Evidence for the intra-uterine programming of adiposity in later life

Ann Hum Biol. 2011 Jul;38(4):410-28. doi: 10.3109/03014460.2011.592513. Epub 2011 Jun 17.


Aim: Research in animals has shown that altering foetal nutrition by under-nourishing or over-nourishing the mother or rendering her diabetic or foetal exposure to glucocorticoids and toxins can programme obesity in later life. The increased adiposity is mediated by permanent changes in appetite, food choices, physical activity and energy metabolism. In humans, increased adiposity has been shown in people who experienced foetal under-nutrition due to maternal famine or over-nutrition due to maternal diabetes. Lower birth weight (a proxy for foetal under-nutrition) is associated with a reduced adult lean mass and increased intra-abdominal fat. Higher birth-weight caused by maternal diabetes is associated with increased total fat mass and obesity in later life. There is growing evidence that maternal obesity, without diabetes, is also a risk factor for obesity in the child, due to foetal over-nutrition effects. Maternal smoking is associated with an increased risk of obesity in the children, although a causal link has not been proven. Other foetal exposures associated with increased adiposity in animals include glucocorticoids and endocrine disruptors.

Conclusions: Reversing the current obesity epidemic will require greater attention to, and better understanding of, these inter-generational (mother-offspring) factors that programme body composition during early development.

MeSH terms

  • Adiposity / physiology*
  • Adult
  • Animals
  • Female
  • Fetus / physiology*
  • Humans
  • Maternal-Fetal Relations
  • Models, Animal
  • Nutritional Status
  • Obesity / embryology*
  • Obesity / epidemiology
  • Obesity / etiology*
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / pathology