title: In utero Programming of Allergic Susceptibility.
abstract: BACKGROUND
  Around 30-40% of the world's population will experience allergy, the most common and earliest-onset noncommunicable disease. With a steady rise in the incidence of allergic disease over recent decades, up to 18% of children will suffer a respiratory, food or skin allergy before their 18th birthday. There is compelling evidence that the risk of developing allergy is influenced by early life events and particularly in utero exposures.
  
  
  METHODS
  A comprehensive literature review was undertaken which outlines prenatal risk factors and potential mechanisms underlying the development of allergy in childhood.
  
  
  RESULTS
  Exposures including maternal cigarette smoking, preterm birth and Caesarean delivery are implicated in predisposing infants to the later development of allergy. In contrast, restricted growth in utero, a healthy maternal diet and a larger family size are protective, but the mechanisms here are unclear and require further investigation.
  
  
  CONCLUSIONS
  To ameliorate the allergy pandemic in young children, we must define prenatal mechanisms that alter the programming of the fetal immune system and also identify specific targets for antenatal interventions.
authors.affiliation: Robinson Research Institute and School of Medicine, University ofAdelaide, Adelaide, S.A., Australia.
authors.forename: Jessica A
authors.initials: JA
authors.lastname: Grieger
authors.forename: Vicki L
authors.initials: VL
authors.lastname: Clifton
authors.forename: Astrud R
authors.initials: AR
authors.lastname: Tuck
authors.forename: Amy L
authors.initials: AL
authors.lastname: Wooldridge
authors.forename: Sarah A
authors.initials: SA
authors.lastname: Robertson
authors.forename: Kathryn L
authors.initials: KL
authors.lastname: Gatford
mesh_terms: D000818:Animals; D019175:DNA Methylation; D004032:Diet; D019587:Dietary Supplements; D004198:Disease Susceptibility; D044127:Epigenesis, Genetic; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology*; D007112:Immunity, Maternally-Acquired; D007231:Infant, Newborn; D018811:Maternal Exposure / Q000009:adverse effects; D010920:Placenta / Q000276:immunology / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors