterations occur at individual CpG dinucleotides.

Purpose of the Study:

• To review recent advances in understanding the mechanisms of early life origins of disease.
• To contextualize these findings within a broader life-course perspective.

Main Methods:

• Review of existing literature on epigenetic regulation and early life exposures.
• Analysis of studies investigating the impact of nutritional interventions on phenotype and epigenotype.

Main Results:

• Epigenetic modifications are key mediators of environmentally induced phenotypic changes.
• Nutritional interventions (e.g., folic acid, methyl donors) can alter induced phenotypes and epigenotypes.
• Interventions show promise for reducing NCD risk but require careful design.

Conclusions:

• Epigenetic regulation plays a critical role in the developmental origins of NCDs.
• Nutritional strategies may offer a pathway to mitigate risks associated with early life exposures.
• Further research and cautious implementation are needed for effective interventions.