Maternal nutrition, intrauterine programming and consequential risks in the offspring

Rev Endocr Metab Disord. 2008 Sep;9(3):203-11. doi: 10.1007/s11154-008-9087-z. Epub 2008 Jul 26.


It is traditionally believed that genetic susceptibility and adult faulty lifestyle lead to type 2 diabetes, a chronic non-communicable disease. The "Developmental Origins of Health and Disease" (DOHaD) model proposes that the susceptibility to type 2 diabetes originates in the intrauterine life by environmental fetal programming, further exaggerated by rapid childhood growth, i.e. a biphasic nutritional insult. Both fetal under nutrition (sometimes manifested as low birth weight) and over nutrition (the baby of a diabetic mother) increase the risk of future diabetes. The common characteristic of these two types of babies is their high adiposity. An imbalance in nutrition seems to play an important role, and micronutrients seem particularly important. Normal to high maternal folate status coupled with low vitamin B(12) status predicted higher adiposity and insulin resistance in Indian babies. Thus, 1-C (methyl) metabolism seems to play a key role in fetal programming. DOHaD represents a paradigm shift in the model for prevention of the chronic non-communicable diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Diabetes Mellitus, Type 2 / etiology*
  • Diabetes Mellitus, Type 2 / genetics
  • Embryonic Development / genetics
  • Embryonic Development / physiology*
  • Epigenesis, Genetic / physiology*
  • Female
  • Humans
  • Maternal Nutritional Physiological Phenomena*
  • Models, Biological
  • Pregnancy
  • Prenatal Exposure Delayed Effects / etiology*
  • Prenatal Exposure Delayed Effects / genetics
  • Risk Factors