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Does breast feeding influence liver biochemistry?
Marianne Hørby Jørgensen1, Peter Ott, Anders Juul
1Department of Paediatrics, Hillerød Hospital, Hillerød, Denmark.
Insights
Breastfeeding may elevate aspartate aminotransferase (AST) and bilirubin in infants, but not indicate liver disease. Human milk factors may induce hepatocytes, supported by higher albumin and AST-IGF-I association.
Area of Science:
- Pediatric Gastroenterology
- Neonatal Nutrition
- Biochemistry
Background:
- Breastfed infants have higher hyperbilirubinemia risk than formula-fed infants.
- Early feeding practices may influence infant liver biochemistry.
- Understanding feeding mode's impact on liver enzymes is crucial for infant health.
Purpose of the Study:
- To investigate the effect of feeding mode on liver biochemistry in healthy term infants.
- To compare liver enzyme levels between breast-fed and formula-fed infants.
- To explore potential factors influencing liver biochemistry based on diet.
Main Methods:
- Longitudinal study of healthy term infants with monthly feeding mode questionnaires.
- Blood samples collected at 2, 6, and 9 months of age.
- Assessed liver biochemistry (albumin, alkaline phosphatase, lactic dehydrogenase, AST, bilirubin), IGF-I, and IGFBP-3.
Main Results:
- Higher mean AST and bilirubin levels observed in breast-fed infants at 2 and 6 months.
- Elevated mean albumin levels in breast-fed infants at 2 months.
- No significant differences in alkaline phosphatase, IGF-I, IGFBP-3, or lactic dehydrogenase between groups; AST correlated positively with IGF-I at 2 months.
Conclusions:
- Elevated AST in breast-fed infants is unlikely due to CMV, vitamin K deficiency, or macromolecular AST, as no other liver disease signs were present.
- The study speculates that factors in human milk may induce hepatocytes, leading to higher AST levels.
- Higher albumin and the AST-IGF-I association support the hypothesis of hepatocyte induction by human milk components.
Objective:
It is assumed that early feeding can affect liver biochemistry because breast-fed infants have a higher risk of hyperbilirubinemia than formula-fed infants. The authors sought to determine how feeding mode affected liver biochemistry in healthy term infants.
Methods:
Healthy term infants were followed up during infancy with a monthly questionnaire about feeding mode. Blood samples were obtained at 2, 6, and 9 months. Liver biochemistry (serum albumin, alkaline phosphatase, lactic dehydrogenase, aspartate aminotransferase [AST], and bilirubin), total insulin-like growth factor 1 (IGF-I), and insulin growth factor binding protein 3 (IGFBP-3) were determined at all ages.
Results:
Mean AST and bilirubin were significantly higher in breast-fed infants at 2 and 6 months. In addition, mean albumin levels were higher in breast-fed infants at 2 months. Alkaline phosphatase, IGF-I, IGFBP-3, and lactic dehydrogenase levels did not differ between the feeding groups. AST levels did not correlate significantly with bilirubin, albumin, alkaline phosphatase, or lactic dehydrogenase values. There was a strong positive association between AST and IGF-I at 2 months (r = 0.47, P = 0.004).
Conclusion:
Cytomegalovirus infection, vitamin K deficiency, and macromolecular forms of AST could be an explanation for a higher AST level among breast-fed infants. However, no other clinical or paraclinical sign of liver disease was seen, all infants were given oral vitamin K, and the AST did not rise to levels comparable to those seen in individuals with macromolecular AST. The authors speculate the most likely explanation of the elevated AST is induction of hepatocytes by factors in human milk. This is supported by the higher albumin levels in breast-fed infants and the positive association between AST and IGF-I.
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