Jaundice causes a yellowish discoloration of the skin and the whites of the eyes due to elevated bilirubin levels (hyperbilirubinemia) in the blood. Bilirubin is a yellow pigment produced when red blood cells break down, and the newborn’s immature liver often processes this substance slowly. This condition is common, affecting approximately 60% of full-term and 80% of preterm infants in the first week of life. While most jaundice is transient and resolves, a significant portion of cases are linked specifically to breastfeeding.
Types of Jaundice in Breastfed Infants
The term “breastfed jaundice” is often used broadly, but medical professionals distinguish between two separate conditions based on timing and underlying cause: breastfeeding jaundice and breast milk jaundice. Both result in unconjugated hyperbilirubinemia, meaning the bilirubin has not yet been processed by the liver.
Breastfeeding Jaundice (Early-Onset)
Breastfeeding jaundice, also called suboptimal intake jaundice, typically appears in the first week of life. It is caused by insufficient milk intake, often due to poor latch, inadequate supply, or infrequent feedings. Reduced fluid and caloric intake lead to mild dehydration and slower bowel movements, preventing bilirubin excretion. This lack of excretion causes bilirubin to be reabsorbed into the bloodstream from the intestines.
Breast Milk Jaundice (Late-Onset)
Breast milk jaundice is a late-onset condition that generally appears after the first week of life, often peaking around two to three weeks, and can persist for a month or longer. Infants with this type are usually feeding well, gaining weight appropriately, and producing normal amounts of urine and stool. This condition is related to components within the milk that interfere with bilirubin metabolism, unlike breastfeeding jaundice, which is a function of inadequate intake.
The Role of Breast Milk in Bilirubin Processing
The mechanism behind breast milk jaundice involves the enterohepatic circulation, where bilirubin cycles between the liver, the intestine, and the bloodstream. After the liver conjugates bilirubin to make it water-soluble for excretion, it is passed into the intestine. In newborns, an enzyme called beta-glucuronidase is highly active in the intestine, and its presence is significantly higher in breastfed infants.
This enzyme works by “deconjugating” the bilirubin, reversing the liver’s processing step, which turns the water-soluble form back into its fat-soluble, unconjugated form. Once unconjugated, the bilirubin can be easily reabsorbed through the intestinal wall and returned to the bloodstream, raising the serum level. Components within breast milk, such as beta-glucuronidase and certain nonesterified fatty acids, are thought to promote this deconjugation or inhibit the liver’s ability to initially conjugate the bilirubin, prolonging the condition.
Specific milk components, including an unusual progesterone metabolite or high levels of epidermal growth factor, have also been investigated for their potential to inhibit the liver enzyme responsible for conjugation or increase intestinal absorption. Additionally, a genetic predisposition, such as a mutation in the UGT1A1 gene, is often identified in infants with prolonged breast milk jaundice. This combination of an infant’s genetic makeup and the unique composition of breast milk contributes to a slower decline in bilirubin levels than is seen in formula-fed infants.
Diagnosis, Treatment, and Long-Term Outlook
Diagnosis of hyperbilirubinemia begins with a physical assessment of the infant’s skin color, followed by objective measurement of bilirubin levels. Screening is often performed using a transcutaneous bilirubinometer (TcB), a non-invasive device that measures bilirubin by shining light through the skin. If the TcB reading is high, a definitive total serum bilirubin (TSB) level is confirmed via a blood test.
Medical professionals use age-specific nomograms to plot the TSB level and determine the risk zone for the infant, helping to differentiate between physiological jaundice, the two types of breastfed jaundice, and pathological conditions.
Treatment Approaches
For cases of early-onset breastfeeding jaundice, the treatment focuses on optimizing feeding by increasing frequency, aiming for 8 to 12 feeds per day, and correcting any latch or supply issues, often with the help of a lactation specialist. This ensures adequate hydration and caloric intake to promote regular stooling and bilirubin excretion.
If TSB levels reach a threshold that poses a risk of neurotoxicity, the infant is treated with phototherapy, where special blue-green lights convert the unconjugated bilirubin into water-soluble isomers that the body can excrete without liver processing.
In cases of breast milk jaundice where levels are very high, a brief 12- to 48-hour interruption of breastfeeding, known as a “break test,” may be recommended, though this is now less common. This temporary switch to formula or expressed milk allows healthcare providers to observe a rapid drop in bilirubin, confirming the diagnosis.
The long-term outlook for infants with breast milk jaundice is generally excellent, as it is a benign, self-limiting condition that rarely causes permanent harm. The jaundice typically resolves spontaneously, often by 4 to 12 weeks of age, and continued breastfeeding is recommended in almost all cases.
Parents should seek immediate medical attention if the baby is lethargic, has a high-pitched cry, is feeding poorly, or if the yellowing of the skin spreads rapidly or to the palms and soles of the feet. These signs may indicate that bilirubin levels are approaching a threshold that risks a rare but severe complication known as kernicterus, which can cause permanent brain damage.