Editing Maternal effect (section)

===High protein diet during gestation correlated with higher blood pressure and adiposity===
Further studies have examined the epigenetic changes resulting from a high protein/low carbohydrate diet during pregnancy.  This diet caused epigenetic changes that were associated with higher blood pressure, higher [[cortisol]] levels, and a heightened [[Hypothalamic–pituitary–adrenal axis|Hypothalamic-pituitary-adrenal (HPA) axis]] response to stress.  Increased methylation in the 11β-hydroxysteroid dehydrogenase type 2 (HSD2), [[Glucocorticoid receptor|glucocorticoid receptor (GR)]], and [[H19 (gene)|H19]] ICR were positively correlated with adiposity and blood pressure in adulthood.  Glucocorticoids play a vital role in tissue development and maturation as well as having effects on metabolism.  Glucocorticoids’ access to GR is regulated by HSD1 and HSD2.  H19 is an imprinted gene for a [[Long non-coding RNA|long coding RNA (lncRNA)]], which has limiting effects on body weight and cell proliferation.  Therefore, higher methylation rates in H19 ICR repress transcription and prevent the lncRNA from regulating body weight.  Mothers who reported higher meat/fish and vegetable intake and lower bread/potato intake in late pregnancy had a higher average methylation in GR and HSD2.  However, one common challenge of these types of studies is that many epigenetic modifications have tissue and cell-type specificity DNA methylation patterns.  Thus, epigenetic modification patterns of accessible tissues, like peripheral blood, may not represent the epigenetic patterns of the tissue involved in a particular disease.<ref>{{cite journal |vauthors=Drake AJ, McPherson RC, Godfrey KM, Cooper C, [[Karen A. Lillycrop|Lillycrop KA]], Hanson MA, Meehan RR, Seckl JR, Reynolds RM |title=An unbalanced maternal diet in pregnancy associates with offspring epigenetic changes in genes controlling glucocorticoid action and foetal growth |journal=Clinical Endocrinology |volume=77 |issue=6 |pages=808–15 |year=2012 |pmid=22642564 |doi=10.1111/j.1365-2265.2012.04453.x |s2cid=28199749 |doi-access=free }}</ref>