In Utero Life and Epigenetic Predisposition for Disease

Abstract

Regulatory regions of the human genome can be modified through epigenetic processes during prenatal life to make an individual more likely to suffer chronic diseases when they reach adulthood. The modification of chromatin and DNA contributes to a larger well-documented process known as “programming” whereby stressors in the womb give rise to adult onset diseases, including cancer. It is now well known that death from ischemic heart disease is related to birth weight; the lower the birth weight, the higher the risk of death from cardiovascular disease as well as type 2 diabetes and osteoporosis. Recent epidemiological data link rapid growth in the womb to metabolic disease and obesity and also to breast and lung cancers. There is increasing evidence that “marked” regions of DNA can become “unmarked” under the influence of dietary nutrients. This gives hope for reversing propensities for cancers and other diseases that were acquired in the womb. For several cancers, the size and shape of the placenta are associated with a person’s cardiovascular and cancer risks as are maternal body mass index and height. The features of placental growth and nutrient transport properties that lead to adult disease have been little studied. In conclusion, several cancers have their origins in the womb, including lung and breast cancer. More research is needed to determine the epigenetic processes that underlie the programming of these diseases.

Developmental programming of the metabolic syndrome - critical windows for intervention

“…There is increasing evidence that "marked" regions of DNA can become "unmarked" under the influence of dietary nutrients. This gives hope for reversing propensities for metabolic disorders and other diseases that were acquired in the womb [101] . Experimental data in rodents and recent observations in humans suggest that epigenetic changes in regulatory and growth-related genes play a significant role in mediating the patho-physiological phenotypes derived from developmental programming [102,103] .…”

Placental and Cord Blood Methylation of Genes Involved in Energy Homeostasis: Association With Fetal Growth and Neonatal Body Composition

“…Although DNA methylation has traditionally been viewed as an epigenetic "silencing" mark, recent advances suggest that the impact of DNA methylation on gene expression depends more on the genomic location of the CpG site (7). An adverse intrauterine environment can modify placental epigenetic marks and gene expression profiles, resulting in fetal growth restraint (8)(9)(10). Differential patterns of placental and cord blood methylation and/or expression have been described in selected imprinted and nonimprinted genes (11,12) in heterogeneous populations, including preterm infants (11) and growth-restricted fetuses from pregnancies complicated by hypertension or preeclampsia (12).…”

Вплив Екзогенних Факторів На Геномний Імпринтинг . 1. Вплив Дієти І Забезпеченості Мікронутрієнтами Матері На Геномний Імпринтинг Нащадків

“…В настоящее время представлены научные до-казательства того, что характер питания и опреде-ленные ингредиенты продуктов питания матери могут индуцировать эпигенетические изменения генома плода, детерминирующие развитие не-обратимых изменений его фенотипа [30,33,42]. Влияние питания матери на функционирование эпигенетических механизмов ребенка носит неод-нозначный характер.…”