An estimated 5-20% of premenopausal women are affected by polycystic ovary syndrome (PCOS) across the globe. Not only is it one of the leading causes of infertility, but a significant number of females with PCOS also exhibit metabolic abnormalities, leading to higher risks for development of metabolic syndrome, cardiovascular disease, gestational diabetes, as well as type 2 diabetes. While the exact cause of PCOS is unknown, it has been determined that PCOS is characterized by methyl group imbalances. Methyl group metabolism involves several substrates and cofactors. Specifically, sources of methyl groups include methionine, betaine and choline, while the cofactors involved include the B-vitamins folate, B12, and B6. Disruption to the interplay of these key nutrients may have significant consequences on gene expression. Dietary eggs are considered an excellent food source for these key nutrients, particularly choline. Thus we propose to use two models of PCOS, a genetic and chemically-induced model to characterize abnormal metabolism of these pathways, thus forming a potential mechanistic link between methyl groups, epigenetic modifications, metabolic complications and PCOS owing to methyl group insufficiency. This hypothesis provides a strategic means by which dietary intervention, via whole egg consumption, can manage PCOS as well as its complications.
The purpose of this study is to more clearly understand how whole egg consumption influences polycystic ovary syndrome (PCOS) and establish its impact on the metabolic complications associated with PCOS. This knowledge will influence future dietary guidelines and intervention strategies to improve management of PCOS.
