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Breast milk jaundice

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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In the breastfed infant, prolongation of unconjugated hyperbilirubinemia into the third and later weeks of life in the healthy newborn is a normal and regularly occurring extension of physiologic jaundice. This is known as breastmilk jaundice (1,2)

  • breast milk jaundice, benign unconjugated hyperbilirubinaemia associated with breast feeding, is a common cause of prolonged jaundice in the otherwise healthy breastfed infant born at term
  • at least one third of all breastfed infants are clinically jaundiced in the third week of life and that two thirds have significant unconjugated hyperbilirubinemia in the third week (1)
  • breast milk jaundice presents in the first or second week of life, and can persist for as long as 12 weeks before spontaneous resolution (2)

Breast milk jaundice is a relatively common cause of prolonged neonatal jaundice. It was thought to be due to a complex steroid in breast milk, 3-alpha, 20-beta pregnanediol, which inhibits hepatic glucuronyl transferase but no definitive cause has been identified. Mild jaundice may last for weeks.


  • recognition that at least two thirds of all breastfed infants will have serum bilirubin concentrations in the third week of life that are significantly higher than the adult normal value is an important foundation for diagnosis
  • diagnosis of breastmilk jaundice can usually be made in the healthy, thriving breastfed infant with good weight gain in whom hemolysis and other pathologic causes of jaundice have been ruled out by clinical or laboratory study


  • clinical management of the infant with breastmilk jaundice is of considerable interest and importance
  • interruption of breast feeding to diagnose breast milk jaundice is not advised
    • cessation of breast feeding, however brief, may jeopardise an infant's ability to return to exclusive breast feeding, which is unnecessarily harmful to the infant and traumatic for parents
    • a trial of breastfeeding cessation may be falsely reassuring
      • may obscure a potentially serious underlying aetiology for prolonged hyperbilirubinaemia e.g a breastfed infant in whom breast milk jaundice occurs concomitantly with G6PD deficiency may exhibit clinical improvement in jaundice when breast feeding is discontinued, and a potentially significant underlying condition may go undiagnosed
  • infants with breast milk jaundice require no treatment if clinically well and if the total serum bilirubin concentration remains below that recommended for phototherapy
    • if total bilirubin exceeds 200 µmol/l (12 mg/dl), further investigation and the diagnosis of breast milk jaundice alone cannot be made. In the event of a negative investigation and persistent hyperbilirubinaemia above 200 µmol/l (12 mg/dl), then consider the possibility of the additional presence of an UGT 1A1(uridine diphosphate glucuronosyltransferase 1A1) mutation or G6PD deficiency
    • for total serum bilirubin over 350 µmol/l (20 mg/dl), treatment with phototherapy is recommended


  • in the hepatocyte, bilirubin undergoes conjugation via the hepatic enzyme UGT 1A1 (uridine diphosphate glucuronosyltransferase 1A1)
  • mothers should be encouraged to continue with breast feeding as the condition resolves spontaneously
  • breast milk jaundice may be confused for jaundice due to fluid deprivation
    • insufficient caloric intake resulting from maternal and/or infant breastfeeding difficulties may also increase serum unconjugated bilirubin concentrations. This is the infantile equivalent of adult starvation jaundice. It is known as breastfeeding jaundice or "breast-nonfeeding jaundice."
    • great majority of full -term breastfed infants who developed kernicterus had excessive weight loss of more than 10%, suggesting a period of lethargy and poor feeding, possibly secondary to the rising serum bilirubin


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